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1
NIELSEN, METTE O., TORBEN G. MADSEN, and ANNE MARIE HEDEBOE. "Regulation of mammary glucose uptake in goats: role of mammary gland supply, insulin, IGF-1 and synthetic capacity." Journal of Dairy Research 68, no. 3 (August 2001): 337–49. http://dx.doi.org/10.1017/s002202990100499x.
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Variations in mammary glucose uptake were measured during the normal pregnancy-lactation cycle in dairy goats. In addition mammary glucose uptake was studied in response to somatotropin (ST) treatment in mid-lactation and acute increases in glucose concentration induced by sodium-propionate challenge in early lactation. Mammary glucose uptake was independent of arterial glucose, insulin and Insulin-like Growth Factor-1 (IGF-1) concentrations during lactation and during acute increases in arterial glucose concentration. Glucose uptake in the lactating mammary gland of the goat must therefore be carried out by an insulin-independent carrier, possible GLUT1, and glucose supply is not a limiting factor for uptake under in vivo conditions. Extraction of glucose uptake changed markedly during the normal course of lactation, following the overall changes in milk yield. Concentrations of glucose in skimmed milk, believed to reflect intracellular glucose concentration, changed in opposite directions, resulting in decreasing ratios of arterialratioskimmed milk glucose concentration with progressing lactation. Thus, mammary synthetic capacity also involves a capacity for glucose uptake, which may be influenced by variations in glucose carrier numbers, as well as mammary metabolic activity (intracellular glucose concentration). In contrast to the situation during the normal course of lactation, ST stimulated milk yield, despite less efficient glucose extraction.
2
Xu, Jing, Melissa A. Kirigiti, Kevin L. Grove, and M. Susan Smith. "Regulation of Food Intake and Gonadotropin-Releasing Hormone/Luteinizing Hormone during Lactation: Role of Insulin and Leptin." Endocrinology 150, no. 9 (May 21, 2009): 4231–40. http://dx.doi.org/10.1210/en.2009-0190.
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Abstract Negative energy balance during lactation is reflected by low levels of insulin and leptin and is associated with chronic hyperphagia and suppressed GnRH/LH activity. We studied whether restoration of insulin and/or leptin to physiological levels would reverse the lactation-associated hyperphagia, changes in hypothalamic neuropeptide expression [increased neuropeptide Y (NPY) and agouti-related protein (AGRP) and decreased proopiomelanocortin (POMC), kisspeptin (Kiss1), and neurokinin B (NKB)] and suppression of LH. Ovariectomized lactating rats (eight pups) were treated for 48 h with sc minipumps containing saline, human insulin, or rat leptin. The arcuate nucleus (ARH) was analyzed for NPY, AGRP, POMC, Kiss1, and NKB mRNA expression; the dorsal medial hypothalamus (DMH) was analyzed for NPY mRNA. Insulin replacement reversed the increase in ARH NPY/AGRP mRNAs, partially recovered POMC, but had no effect on recovering Kiss1/NKB. Leptin replacement only affected POMC, which was fully recovered. Insulin/leptin dual replacement had similar effects as insulin replacement alone but with a slight increase in Kiss1/NKB. The lactation-induced increase in DMH NPY was unchanged after treatments. Restoration of insulin and/or leptin had no effect on food intake, body weight, serum glucose or serum LH. These results suggest that the negative energy balance of lactation is not required for the hyperphagic drive, although it is involved in the orexigenic changes in the ARH. The chronic hyperphagia of lactation is most likely sustained by the induction of NPY in the DMH. The negative energy balance also does not appear to be a necessary prerequisite for the suppression of GnRH/LH activity.
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Metcalf, John A., and Timothy E. C. Weekes. "Effect of plane of nutrition on insulin sensitivity during lactation in the ewe." Journal of Dairy Research 57, no. 4 (November 1990): 465–78. http://dx.doi.org/10.1017/s0022029900029514.
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SummaryThe hyperinsulinaemic euglycaemic insulin clamp technique was used to compare insulin sensitivity in lactating ewes at two levels of feeding. Clamps were performed at two (restricted intake) or three (ad libitum intake) stages of lactation and also 30 d after drying off. Dose response curves for insulin were constructed using the glucose metabolic clearance rate (MCR) as the measure of glucose metabolism and these were statistically compared between stages of lactation within the feeding levels, and also between feeding regimes. Animals on a restricted feed intake showed a weight loss throughout lactation, coupled with a lower insulin sensitivity, as measured by the ED50 (concentration of insulin required to produce a half maximal increase in MCR), while those on ad libitum feeding showed a weight gain and a decreased insulin sensitivity in the dry period. Endogenous glucose production was less sensitive to inhibition by insulin in the animals subjected to restricted food intake, compared with those on the ad libitum regime, which suggested a major role for the plane of nutrition in adjusting the homeorhetic control of metabolism during lactation.
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Travers, MT, RG Vernon, and MC Barber. "Repression of the acetyl-CoA carboxylase gene in ovine adipose tissue during lactation: the role of insulin responsiveness." Journal of Molecular Endocrinology 19, no. 2 (October 1, 1997): 99–107. http://dx.doi.org/10.1677/jme.0.0190099.
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We have investigated the mechanisms whereby lipogenesis is markedly suppressed in adipose tissue depots of lactating sheep. Expression of the gene encoding acetyl-CoA carboxylase (ACC), the flux-determining enzyme of the lipogenic pathway, is reduced approximately threefold in both omental and subcutaneous adipose tissue depots during late pregnancy and remains so into lactation when compared with non-pregnant, non-lactating animals. By comparison, total ACC enzyme activity in these adipose depots is suppressed approximately 25- to 30-fold in lactation. Culture of explants from the subcutaneous depot of lactating sheep with insulin plus dexamethasone for 72 h resulted in an approximately sevenfold increase in ACC mRNA, a fivefold increase in total enzyme activity and a marked increase in the proportion of the enzyme in the active state when compared with explants cultured with no added hormones for the same period. However, there was a lag of between 32 and 48 h before marked induction of any of these parameters by insulin plus dexamethasone was observed. Induction of the alpha-tubulin gene paralleled that of the ACC gene, suggesting that cytoskeletal rearrangements are associated with the aquisition of sensitivity to insulin plus dexamethasone. These results demonstrate that the reduction in lipogenic capacity in ovine adipose tissue during lactation is related to repression of the ACC gene, both at the level of steady-state mRNA abundance and possibly at translation, as well as to suppression of the mechanisms that regulate the proportion of ACC in the active state, and these are further related to the marked insensitivity of these parameters to insulin plus dexamethasone in vitro.
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Kunjara, S., M. Sochor, N. Salih, P. McLean, and A. L. Greenbaum. "Phosphoribosyl pyrophosphate and phosphoribosyl pyrophosphate synthetase in rat mammary gland. Changes in the lactation cycle and effects of diabetes, insulin and phenazine methosulphate." Biochemical Journal 238, no. 2 (September 1, 1986): 553–59. http://dx.doi.org/10.1042/bj2380553.
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Changes in the tissue content of phosphoribosyl pyrophosphate (PPRibP), glucose 6-phosphate, ribose 5-phosphate (Rib5P), RNA and DNA, of the activity of PPRibP synthetase (EC 2.7.6.1) and the conversion of [1-14C]- and [6-14C]-glucose into 14CO2 were measured at mid-lactation in the normal and diabetic rat and in pregnancy, lactation and mammary involution in the normal rat. The PPRibP, glucose 6-phosphate and Rib5P contents increase during pregnancy and early lactation to reach a plateau value at mid-lactation, before falling sharply during weaning. The PPRibP content, PPRibP synthetase activity and flux of glucose through the oxidative pentose phosphate pathway (PPP) all change in parallel during the lactation cycle. Similarly, after 3 and 5 days duration of streptozotocin-induced diabetes, ending on day 10 of lactation, there were parallel declines in PPRibP content, PPRibP synthetase and PPP activity. The effect of streptozotocin was prevented by pretreatment with nicotinamide and partially reversed by insulin administration. Addition of insulin to lactating rat mammary-gland slices incubated in vitro significantly raised the PPRibP content (+47%) and the activity of the PPP (+40%); phenazine methosulphate, which gives a 2-fold increase in PPP activity, raised the PPRibP content of lactating mammary gland slices by approx. 3-fold. It is concluded that Rib5P, generated in the oxidative segment of the PPP, is an important determinant of PPRibP synthesis in the lactating rat mammary gland and that insulin plays a central role in the regulation of the bioavailability of this precursor of nucleotide and nucleic acid synthesis.
6
Vernon, R. G., and E. Finley. "Roles of insulin and growth hormone in the adaptations of fatty acid synthesis in white adipose tissue during the lactation cycle in sheep." Biochemical Journal 256, no. 3 (December 15, 1988): 873–78. http://dx.doi.org/10.1042/bj2560873.
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1. Lactation results in a substantial fall in the rate of fatty acid synthesis in sheep adipose tissue. 2. Maintenance of adipose tissue from non-lactating sheep in tissue culture for 24 or 48 h with insulin increased the rate of fatty acid synthesis. Dexamethasone, a glucocorticoid analogue, alone inhibited the rate of fatty acid synthesis, but enhanced the stimulatory effect of insulin. Growth hormone (somatotropin) antagonized the increase in the rate of fatty acid synthesis induced by insulin or insulin plus dexamethasone. 3. Maintenance of adipose tissue from lactating sheep in tissue culture resulted in a small increase in the rate of fatty acid synthesis after 24 h, and then a large increase in rate between 24 and 48 h of culture. The increase during the second 24 h period was dependent on the presence of insulin; this effect was enhanced by dexamethasone and inhibited by growth hormone. 4. The increase in the rate of fatty acid synthesis in tissue from non-lactating sheep and in tissue from lactating sheep during the major increase in rate was prevented by actinomycin D, an inhibitor of transcription. 5. Effects of insulin and growth hormone were observed with physiological concentrations of the hormones. 6. The study suggests that known changes in the serum concentrations of insulin and growth hormone are the primary causes of the changes in fatty acid synthesis in adipose tissue during the lactation cycle in sheep. 7. During lactation, adipose tissue becomes refractory to insulin in sheep; responsiveness is partly restored by tissue culture in the presence of insulin and dexamethasone.
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Debras, E., J. Grizard, E. Aina, S. Tesseraud, C. Champredon, and M. Arnal. "Insulin sensitivity and responsiveness during lactation and dry period in goats." American Journal of Physiology-Endocrinology and Metabolism 256, no. 2 (February 1, 1989): E295—E302. http://dx.doi.org/10.1152/ajpendo.1989.256.2.e295.
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To investigate the role of insulin in partitioning nutrients between the mammary gland and other tissues during lactation in ruminants, euglycemic-hyperinsulinemic clamps were performed in goats during early lactation (15-26 days postpartum), midlactation (78-91 days postpartum), and dry period (169-194 days postpartum). Insulin was infused at 0.4, 0.7, 1.9, 4.4, and 10 micrograms/min. Basal plasma glucose was constant during all periods despite the fact that basal glucose utilization was approximately 3 times higher during lactation than dry period. Basal plasma insulin was similar during early lactation and dry period but increased during midlactation. Insulin infusion resulted in a dose-dependent stimulation of glucose utilization. The insulin-stimulated glucose utilization above basal was greatly impaired during early lactation when compared with dry period, but this only occurred at very high plasma insulin. Insulin infusion also resulted in a decrease in glucose production; the maximal insulin effect is achieved at the lowest insulin infusion rate. The ability of insulin to decrease glucose production was significantly improved during early lactation when compared with dry period. This phenomenon may provide a mechanism to save gluconeogenic substrates during early lactation. In contrast, midlactation did not result in any significant change in insulin action with both glucose utilization and glucose production.
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Sladek, Celia D., Wanida Stevens, Zhilin Song, Ginger C. Johnson, and Paul S. MacLean. "The “metabolic sensor” function of rat supraoptic oxytocin and vasopressin neurons is attenuated during lactation but not in diet-induced obesity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 310, no. 4 (February 15, 2016): R337—R345. http://dx.doi.org/10.1152/ajpregu.00422.2015.
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The oxytocin (OT) and vasopressin (VP) neurons of the supraoptic nucleus (SON) demonstrate characteristics of “metabolic sensors”. They express insulin receptors and glucokinase (GK). They respond to an increase in glucose and insulin with an increase in intracellular [Ca2+] and increased OT and VP release that is GK dependent. Although this is consistent with the established role of OT as an anorectic agent, how these molecules function relative to the important role of OT during lactation and whether deficits in this metabolic sensor function contribute to obesity remain to be examined. Thus, we evaluated whether insulin and glucose-induced OT and VP secretion from perifused explants of the hypothalamo-neurohypophyseal system are altered during lactation and by diet-induced obesity (DIO). In explants from female day 8 lactating rats, increasing glucose (Glu, 5 mM) did not alter OT or VP release. However, insulin (Ins; 3 ng/ml) increased OT release, and increasing the glucose concentration in the presence of insulin (Ins+Glu) resulted in a sustained elevation in both OT and VP release that was not prevented by alloxan, a GK inhibitor. Explants from male DIO rats also responded to Ins+Glu with an increase in OT and VP regardless of whether obesity had been induced by feeding a high-fat diet (HFD). The HFD-DIO rats had elevated body weight, plasma Ins, Glu, leptin, and triglycerides. These findings suggest that the role of SON neurons as metabolic sensors is diminished during lactation, but not in this animal model of obesity.
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Kraetz, W. D., C. Zimmer, D. Schneider, and D. Schams. "Secretion pattern of growth hormone, prolactin, insulin and insulin-like growth factor-1 in the periparturient sow depending on the metabolic state during lactation." Animal Science 67, no. 2 (October 1998): 339–47. http://dx.doi.org/10.1017/s1357729800010110.
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AbstractThe aim of the study was to investigate the influence of different energy levels during a 4-week lactation on the regulation of the metabolic hormones somatotropin (GH), prolactin, insulin and insulin-like growth factor-1 (IGF-1). A total of 21 crossbred sows (German Landrace × Duroc) were cannulated for daily blood collection from 3 weeks before parturition until 2 weeks after weaning and for weekly window sampling (every 20 min for 10 h). Nineteen sows were given 2·8 kg food during late gestation, 5·0 kg food during lactation and 2·8 kg food per day after weaning and two sows were given food at a restricted level (3·0 kg) during lactation. In the 19 sows, the different energy balance was induced by allocation of different numbers of sucking piglets to the respective sows. One group of sows suckled seven piglets and served as a control (C; no. = 7) and another group suckled 10 to 12 piglets and was energy deficient (D). After the study, the sows of the deficient group were, based on their litter weight gain from parturition until weaning, divided into low (D-L; no. = 6) or high (D-H; no. = 6) litter weight gain. The D-H sows lost more body weight during lactation than C and had lower glucose and higher nonesterified fatty acids levels before morning feeding. GH and prolactin increased around parturition and their secretory profiles during lactation were altered by the frequent sucking stimulus, whereby the access of the piglets to their dams was not controlled. During lactation, GH and prolactin were highest in D-H sows. The results suggest a possible role of not only GH but also of prolactin in nutrient partitioning to the mammary gland just before the start of lactation and for minimizing the adverse effects of a negative energy balance. Furthermore, insulin and IGF-1 increased around parturition in all sows. Insulin was higher before and after feeding and the highest levels were found in C and D-L sows. The regulation patterns of insulin and IGF-1 indicate that the lactating sow is able to mobilize enough energy from body reserves to prevent metabolic disorders, even during a period with deficient energy supply. This is contrary to the regulation in the dairy cow, where the negative energy balance is coupled with a severe glucose deficit during phases of high milk yield, which causes decreased levels of insulin and IGF-1. In the sow, the glucose intake with the food meets the glucose requirement for metabolic pathways also during a deficient lactational energy intake. Therefore, in sows IGF-1 can be stimulated by increased GH levels via the GH receptor in the liver during a state of nutritional energy deficiency and the fact that sows can compensate a deficient metabolic state much better than cows is also reflected in the respective endocrinology.
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Sano, H., H. Arai, A. Takahashi, H. Takahashi, and Y. Terashima. "Insulin and glucagon responses to intravenous injections of glucose, arginine and propionate in lactating cows and growing calves." Canadian Journal of Animal Science 79, no. 3 (September 1, 1999): 309–14. http://dx.doi.org/10.4141/a98-115.
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Plasma insulin and glucagon responses to glucose, arginine and propionate injections were measured to establish indicators of the endocrine status in lactating cows and growing calves. The metabolites were intravenously injected at a dose of 0.625 mmol kg−1 and the time courses of changes in plasma insulin and glucagon concentrations were determined. Basal plasma glucagon concentrations were higher (P < 0.05) for lactating cows than for growing calves, while basal plasma insulin concentrations did not differ between animal groups. Concentrations of plasma insulin increased (P < 0.01) after glucose injection, whereas plasma glucagon concentrations decreased in both lactating cows (P < 0.05) and growing calves (P < 0.01). Plasma insulin and glucagon concentrations increased in response to arginine (P < 0.01) and propionate (P < 0.01 except insulin for lactating cows at P < 0.05) injections. Plasma insulin and glucagon responses were greater (P < 0.05) to arginine than to glucose or propionate. Plasma glucagon responses to arginine were greater (P < 0.05) for lactating cows than for growing calves. The insulin:glucagon molar ratio increased in response to the metabolite injections except following injections of arginine and propionate into lactating cows, when the ratio did not increase significantly. It is possible that in cows the enhanced responsiveness of glucagon secretion plays a role in the maintenance of lactation. Key words: Insulin, glucagon, arginine, propionate, lactating cow, growing calf
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Hafner, Hannah, Eric Chang, Zach Carlson, Allen Zhu, Mita Varghese, Jeremy Clemente, Simin Abrishami, et al. "Lactational High-Fat Diet Exposure Programs Metabolic Inflammation and Bone Marrow Adiposity in Male Offspring." Nutrients 11, no. 6 (June 21, 2019): 1393. http://dx.doi.org/10.3390/nu11061393.
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Overnutrition during critical windows of development plays a significant role in life-long metabolic disease risk. Early exposure to excessive nutrition may result in altered programming leading to increased susceptibility to obesity, inflammation, and metabolic complications. This study investigated the programming effects of high-fat diet (HFD) exposure during the lactation period on offspring adiposity and inflammation. Female C57Bl/6J dams were fed a normal diet or a 60% HFD during lactation. Offspring were weaned onto a normal diet until 12 weeks of age when half were re-challenged with HFD for 12 weeks. Metabolic testing was performed throughout adulthood. At 24 weeks, adipose depots were isolated and evaluated for macrophage profiling and inflammatory gene expression. Males exposed to HFD during lactation had insulin resistance and glucose intolerance as adults. After re-introduction to HFD, males had increased weight gain and worsened insulin resistance and hyperglycemia. There was increased infiltration of pro-inflammatory CD11c+ adipose tissue macrophages, and bone marrow was primed to produce granulocytes and macrophages. Bone density was lower due to enhanced marrow adiposity. This study demonstrates that maternal HFD exposure during the lactational window programs offspring adiposity, inflammation, and impaired glucose homeostasis.
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Bionaz, Massimo, and Juan J. Loor. "Gene Networks Driving Bovine Mammary Protein Synthesis during the Lactation cycle." Bioinformatics and Biology Insights 5 (January 2011): BBI.S7003. http://dx.doi.org/10.4137/bbi.s7003.
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A crucial role for both insulin and mTOR in the regulation of milk protein synthesis is emerging. Bovine mammary biopsies harvested during late-pregnancy through end of subsequent lactation were used to evaluate via quantitative PCR the expression of 44 genes involved in pathways of insulin, mTOR, AMPK, and Jak2-Stat5 signalling and also glucose and amino acid (AA) transporters. We observed an increased expression during lactation of ELF5, AA and glucose transporters, insulin signaling pathway components, MAPK14, FRAP1, EIF4EBP2, GSK3A and TSC1 among mTOR signaling-related genes. Among ribosomal components RPL22 was down-regulated. The overall data support a central role of AA and glucose transporters and insulin signaling through mTOR for the regulation of protein synthesis in bovine mammary gland. Furthermore, the existence of translational competition favoring the translation of milk protein transcripts was inferred from the combined dataset.
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Whitmore, T. J., N. J. Trengove, D. F. Graham, and P. E. Hartmann. "Analysis of Insulin in Human Breast Milk in Mothers with Type 1 and Type 2 Diabetes Mellitus." International Journal of Endocrinology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/296368.
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Despite the important role that insulin plays in the human body, very little is known about its presence in human milk. Levels rapidly decrease during the first few days of lactation and then, unlike other serum proteins of similar size, achieve comparable levels to those in serum. Despite this, current guides for medical treatment suggest that insulin does not pass into milk, raising the question of where the insulin in milk originates. Five mothers without diabetes, 4 mothers with type 1, and 5 mothers with type 2 diabetes collected milk samples over a 24-hour period. Samples were analysed for total and endogenous insulin content and for c-peptide content. All of the insulin present in the milk of type 1 mothers was artificial, and c-peptide levels were 100x lower than in serum. This demonstrates that insulin is transported into human milk at comparable concentration to serum, suggesting an active transport mechanism. The role of insulin in milk is yet to be determined; however, there are a number of potential implications for the infant of the presence of artificial insulins in milk.
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Da Costa, T. H. M., and D. H. Williamson. "Effects of exogenous insulin or vanadate on disposal of dietary triacylglycerols between mammary gland and adipose tissue in the lactating rat: insulin resistance in white adipose tissue." Biochemical Journal 290, no. 2 (March 1, 1993): 557–61. http://dx.doi.org/10.1042/bj2900557.
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The effects of exogenous insulin or vanadate (an insulin mimetic) on the disposal of dietary [14C]lipid between oxidation to 14CO2, deposition in adipose tissue or uptake by mammary gland and transfer to suckling pups were studied in virgin and lactating rats. After an oral load of [1-14C]triolein, virgin rats treated with a supraphysiological dose of insulin over 24 h showed a decrease (58%) in 14CO2 production and increased accumulation of [14C]lipid in carcass and white adipose tissue. There was a 2.5-fold increase in lipoprotein lipase activity in the latter. Chronic vanadate administration (12 days) had no effect on these parameters. In lactating rats, the stimulation of the deposition of [14C]lipid in adipose tissue by exogenous insulin was about 10% of that in virgin rats. In prolactin-deficient lactating rats there was no stimulation of [14C]lipid deposition in adipose tissue by insulin. However, both insulin and vanadate treatment increased the accumulation of [14C]lipid in mammary gland to the values seen in the mammary glands plus pups of normal lactating rats. Lipoprotein lipase activity in the gland was also restored to normal values. It is concluded that in lactation there is resistance to insulin stimulation of dietary lipid deposition in adipose tissue, and that this is not due to circulating prolactin. In addition, exogenous insulin plays a role in the regulation of lipoprotein lipase and hence of dietary lipid uptake into lactating mammary gland.
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Sartin, J. L., K. A. Cummins, R. J. Kemppainen, D. N. Marple, C. H. Rahe, and J. C. Williams. "Glucagon, insulin, and growth hormone responses to glucose infusion in lactating dairy cows." American Journal of Physiology-Endocrinology and Metabolism 248, no. 1 (January 1, 1985): E108—E114. http://dx.doi.org/10.1152/ajpendo.1985.248.1.e108.
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Early lactation in the dairy cow is associated with an increased demand for energy that can only be met by hormone-mediated partitioning of nutrients. The purpose of this study was to determine adaptive responses of basal and glucose-stimulated glucagon (IRG), insulin (IRI), and growth hormone (GH) concentrations to early lactation. Blood was collected via jugular cannulas from nonpregnant nonlactating (NPNL) cows and cows 14 days antepartum (AP) and 5 and 30 days postpartum (PP). Basal concentrations of IRI decreased with lactation, IRG was essentially unchanged, and GH was increased with lactation. The molar IRI/IRG (I/G) ratio was decreased from 4.6 at day 14 AP to 1.3 at day 30 PP. The effects of exogenous glucose (0.56 mM/kg body wt) on IRI were greatest during pregnancy and declined with lactation. IRG responses to glucose were similar except in NPNL cows, which had a minimal but prolonged IRG inhibition, GH responses to glucose infusion were absent in NPNL cows and were most significant at 5 days PP. The decreased I/G and elevated GH concentrations suggests that both IRG and GH play a role in nutrient partitioning during early lactation.
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Sartin, J. L., K. A. Cummins, R. J. Kemppainen, R. Carnes, D. G. McClary, and J. C. Williams. "Effect of propionate infusion on plasma glucagon, insulin and growth hormone concentrations in lactating dairy cows." Acta Endocrinologica 109, no. 3 (July 1985): 348–54. http://dx.doi.org/10.1530/acta.0.1090348.
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Abstract. Altered concentrations of metabolic hormones have been suggested as important mediators of energy partitioning during early lactation. This study was initiated to determine the effects of propionate (1.0 mmol/kg body weight) infusion on plasma concentrations of glucagon, insulin, growth hormone, propionate and glucose at 14 days ante-partum (AP) and days 5 and 30 postpartum (PP). No differences were seen in propionate concentrations between sampling days. Glucose concentrations were elevated following propionate infusion in pregnant cows but were not elevated in the PP cows. Insulin responses to propionate infusion did not differ between days while the glucagon response was blunted at day 5 PP. Basal glucagon concentrations were elevated between days 5 and 30 PP, insulin concentrations were unchanged between days, while the molar insulin/glucagon ratio was decreased during early lactation. Basal growth hormone (GH) concentrations were elevated between day 14 AP and day 30 PP. GH responsiveness to declining propionate concentrations was greatest at day 5 PP. These data further suggest a role for glucagon as well as GH in nutrient partitioning during early lactation.
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Farney, Jaymelynn K., Laman K. Mamedova, Johann F. Coetzee, Butch KuKanich, Lorraine M. Sordillo, Sara K. Stoakes, J. Ernest Minton, Larry C. Hollis, and Barry J. Bradford. "Anti-inflammatory salicylate treatment alters the metabolic adaptations to lactation in dairy cattle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 305, no. 2 (July 15, 2013): R110—R117. http://dx.doi.org/10.1152/ajpregu.00152.2013.
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Adapting to the lactating state requires metabolic adjustments in multiple tissues, especially in the dairy cow, which must meet glucose demands that can exceed 5 kg/day in the face of negligible gastrointestinal glucose absorption. These challenges are met through the process of homeorhesis, the alteration of metabolic setpoints to adapt to a shift in physiological state. To investigate the role of inflammation-associated pathways in these homeorhetic adaptations, we treated cows with the nonsteroidal anti-inflammatory drug sodium salicylate (SS) for the first 7 days of lactation. Administration of SS decreased liver TNF-α mRNA and marginally decreased plasma TNF-α concentration, but plasma eicosanoids and liver NF-κB activity were unaltered during treatment. Despite the mild impact on these inflammatory markers, SS clearly altered metabolic function. Plasma glucose concentration was decreased by SS, but this was not explained by a shift in hepatic gluconeogenic gene expression or by altered milk lactose secretion. Insulin concentrations decreased in SS-treated cows on day 7 compared with controls, which was consistent with the decline in plasma glucose concentration. The revised quantitative insulin sensitivity check index (RQUICKI) was then used to assess whether altered insulin sensitivity may have influenced glucose utilization rate with SS. The RQUICKI estimate of insulin sensitivity was significantly elevated by SS on day 7, coincident with the decline in plasma glucose concentration. Salicylate prevented postpartum insulin resistance, likely causing excessive glucose utilization in peripheral tissues and hypoglycemia. These results represent the first evidence that inflammation-associated pathways are involved in homeorhetic adaptations to lactation.
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FAULKNER, ANNE, and PAMELA A. MARTIN. "Changes in the concentrations of glucagon-like peptide-1(7–36)amide and gastric inhibitory polypeptide during the lactation cycle in goats." Journal of Dairy Research 65, no. 3 (August 1998): 433–41. http://dx.doi.org/10.1017/s0022029998002957.
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Plasma concentrations of glucagon-like peptide-1(7–36)amide (GLP) and gastric inhibitory polypeptide (GIP) were determined at fortnightly intervals for over a year throughout the pregnancy–lactation cycle of goats. Both GIP and GLP concentrations were elevated during lactation and fell rapidly when milk secretion was terminated. At the onset of lactation GLP concentrations rose rapidly whereas GIP concentrations showed a delayed response. GLP concentrations remained high throughout lactation but those of GIP declined linearly as milk yields fell. Serum insulin concentrations correlated positively with plasma glucose concentrations but not with either GIP or GLP concentrations. Negative correlations were found between serum insulin concentrations and milk yield and plasma non-esterified fatty acid concentrations. The results are consistent with plasma GIP and GLP concentrations being determined by other factors in addition to nutrient intake and absorption. Changes in GIP concentrations mirrored reported changes in the hypertrophy and atrophy of the intestine in ruminants while GLP concentrations may be more dependent on the neural and endocrine factors associated with lactation. The elevated concentrations of both peptides indicated a specific role in lactation independent of their normal anabolic and insulinotropic effects.
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Leury, Brian J., Lance H. Baumgard, Stephanie S. Block, Nthabisheng Segoale, Richard A. Ehrhardt, Robert P. Rhoads, Dale E. Bauman, Alan W. Bell, and Yves R. Boisclair. "Effect of insulin and growth hormone on plasma leptin in periparturient dairy cows." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 5 (November 2003): R1107—R1115. http://dx.doi.org/10.1152/ajpregu.00320.2003.
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After parturition, dairy cows suffer from an intense energy deficit caused by the onset of copious milk secretion and an inadequate increase in voluntary food intake. We previously showed that this energy deficit contributes to a decline in plasma leptin. This decline mirrors that of plasma insulin but is reciprocal to the profile of plasma growth hormone (GH), suggesting that both hormones may regulate plasma leptin in periparturient dairy cows. To study the role of insulin, hyperinsulinemic-euglycemic clamps were performed on six dairy cows in late pregnancy (LP, 31 days prepartum) and early lactation (EL, 7 days postpartum). Infusion of insulin (1 μg·kg body wt-1·h-1) caused a progressive rise in the plasma concentration of leptin that reached maximum levels at 24 h during both physiological states. At steady states, the absolute increase in plasma leptin was greater in LP than in EL cows (2.4 vs. 0.4 ng/ml). Insulin infusion increased leptin mRNA in adipose tissue during LP but not during EL. During lactation, mammary epithelial cells expressed leptin mRNA but insulin did not increase milk leptin output. In contrast, a 3-day period of GH administration had no effect on plasma leptin during LP or EL. Therefore, insulin increases plasma leptin in LP by stimulating adipose tissue synthesis but has only marginal effects in EL, when cows are in negative energy balance. Other factors, such as increased response of adipose tissue to β-adrenergic signals, probably contribute to the reduction of plasma leptin in early lactating dairy cows.
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Stringer, J. M., G. Shaw, A. Pask, and M. B. Renfree. "137. GENOMIC IMPRINTING IN THE MARSUPIAL MAMMARY GLAND." Reproduction, Fertility and Development 22, no. 9 (2010): 55. http://dx.doi.org/10.1071/srb10abs137.
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Genomic imprinting is an epigenetic mechanism that differentially regulates the expression of certain genes, resulting in expression from only one parental allele. In mammals, genomic imprinting occurs in the placenta of both eutherians and marsupials, and plays an important role in regulating nutrition and growth of the developing fetus. The mammary gland also provides a critical source of nutrition for the neonate in all mammals, but there are few imprinting studies of this organ. Marsupials deliver tiny, altricial young that complete development during an extended lactation. INS (insulin) is paternally expressed in the eutherian and marsupial yolk sac and curiously is the only gene that is solely imprinted in this organ (1, 2). Insulin regulates carbohydrate metabolism, protein synthesis and cell growth. Insulin, (plus cortisol and prolactin) is required for the onset of lactation and the synthesis of milk (3). We characterised INS expression and examined its imprint status in the mammary gland of the tammar wallaby. INS mRNA is expressed in the mammary gland of the tammar from birth and throughout of lactation with highest expression at the initiation of lactation (Phase 1-2a) and around Phase 3 of lactation. Direct sequencing of 7 individuals at various stages of lactation confirmed that INS is imprinted in the mammary gland. Surprisingly, INS may also be imprinted in several other organs in the adult and juvenile wallaby. Preliminary bisulfite sequencing suggests there is a differentially methylated region located upstream of INS which may help to regulate INS expression. This is the first study to identify INS imprinting outside the yolk sac. As INS is critical for lactation, this is also the first indication that genomic imprinting may regulate lactation, suggesting that imprinting in the mammary gland may be as critical for post-natal survival as placental imprinting is for pre-natal development. (1) Deltour LX, et al. (1995). Tissue- and developmental stage-specific imprinting of the mouse proinsulin gene, Ins2. Dev Biol 168(2): 686–688.(2) Ager EI, et al. (2007). Insulin is imprinted in the placenta of the marsupial, Macropus eugenii. Dev Biol 309: 317–328.(3) Bolander FF, et al. (1981). Insulin is essential for accumulation of casein mRNA in mouse mammary epithelial cells. Proc Natl Acad Sci USA 78(9): 5682–5684.
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Cohick, W. S. "Role of the Insulin-like Growth Factors and Their Binding Proteins in Lactation." Journal of Dairy Science 81, no. 6 (June 1998): 1769–77. http://dx.doi.org/10.3168/jds.s0022-0302(98)75746-7.
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Rogowska, Monika D., Uriel N. V. Pena, Nimrat Binning, and Julian K. Christians. "Recovery of the maternal skeleton after lactation is impaired by advanced maternal age but not by reduced IGF availability in the mouse." PLOS ONE 16, no. 9 (September 1, 2021): e0256906. http://dx.doi.org/10.1371/journal.pone.0256906.
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Background Lactation results in substantial maternal bone loss that is recovered following weaning. However, the mechanisms underlying this recovery, and in particular the role of insulin-like growth factor 1 (IGF-I), is not clear. Furthermore, there is little data regarding whether recovery is affected by advanced maternal age. Methods Using micro-computed tomography, we studied bone recovery following lactation in mice at 2, 5 and 7 months of age. We also investigated the effects of reduced IGF-I availability using mice lacking PAPP-A2, a protease of insulin-like growth factor binding protein 5 (IGFBP-5). Results In 2 month old mice, lactation affected femoral trabecular and cortical bone, but only cortical bone showed recovery 3 weeks after weaning. This recovery was not affected by deletion of the Pappa2 gene. The amount of trabecular bone was reduced in 5 and 7 month old mice, and was not further reduced by lactation. However, the recovery of cortical bone was impaired at 5 and 7 months compared with at 2 months. Conclusions Recovery of the maternal skeleton after lactation is impaired in moderately-aged mice compared with younger mice. Our results may be relevant to the long-term effects of breastfeeding on the maternal skeleton in humans, particularly given the increasing median maternal age at childbearing.
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Ehrhardt, Richard A., Andreas Foskolos, Sarah L. Giesy, Stephanie R. Wesolowski, Christopher S. Krumm, W. Ronald Butler, Susan M. Quirk, Matthew R. Waldron, and Yves R. Boisclair. "Increased plasma leptin attenuates adaptive metabolism in early lactating dairy cows." Journal of Endocrinology 229, no. 2 (May 2016): 145–57. http://dx.doi.org/10.1530/joe-16-0031.
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Mammals meet the increased nutritional demands of lactation through a combination of increased feed intake and a collection of adaptations known as adaptive metabolism (e.g., glucose sparing via insulin resistance, mobilization of endogenous reserves, and increased metabolic efficiency via reduced thyroid hormones). In the modern dairy cow, adaptive metabolism predominates over increased feed intake at the onset of lactation and develops concurrently with a reduction in plasma leptin. To address the role of leptin in the adaptive metabolism of early lactation, we asked which adaptations could be countered by a constant 96-h intravenous infusion of human leptin (hLeptin) starting on day 8 of lactation. Compared to saline infusion (Control), hLeptin did not alter energy intake or milk energy output but caused a modest increase in body weight loss. hLeptin reduced plasma glucose by 9% and hepatic glycogen content by 73%, and these effects were associated with a 17% increase in glucose disposal during an insulin tolerance test. hLeptin attenuated the accumulation of triglyceride in the liver by 28% in the absence of effects on plasma levels of the anti-lipolytic hormone insulin or plasma levels of free fatty acids, a marker of lipid mobilization from adipose tissue. Finally, hLeptin increased the plasma concentrations of T4and T3by nearly 50% without affecting other neurally regulated hormones (i.e., cortisol and luteinizing hormone (LH)). Overall these data implicate the periparturient reduction in plasma leptin as one of the signals promoting conservation of glucose and energy at the onset of lactation in the energy-deficient dairy cow.
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Fodor, Anna, Ottó Pintér, Ágnes Domokos, Kristina Langnaese, István Barna, Mario Engelmann, and Dóra Zelena. "Blunted HPA axis response in lactating, vasopressin-deficient Brattleboro rats." Journal of Endocrinology 219, no. 2 (August 13, 2013): 89–100. http://dx.doi.org/10.1530/joe-13-0224.
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Adaptation to stress is a basic phenomenon in mammalian life that is mandatorily associated with the activity of the hypothalamic–pituitary–adrenal (HPA) axis. An increased resting activity of the HPA axis can be measured during pregnancy and lactation, suggesting that these reproductive states lead to chronic load in females. In this study, we examined the consequences of the congenital lack of vasopressin on the activity of the HPA axis during lactation using vasopressin-deficient Brattleboro rats. Virgin and lactating, homozygous vasopressin-deficient rats were compared with control, heterozygous rats. In control dams compared with virgins, physiological changes similar to those observed in a chronic stress state (thymus involution, adrenal gland hyperplasia, elevation of proopiomelanocortin mRNA levels in the adenohypophysis, and resting plasma corticosterone levels) were observed. In vasopressin-deficient dams, adrenal gland hyperplasia and resting corticosterone level elevations were not observed. Corticotropin-releasing hormone (Crh) mRNA levels in the hypothalamic paraventricular nucleus were elevated in only the control dams, while oxytocin (OT) mRNA levels were higher in vasopressin-deficient virgins and lactation induced a further increase in both the genotypes. Suckling-induced ACTH and corticosterone level elevations were blunted in vasopressin-deficient dams. Anaphylactoid reaction (i.v. egg white) and insulin-induced hypoglycemia stimulated the HPA axis, which were blunted in lactating rats compared with the virgins and in vasopressin-deficient rats compared with the controls without interaction of the two factors. Vasopressin seems to contribute to the physiological changes observed during lactation mimicking a chronic stress state, but its role in acute HPA axis regulation during lactation seems to be similar to that observed in virgins. If vasopressin is congenitally absent, OT, but not the CRH, compensates for the missing vasopressin; however, the functional restitution remains incomplete.
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Takaya, Junji, Sohsaku Yamanouchi, Jiro Kino, Yuko Tanabe, and Kazunari Kaneko. "A Calcium-Deficient Diet in Dams during Gestation Increases Insulin Resistance in Male Offspring." Nutrients 10, no. 11 (November 13, 2018): 1745. http://dx.doi.org/10.3390/nu10111745.
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Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. Osteocalcin (OC), a bone formation biomarker, acts directly on β-cells and increases insulin secretion. We determined the effects of Ca deficiency during pregnancy and/or lactation on insulin resistance in offspring. Female Wistar rats consumed either a Ca-deficient or control diet ad libitum from three weeks preconception to 21 days postparturition. Pups were allowed to nurse their original mothers until weaning. The offspring were fed a control diet beginning at weaning and were killed on day 180. Serum carboxylated OC (Gla-OC) and undercarboxylated OC (Glu-OC), insulin and adipokines in offspring were measured. In males, mean levels of insulin, glucose, and HOMA-IR were higher in the Ca-deficient group than in the control group. In addition, ionized Ca (iCa) was inversely associated with serum Glu-OC and adiponectin in males. In females, mean levels of Glu-OC and Gla-OC in the Ca-deficient group were higher than in the control group. In all offspring, serum leptin levels were correlated with serum insulin levels, and inversely correlated with iCa. In conclusion, maternal Ca restriction during pregnancy and/or lactation influences postnatal offspring Ca metabolism and insulin resistance in a sex-specific manner.
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Gravena, C., PC Mathias, and SJ Ashcroft. "Acute effects of fatty acids on insulin secretion from rat and human islets of Langerhans." Journal of Endocrinology 173, no. 1 (April 1, 2002): 73–80. http://dx.doi.org/10.1677/joe.0.1730073.
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Fatty acids have both stimulatory and inhibitory effects on insulin secretion. Long-term exposure to fatty acids results in impaired insulin secretion whilst acute exposure has generally been found to enhance insulin release. However, there are conflicting data in the literature as to the relative efficacy of various fatty acids and on the glucose dependency of the stimulatory effect. Moreover, there is little information on the responses of human islets in vitro to fatty acids. We have therefore studied the acute effects of a range of fatty acids on insulin secretion from rat and human islets of Langerhans at different glucose concentrations. Fatty acids (0.5 mM) acutely stimulated insulin release from rat islets of Langerhans in static incubations in a glucose-dependent manner. The greatest effect was seen at high glucose concentration (16.7 mM) and little or no response was elicited at 3.3 or 8.7 mM glucose. Long-chain fatty acids (palmitate and stearate) were more effective than medium-chain (octanoate). Saturated fatty acids (palmitate, stearate) were more effective than unsaturated (palmitoleate, linoleate, elaidate). Stimulation of insulin secretion by fatty acids was also studied in perifused rat islets. No effects were observed at 3.3 mM glucose but fatty acids markedly potentiated the effect of 16.7 mM glucose. The combination of fatty acid plus glucose was less effective when islets had been first challenged with glucose alone. The insulin secretory responses to fatty acids of human islets in static incubations were similar to those of rat islets. In order to examine whether the responses to glucose and to fatty acids could be varied independently we used an animal model in which lactating rats are fed a low-protein diet during early lactation. Islets from rats whose mothers had been malnourished during lactation were still able to respond effectively to fatty acids despite a lowered secretory response to glucose. These data emphasise the complex interrelationships between nutrients in the control of insulin release and support the view that fatty acids play an important role in glucose homeostasis during undernutrition.
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Flint, D. J., E. Tonner, J. Beattie, and D. Panton. "Investigation of the mechanism of action of growth hormone in stimulating lactation in the rat." Journal of Endocrinology 134, no. 3 (September 1992): 377–83. http://dx.doi.org/10.1677/joe.0.1340377.
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ABSTRACT The role of GH was examined using an antiserum to rat GH (anti-rGH). When administered to lactating rats on day 2 of lactation it was without effect, whereas bromocriptine markedly suppressed milk production, with no additional effect of combined treatment. On day 6 of lactation, treatment with anti-rGH was also without effect, whilst bromocriptine again suppressed milk production. Combined treatment, however, suppressed milk synthesis completely, suggesting that GH was capable of maintaining about 50% of normal milk yield in the absence of prolactin at day 6 of lactation. By day 14 of lactation, anti-rGH treatment alone was capable of decreasing milk yield by about 20%, and again milk secretion only stopped completely when GH and prolactin were suppressed. These data suggest that the role of GH in supporting lactation increases as lactation progresses. The effects of GH in stimulating growth and in increasing milk yield in ruminants have been proposed to be mediated via insulin-like growth factor-I (IGF-I). In rats treated with anti-rGH, both IGF-I and IGF-II were decreased in serum. The concentration of the major IGF-binding protein (IGFBP-3) was not, however, affected by inhibition of GH or prolactin individually, but was decreased in animals treated with bromocriptine and anti-rGH. In animals given both bromocriptine and anti-rGH, concurrent treatment with recombinant bovine GH maintained milk yield at 50% of control values and normalized serum IGF-I, IGF-II and IGFBP-3 concentrations. By contrast, concurrent treatment with IGF-I or IGF-II, despite normalizing their respective concentrations in serum, failed to affect milk yield. These results suggest that neither IGF-I nor IGF-II is capable of mediating the effects of GH alone. It is, however, possible that they play a part in a coordinated series of responses to GH involving IGF-I, IGF-II and IGFBP-3. Journal of Endocrinology (1992) 134, 377–383
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Herrera, López-Soldado, Limones, Amusquivar, and Ramos. "Lipid Metabolism During the Perinatal Phase, and its Implications on Postnatal Development." International Journal for Vitamin and Nutrition Research 76, no. 4 (July 1, 2006): 216–24. http://dx.doi.org/10.1024/0300-9831.76.4.216.
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During pregnancy, lipid metabolism plays a major role to warrant the availability of substrates to the foetus. By using different experimental designs in the rat we have been able to answer several questions that were open about the short- and long-term effects of alterations of lipid metabolism during the perinatal stage. The first one was to demonstrate the importance of maternal body fat depot accumulation during the first half of pregnancy. We found that conditions like undernutrition circumscribed to this specific period when foetal growth is still small, that impede such fat accumulation not only restrain intrauterine development but also have long-term consequences, as shown by an impaired glucose tolerance when adults. Secondly, undernutrition during suckling has major long-term effect decreasing body weight, even though food intake was kept normal from the weaning period. Present findings also show that a diet rich in ω-3 fatty acids during pregnancy and lactation has negative effects on offspring development, but cross fostered experiments showed that the effect was a consequence of the intake of these fatty acids during the lactation period rather than during pregnancy. Pups from dams that were fed a fish oil-rich diet during pregnancy and lactation were found to have altered glucose/insulin relationship at the age of 10 weeks. Since a ω-3 fatty acid-rich diet decreases milk yield during lactation, additional experiments were carried out to determine whether decreased food intake, altered dietary fatty acid composition, or both were responsible for the long-term effects on the glucose/insulin axis. Results show that the decreased food intake caused by a ω-3 fatty acid-rich diet rather than the change in milk composition during suckling was responsible for the reduced pancreatic glucose responsiveness to insulin release at 16 weeks of age. In conclusion, present findings indicate that impaired maternal fat accumulation during early pregnancy and food intake during lactation, rather than a difference in dietary fatty acid composition have a greater influence on postnatal development and affect glucose/insulin relationships in adult rats.
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Teixeira, Pryscila D. S., Gisele C. Couto, Isadora C. Furigo, Edward O. List, John J. Kopchick, and Jose Donato. "Central growth hormone action regulates metabolism during pregnancy." American Journal of Physiology-Endocrinology and Metabolism 317, no. 5 (November 1, 2019): E925—E940. http://dx.doi.org/10.1152/ajpendo.00229.2019.
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The maternal organism undergoes numerous metabolic adaptations to become prepared for the demands associated with the coming offspring. These metabolic adaptations involve changes induced by several hormones that act at multiple levels, ultimately influencing energy and glucose homeostasis during pregnancy and lactation. Previous studies have shown that central growth hormone (GH) action modulates glucose and energy homeostasis. However, whether central GH action regulates metabolism during pregnancy and lactation is still unknown. In the present study, we generated mice carrying ablation of GH receptor (GHR) in agouti-related protein (AgRP)–expressing neurons, in leptin receptor (LepR)–expressing cells or in the entire brain to investigate the role played by central GH action during pregnancy and lactation. AgRP-specific GHR ablation led to minor metabolic changes during pregnancy and lactation. However, while brain-specific GHR ablation reduced food intake and body adiposity during gestation, LepR GHR knockout (KO) mice exhibited increased leptin responsiveness in the ventromedial nucleus of the hypothalamus during late pregnancy, although their offspring showed reduced growth rate. Additionally, both Brain GHR KO and LepR GHR KO mice had lower glucose tolerance and glucose-stimulated insulin secretion during pregnancy, despite presenting increased insulin sensitivity, compared with control pregnant animals. Our findings revealed that during pregnancy central GH action regulates food intake, fat retention, as well as the sensitivity to insulin and leptin in a cell-specific manner. Together, the results suggest that GH acts in concert with other “gestational hormones” to prepare the maternal organism for the metabolic demands of the offspring.
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Stelwagen, K., and D. G. Grieve. "Effect of plane of nutrition between 6 and 16 months of age on body composition, plasma hormone concentrations and first-lactation milk production in Holstein heifers." Canadian Journal of Animal Science 72, no. 2 (June 1, 1992): 337–46. http://dx.doi.org/10.4141/cjas92-041.
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In a completely randomized design, 47 dairy heifers (6–8 mo of age) were assigned to a low (L), medium (M) or high (H) plane of nutrition to determine its effect on body composition (Slaughter Group, n = 23), subsequent first lactation (260 d) milk production (Production Group, n = 24) and blood somatotropin and insulin concentrations (n = 12 from each Slaughter and Production group). Actual daily gains between 6 and 16 mo of age were 611 g (L), 737 g (M) and 903 g (H). The proportion of carcass fat in heifers sacrificed at 16 mo increased while the proportion of lean and bone tissue decreased with increasing plane of nutrition. Concentrations of somatotropin measured at 9 and 14 mo of age decreased but insulin did not differ (9 mo) or tended (P < 0.10) to increase (14 mo) with increasing feeding level. Insulin concentrations at 9 and 14 mo of age were correlated positively with mammary crude protein and dry fat-free tissue at slaughter (9 mo, P < 0.05; 14 mo, P < 0.07), implying that insulin may play a role in mammogenesis in vivo. Plane of nutrition during the rearing period did not significantly affect production and composition of milk in the first lactation. It is speculated that this may be due to the fact that the heifers weighed approximately 200 kg at the start of the experiment, because recent research has demonstrated that the critical weight range during which mammary gland development is affected by plane of nutrition is between 90 and 200 kg. Key words: Heifer, somatotropin, insulin, lactation, plane of nutrition, body composition
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de Souza Rodrigues Cunha, Alessandra Cordeiro, Renata Oliveira Pereira, Mario José dos Santos Pereira, Vivian de Melo Soares, Mariana Renovato Martins, Michelle Teixeira Teixeira, Érica Patrícia Garcia Souza, and Anibal Sanchez Moura. "Long-term effects of overfeeding during lactation on insulin secretion — the role of GLUT-2." Journal of Nutritional Biochemistry 20, no. 6 (June 2009): 435–42. http://dx.doi.org/10.1016/j.jnutbio.2008.05.002.
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Menzies, K. K., K. L. Macmillan, K. R. Nicholas, C. Lefevre, and C. Ormandy. "281. The role of insulin in milk protein synthesis." Reproduction, Fertility and Development 17, no. 9 (2005): 117. http://dx.doi.org/10.1071/srb05abs281.
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The mammary explant culture model has been frequently used to mimic lactation and to examine the endocrine control of milk protein gene expression. Studies in the mouse show the expression of the milk protein genes in explants requires insulin in the presence of prolactin and cortisol. The role of insulin in milk protein synthesis in the dairy cow is not as clear. The bovine mammary explant culture model has been utilised to show that insulin is essential for alpha-s1-casein gene expression and the synthesis of the casein proteins. In addition, mouse culture experiments were undertaken to provide an insight into the underlying molecular mechanisms of insulin action in hte mammary gland. A global analysis of the genes induced in the cultured explants was done using Affymetrix microarray and showed 132 genes, including the major milk protein genes, required the complement of insulin, cortisol and prolactin for maximal expression. Twenty-seven genes showed a 3-fold change in gene expression in response to insulin. The function of these genes can be largely categorised into maintenance of cell integrity, signal transduction, transport mechanisms, cellular metabolism and a direct effect on gene transcription in the nucleus. The requirement for insulin in milk protein synthesis is highlighted by its role in inducing the STAT5 gene, known to be a key transcription factor for the milk protein genes. Interestingly, dairy cows of high genetic merit have unusually low serum concentrations of insulin. This has occured in association with a high selection pressure for milk volume that has altered the regulation of blood glucose homeostasis. Our study indicates that this intensity of selection for high milk volume could be compromising the dairy cow’s potential for milk protein production: Has selecting for milk volume in many populations of dairy cows been achieved by lowering circulating insulin levels with consequent effects on the efficiency for milk protein yield as well as compromised reproductive performance.
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Thorn, Stephanie R., Richard A. Ehrhardt, W. Ronald Butler, Susan M. Quirk, and Yves R. Boisclair. "Insulin regulates hepatic leptin receptor expression in early lactating dairy cows." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 5 (November 2008): R1455—R1462. http://dx.doi.org/10.1152/ajpregu.90546.2008.
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Energy balance controls the expression of the leptin receptor (Lepr) in the ruminant hypothalamus but whether similar regulation occurs in peripheral tissues is unknown. To address this issue, we measured Lepr expression in the liver and adipose tissue of dairy cows during the transition from late pregnancy (LP) to early lactation (EL). This period is characterized by the development of a profound state of energy insufficiency and is associated with reduced plasma insulin and leptin and with increased plasma growth hormone. Hepatic expression of the short (Lepr-a) and long (Lepr-b) isoforms was 40% higher during EL (8 days postpartum) than LP (30 days prepartum). A similar effect was observed when negative energy balance was induced in nonpregnant, late-lactation dairy cows by food restriction, implicating energy insufficiency as a specific cause in EL. The stimulation of hepatic Lepr expression was reversed after a 48-h period of hyperinsulinemic euglycemia in EL. Changes in hepatic Lepr expression during chronic elevation of plasma leptin in EL or plasma growth hormone in nonpregnant, late-lactation cows did not support a role for these hormones in mediating the effects of energy insufficiency on hepatic Lepr expression. In adipose tissue, Lepr expression was increased 10-fold during the transition from LP to EL. Overall, these data indicate that hypoinsulinemia is partly responsible for the induction of Lepr expression in the liver, and perhaps adipose tissue, of energy-deficient dairy cows.
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Barber, M. C., M. T. Travers, E. Finley, D. J. Flint, and R. G. Vernon. "Growth-hormone-prolactin interactions in the regulation of mammary and adipose-tissue acetyl-CoA carboxylase activity and gene expression in lactating rats." Biochemical Journal 285, no. 2 (July 15, 1992): 469–75. http://dx.doi.org/10.1042/bj2850469.
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The factors and mechanisms responsible for the reciprocal changes in lipogenesis in rat mammary gland and adipose tissue during the lactation cycle have been investigated. Lactation decreased the activation status and mRNA concentration of acetyl-CoA carboxylase in adipose tissue. Litter removal decreased the mRNA concentration of acetyl-CoA carboxylase in the mammary gland and increased the enzyme's mRNA concentration and activation status in adipose tissue. Lowering serum prolactin concentration in lactating rats decreased the amount of mammary acetyl-CoA carboxylase mRNA and increased that of adipose tissue, and increased the activation status of the enzyme in adipose tissue. Decreasing serum growth hormone (GH) alone had little effect on acetyl-CoA carboxylase in lactating rats, although it did lower pup growth rate and serum concentration of insulin-like growth factor-I. Lowering serum GH concentration exacerbated the effects of decreasing serum prolactin on mammary-gland (but not adipose-tissue) acetyl-CoA carboxylase mRNA and further increased the rise in activation status of the adipose-tissue enzyme induced by decreasing serum prolactin. Changes in acetyl-CoA carboxylase mRNA in both mammary and adipose tissue were paralleled by changes in total enzyme activity except after litter removal, when there was a disproportionately large decrease in total enzyme activity of the mammary gland. Thus prolactin has a major and GH a minor role in the regulation of acetyl-CoA carboxylase activity during lactation. Changes in mammary activity in response to prolactin and GH are primarily due to alterations in gene transcription, whereas adaptation in adipose tissue involves both changes in gene transcription and activation status.
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Passos, Magna Cottini Fonseca, Fabiane Pereira Toste, Sheila Cristina Potente Dutra, Paula Affonso Trotta, Fernanda Pereira Toste, Patrícia Cristina Lisboa, and Egberto Gaspar de Moura. "Role of neonatal hyperleptinaemia on serum adiponectin and suppressor of cytokine signalling-3 expression in young rats." British Journal of Nutrition 101, no. 2 (August 5, 2008): 250–56. http://dx.doi.org/10.1017/s0007114508006521.
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Previously we had shown that neonatal leptin treatment programmes for both hyperleptinaemia and hyperinsulinaemia, which lead to leptin resistance and low expression of the hypothalamic leptin receptor (OB-Rb) of rats aged 150 d. Here we investigated in young post-weaned rats (age 30 d) if leptin treatment during lactation induces leptin and insulin resistance and if those changes are accompanied by changes in the suppressor of cytokine signalling-3 (SOCS-3) expression and serum adiponectin concentration. After delivery, the pups were divided into two groups: (1) a leptin group (Lep) that were injected with leptin daily (8 μg/100 g body weight subcutaneously) for the first 10 d of lactation; (2) a control (C) group, receiving saline. After weaning (day 21), body weight was monitored until the animals were age 30 d. They were tested for food intake in response to either leptin (0·5 mg/kg body weight intraperitoneally) (CL, LepL) or saline (CSal, LepSal) when they were aged 30 d. The CL group showed lower food intake, but no response was observed in the LepL group, suggesting leptin resistance. The Lep group had hyperleptinaemia (five-fold), hyperinsulinaemia (+42·5 %) and lower levels of serum adiponectin ( − 43·2 %). The hypothalamic expression of OB-Rb was lower ( − 22 %) and SOCS-3 was higher (+52·8 %) in the Lep group. We conclude that neonatal leptin treatment programmes for leptin resistance as soon as 30 d and suggests that SOCS-3 appears to be of particular importance in this event. In the Lep group, the lower serum adiponectin levels were accompanied by higher serum insulin, indicating a probable insulin resistance.
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Butler, S. T., S. H. Pelton, and W. R. Butler. "Insulin increases 17β-estradiol production by the dominant follicle of the first postpartum follicle wave in dairy cows." Reproduction 127, no. 5 (May 2004): 537–45. http://dx.doi.org/10.1530/rep.1.00079.
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Prolonged anovulation following parturition has a negative impact on fertility in dairy cows. Insulin plays an important role in ovarian function in many species, and is profoundly depressed in dairy cows during early lactation. We hypothesized that hypoinsulinemia during early lactation represents a key indicator of nutritional status, resulting in delayed ovulation. Holstein cows (n = 10) were subjected to either a hyperinsulinemic–euglycemic clamp (INS) or saline infusion (CTL) for 96 h, beginning on day 10 after parturition during the first postpartum follicular wave. Insulin was infused continuously (0.3 μg/kg body weight per h) via a jugular catheter, and euglycemia was maintained by infusion of glucose. Circulating insulin concentrations were elevated 2.6-fold in INS cows compared with CTL cows (0.73 ± 0.026 vs 0.28 ± 0.026 ng/ml; P < 0.001). Insulin treatment did not affect (P > 0.05) luteinizing hormone (LH) pulse frequency, pulse amplitude or mean circulating LH. Circulating estradiol was elevated in INS cows (P < 0.01) and circulating testosterone also tended to be higher. The ratio of testosterone to estradiol was not different between treatments for the initial 30 h of infusion, but was significantly reduced thereafter in response to insulin (P < 0.01), suggesting that hyperinsulinemia increased follicular aromatase activity. Insulin treatment also resulted in reduced circulating nonesterified fatty acids, and increased circulating total and free insulin-like growth factor-I concentrations. Insulin infusion increased estradiol secretion by the dominant follicle of the first postpartum follicular wave in dairy cows, and this effect appears not to be mediated through changes in pulsatile LH release.
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Berkovskaya, M. A. "World endocrinology news." Obesity and metabolism 5, no. 2 (June 15, 2008): 45–54. http://dx.doi.org/10.14341/omet2008245-54.
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The role of interleukin-6 in insulin resistance, body fat distribution and energy balance Disorders of glucose metabolism and risk of oral cancer. Duration of lactation is associated with lower prevalence of the metabolic syndrome in midlife--SWAN, the study of women's health across the nation. Vitamin D deficiency and risk of cardiovascular disease. Adypocyte prolactin: regulation of release and putative functions.
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Moullé, Valentine Suzanne, and Patricia Parnet. "Effects of Nutrient Intake during Pregnancy and Lactation on the Endocrine Pancreas of the Offspring." Nutrients 11, no. 11 (November 8, 2019): 2708. http://dx.doi.org/10.3390/nu11112708.
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The pancreas has an essential role in the regulation of glucose homeostasis by secreting insulin, the only hormone with a blood glucose lowering effect in mammals. Several circulating molecules are able to positively or negatively influence insulin secretion. Among them, nutrients such as fatty acids or amino acids can directly act on specific receptors present on pancreatic beta cells. Dietary intake, especially excessive nutrient intake, is known to modify energy balance in adults, resulting in pancreatic dysfunction. However, gestation and lactation are critical periods for fetal development and pup growth and specific dietary nutrients are required for optimal growth. Feeding alterations during these periods will impact offspring development and increase the risk of developing metabolic disorders in adulthood, leading to metabolic programming. This review will focus on the influence of nutrient intake during gestation and lactation periods on pancreas development and function in offspring, highlighting the molecular mechanism of imprinting on this organ.
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Vila, Greisa, Judith Hopfgartner, Gabriele Grimm, Sabina M. Baumgartner-Parzer, Alexandra Kautzky-Willer, Martin Clodi, and Anton Luger. "Lactation and appetite-regulating hormones: increased maternal plasma peptide YY concentrations 3–6 months postpartum." British Journal of Nutrition 114, no. 8 (August 24, 2015): 1203–8. http://dx.doi.org/10.1017/s0007114515002536.
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AbstractBreast-feeding is associated with maternal hormonal and metabolic changes ensuring adequate milk production. In this study, we investigate the impact of breast-feeding on the profile of changes in maternal appetite-regulating hormones 3–6 months postpartum. Study participants were age- and BMI-matched lactating mothers (n 10), non-lactating mothers (n 9) and women without any history of pregnancy or breast-feeding in the previous 12 months (control group, n 10). During study sessions, young mothers breast-fed or bottle-fed their babies, and maternal blood samples were collected at five time points during 90 min: before, during and after feeding the babies. Outcome parameters were plasma concentrations of ghrelin, peptide YY (PYY), leptin, adiponectin, prolactin, cortisol, insulin, glucose and lipid values. At baseline, circulating PYY concentrations were significantly increased in lactating mothers (100·3 (se 6·7) pg/ml) v. non-lactating mothers (73·6 (se 4·9) pg/ml, P=0·008) and v. the control group (70·2 (se 9) pg/ml, P=0·021). We found no differences in ghrelin, leptin and adiponectin values. Baseline prolactin concentrations were over 4-fold higher in lactating mothers (P<0·001). Lactating women had reduced TAG levels and LDL-cholesterol:HDL-cholesterol ratio, but increased waist circumference, when compared with non-lactating women. Breast-feeding sessions further elevated circulating prolactin (P<0·001), but induced no acute effects on appetite-regulating hormones. In summary, one single breast-feeding session did not acutely modulate circulating appetite-regulating hormones, but increased baseline PYY concentrations are associated with prolonged lactation. PYY might play a role in the coordination of energy balance during lactation, increasing fat mobilisation from maternal depots and ensuring adequate milk production for the demands of the growing infant.
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Teixeira, Pryscila D. S., Angela M. Ramos-Lobo, Isadora C. Furigo, and Jose Donato. "Brain STAT5 Modulates Long-Term Metabolic and Epigenetic Changes Induced by Pregnancy and Lactation in Female Mice." Endocrinology 160, no. 12 (October 10, 2019): 2903–17. http://dx.doi.org/10.1210/en.2019-00639.
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Abstract Several metabolic and behavioral adaptations that emerge during pregnancy remain present after weaning. Thus, reproductive experience causes long-lasting metabolic programming, particularly in the brain. However, the isolate effects of pregnancy or lactation and the molecular mechanisms involved in these long-term modifications are currently unknown. In the current study, we investigated the role of brain signal transducer and activator of transcription-5 (STAT5), a key transcription factor recruited by hormones highly secreted during gestation or lactation, for the long-term adaptations induced by reproductive experience. In control mice, pregnancy followed by lactation led to increased body adiposity and reduced ambulatory activity later in life. Additionally, pregnancy+lactation induced long-term epigenetic modifications in the brain: we observed upregulation in hypothalamic expression of histone deacetylases and reduced numbers of neurons with histone H3 acetylation in the paraventricular, arcuate, and ventromedial nuclei. Remarkably, brain-specific STAT5 ablation prevented all metabolic and epigenetic changes observed in reproductively experienced control female mice. Nonetheless, brain-specific STAT5 knockout (KO) mice that had the experience of pregnancy but did not lactate showed increased body weight and reduced energy expenditure later in life, whereas pregnancy KO and pregnancy+lactation KO mice exhibited improved insulin sensitivity compared with virgin KO mice. In summary, lactation is necessary for the long-lasting metabolic effects observed in reproductively experienced female mice. In addition, epigenetic mechanisms involving histone acetylation in neuronal populations related to energy balance regulation are possibly associated with these long-term consequences. Finally, our findings highlighted the key role played by brain STAT5 signaling for the chronic metabolic and epigenetic changes induced by pregnancy and lactation.
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Rodney, R. M., P. Celi, J. J. McGrath, H. M. Golder, S. T. Anderson, D. M. McNeill, D. R. Fraser, and I. J. Lean. "Metabolic and production responses to calcidiol treatment in mid-lactation dairy cows." Animal Production Science 59, no. 3 (2019): 449. http://dx.doi.org/10.1071/an16770.
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The study of vitamin D in cattle has often focussed on its role in calcium and mineral metabolism. However, there is evidence of a wider role for vitamin D in bone and energy metabolism. Two studies were conducted to explore relationships between calcidiol supplementation, blood minerals and metabolites in mid-lactation dairy cows. In Experiment 1, a dose-response study was conducted in which 25 mid-lactation cows were fed one of five supplementary calcidiol doses (0, 0.5, 1, 2 or 4 mg calcidiol/day) for 30 days, with blood samples taken every 10 days. Increasing calcidiol dose increased plasma calcidiol (P=0.001), 24,25-(OH)2-D3 (P=0.001) and serum phosphate (P=0.003) in a curvilinear manner, increased and then decreased plasma 25-OH-D2 (P=0.004) and linearly increased 3-epi 25-OH-D3 (P=0.001) and milk calcidiol concentrations (P=0.001). Calcidiol supplementation did not affect milk yield or composition, bodyweight or condition score. In Experiment 2, relationships between blood calcidiol and mineral and metabolite concentrations over time were explored using time-series analysis. Ten mid-lactation cows were fed either 0 or 0.5 mg calcidiol/day for 27 days, with blood samples taken every 3 days. Feeding calcidiol increased plasma calcidiol (P=0.001), 24,25-OH-D3 (P=0.038), and insulin (P=0.046), but decreased 25-OH-D2 (P=0.008) concentrations. Positive associations were identified between blood calcidiol and concentrations of other metabolites, including cholecalciferol, calcium, osteocalcin, glucose, insulin, non-esterified fatty acids, β-hydroxybutyrate, cholesterol, magnesium, phosphorus and total protein at varying lags (±0, 3 or 6 days), while negative relationships were identified between calcidiol and 24,25-(OH)2-D3, and phosphorus 3 days later. Importantly, strong positive associations between calcidiol and indicators of energy metabolism were identified. Overall, these experiments provide support for a positive effect of calcidiol treatment on dairy cow metabolism.
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Bouanane, Samira, Nassira B. Benkalfat, Fatima-Zohra Baba Ahmed, Hafida Merzouk, Nassima S. Mokhtari, Sid-Ahmed Merzouk, Joseph Gresti, Christian Tessier, and Michel Narce. "Time course of changes in serum oxidant/antioxidant status in overfed obese rats and their offspring." Clinical Science 116, no. 8 (March 16, 2009): 669–80. http://dx.doi.org/10.1042/cs20080413.
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The aim of the present study was to determine the time course of changes in oxidant/antioxidant status, as well as serum glucose, insulin, leptin and lipid levels, liver adipose tissue and muscle lipid and protein contents, in cafeteria-diet-fed dams during gestation and lactation, and in their offspring throughout adulthood. Food intake was also evaluated. The cafeteria diet induced a significant increase in maternal body and relative adipose tissue weights, daily energy intake, and plasma glucose, insulin, leptin and lipid levels at parturition (day 0) and at the end of lactation (day 21). Plasma total antioxidant status [ORAC (oxygen radical absorbance capacity)], erythrocyte catalase and SOD (superoxide dismutase) activities were lower, whereas plasma hydroperoxide and carbonyl protein levels were higher in cafeteria-diet-fed mothers compared with control mothers at days 0 and 21. Pups from cafeteria-diet-fed dams, both males and females, also had consistently higher body and relative adipose tissue weights, and plasma glucose, insulin, leptin, triacylglycerol (triglyceride) and cholesterol levels at birth (day 0), weaning (day 21) and 3 months of age (day 90). These offspring had significantly lower ORAC and catalase activity, and higher plasma hydroperoxide and carbonyl protein levels and SOD activity at birth, at days 21 and 90 compared with control offspring. In conclusion, excessive maternal fat and energy intake can play an important role in the development of metabolic disorders in the offspring. Maternal oxidative stress may be among the responsible factors. Fetal oxidative stress may present an additional confounding influence and probably contributes to additional disorders, aggravating features of the metabolic syndrome. An improvement in maternal oxidant/antioxidant status during pregnancy and lactation, with adequate nutrition, could have beneficial effects on the progeny.
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Chilliard, Yves, Anne Ferlay, Yannick Faulconnier, Muriel Bonnet, Jacques Rouel, and François Bocquier. "Adipose tissue metabolism and its role in adaptations to undernutrition in ruminants." Proceedings of the Nutrition Society 59, no. 1 (February 2000): 127–34. http://dx.doi.org/10.1017/s002966510000015x.
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Changes in the amount and metabolism of adipose tissue (AT) occur in underfed ruminants, and are amplified during lactation, or in fat animals. The fat depot of the tail of some ovine breeds seems to play a particular role in adaptation to undernutrition; this role could be linked to its smaller adipocytes and high sensitivity to the lipolytic effect of catecholamines. Glucocorticoids and growth hormone probably interact to induce teleophoretic changes in the AT responses to adenosine and catecholamines during lactation. Fat mobilization in dry ewes is related both to body fatness and to energy balance. The in vivo β-adrenergic lipolytic potential is primarily related to energy balance, whereas basal postprandial plasma non-esterified fatty acids (NEFA) are related to body fatness, and preprandial plasma NEFA is the best predictor of the actual body lipid loss. Several mechanisms seem to be aimed at avoiding excessive fat mobilization and/or insuring a return to the body fatness homeostatic set point. As well as providing the underfed animal with fatty acids as oxidative fuels, AT acts as an endocrine gland. The yield of leptin by ruminant AT is positively related to body fatness, decreased by underfeeding, β-adrenergic stimulation and short day length, and increased by insulin and glucocorticoids. This finding suggests that the leptin chronic (or acute) decrease in lean (or underfed respectively) ruminants is, as in rodents, a signal for endocrine, metabolic and behavioural adaptations aimed at restoring homeostasis.
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Fan, Xinyang, Lihua Qiu, Xiaohong Teng, Yongyun Zhang, and Yongwang Miao. "Effect of INSIG1 on the milk fat synthesis of buffalo mammary epithelial cells." Journal of Dairy Research 87, no. 3 (August 2020): 349–55. http://dx.doi.org/10.1017/s0022029920000710.
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AbstractWe hypothesized that insulin-induced gene 1 (INSIG1) affects milk fat synthesis in buffalo. For this reason, the protein abundance of INSIG1 in the mammary tissue of buffalo during the peak period of lactation and dry-off period was evaluated. The results showed that the expression of INSIG1 at the peak of lactation was lower than that in the dry-off period. To explore the role of INSIG1 in milk fat synthesis, the buffalo mammary epithelial cells (BMECs) were isolated and purified from buffalo mammary tissue, and INSIG1 gene were overexpressed and knocked down by constructing the recombinant lentivirus vector of INSIG1 gene and transfecting into BMECs. Results revealed that INSIG1 overexpression decreased the expression of INSIG2, SREBP, PPARG, SCD, GPAM, DGAT2 and AGPAT6, which led to reduction of triglycerides (TAG) content in the cell. In contrast, knockdown of INSIG1 had a positive effect on mRNA expression of the above genes. Overall, the data provide strong support for a key role of INSIG1 in the regulation of milk fat synthesis in BMECs.
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VAN DUIJVENVOORDE, PETER M., and BARBARA J. ROLLS. "Body fat regulation during pregnancy and lactation: the roles of diet and insulin." Biochemical Society Transactions 13, no. 5 (October 1, 1985): 824–25. http://dx.doi.org/10.1042/bst0130824.
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Grunewald, Hellmuth, Kirchberg, Mearin, Auricchio, Castillejo, Korponay-Szabo, et al. "Variation and Interdependencies of Human Milk Macronutrients, Fatty Acids, Adiponectin, Insulin, and IGF-II in the European PreventCD Cohort." Nutrients 11, no. 9 (August 30, 2019): 2034. http://dx.doi.org/10.3390/nu11092034.
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Human milk composition is variable. The identification of influencing factors and interdependencies of components may help to understand the physiology of lactation. In this study, we analyzed linear trends in human milk composition over time, the variation across different European countries and the influence of maternal celiac disease. Within a multicenter European study exploring potential prevention of celiac disease in a high-risk population (PreventCD), 569 human milk samples were donated by women from five European countries between 16 and 163 days postpartum. Some 202 mothers provided two samples at different time points. Protein, carbohydrates, fat and fatty acids, insulin, adiponectin, and insulin-like growth factor II (IGF-II) were analyzed. Milk protein and n-6 long chain polyunsaturated fatty acids decreased during the first three months of lactation. Fatty acid composition was significantly influenced by the country of residence. IGF-II and adiponectin concentrations correlated with protein content (r = 0.24 and r = 0.35), and IGF-II also correlated with fat content (r = 0.36), suggesting a possible regulatory role of IGF in milk macronutrient synthesis. Regarding the impact of celiac disease, only the level in palmitic acid was influenced by this disease, suggesting that breastfeeding by celiac disease mothers should not be discouraged.
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Sartori, Chiara, Pietro Lazzeroni, Silvia Merli, Viviana Dora Patianna, Francesca Viaroli, Francesca Cirillo, Sergio Amarri, and Maria Elisabeth Street. "From Placenta to Polycystic Ovarian Syndrome: The Role of Adipokines." Mediators of Inflammation 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/4981916.
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Adipokines are cytokines produced mainly by adipose tissue, besides many other tissues such as placenta, ovaries, peripheral-blood mononuclear cells, liver, muscle, kidney, heart, and bone marrow. Adipokines play a significant role in the metabolic syndrome and in cardiovascular diseases, have implications in regulating insulin sensitivity and inflammation, and have significant effects on growth and reproductive function. The objective of this review was to analyze the functions known today of adiponectin, leptin, resistin, and visfatin from placenta throughout childhood and adolescence. It is well known now that their serum concentrations during pregnancy and lactation have long-term effects beyond the fetus and newborn. With regard to puberty, adipokines are involved in the regulation of the relationship between nutritional status and normal physiology or disorders of puberty and altered gonadal function, as, for example, premature pubarche and polycystic ovarian syndrome (PCOS). Cytokines are involved in the maturation of oocytes and in the regular progression of puberty and pregnancy.
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Berlato, Chiara, and Wolfgang Doppler. "Selective Response to Insulin Versus Insulin-Like Growth Factor-I and -II and Up-Regulation of Insulin Receptor Splice Variant B in the Differentiated Mouse Mammary Epithelium." Endocrinology 150, no. 6 (February 26, 2009): 2924–33. http://dx.doi.org/10.1210/en.2008-0668.
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The terminal differentiation of the mouse mammary gland epithelium during lactation has been shown to require IGFs and/or superphysiological levels of insulin. It has been suggested that IGF receptor I (IGF-IR), in addition to its well-established role in the mammary gland during puberty and pregnancy, serves as the principal mediator of IGFs at this stage of development. However, our analysis of the expression levels of IGF-IR and the two insulin receptor (IR) splice variants, IR-A and IR-B, has revealed a 3- to 4-fold up-regulation of IR-B transcripts and a 6-fold down-regulation of IGF-IR transcripts and protein during terminal differentiation in the developing mammary gland. IR-B expression was also more than 10-fold up-regulated in murine mammary epithelial cell line HC11 during differentiation in vitro. As already described for the human form, murine IR-B cloned from HC11 exhibited selectivity for insulin as compared with IGFs. When differentiated HC11 cells were stimulated by 10 nm insulin, a concentration that is unable to activate IGF-IR, induction of milk protein and lipid synthetic enzyme gene expression, lactate production, and phosphorylation of Akt were observed. In contrast, on differentiated HC11 cells 10 nm IGF-I or 10 nm IGF-II were able to exert growth-promoting effects only. The lack of response of differentiated cells to low levels of IGFs could not be explained by inactivation of IGFs by IGF binding proteins. Our results suggest a previously unrecognized predominant role for IR-B in the differentiated mammary epithelium.
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Takaya, Junji. "Calcium-Deficiency during Pregnancy Affects Insulin Resistance in Offspring." International Journal of Molecular Sciences 22, no. 13 (June 29, 2021): 7008. http://dx.doi.org/10.3390/ijms22137008.
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Prenatal malnutrition is known to affect the phenotype of the offspring through changes in epigenetic regulation. Growing evidence suggests that epigenetics is one of the mechanisms by which nutrients and minerals affect metabolic traits. Although the perinatal period is the time of highest phenotypic plasticity, which contributes largely to developmental programming, there is evidence of nutritional influence on epigenetic regulation during adulthood. Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. Cortisol, the most important glucocorticoid, is considered to lead to insulin resistance and metabolic syndrome. 11β-hydroxysteroid dehydrogenase-1 is a key enzyme that catalyzes the intracellular conversion of cortisone to physiologically active cortisol. This brief review aims to identify the effects of Ca deficiency during pregnancy and/or lactation on insulin resistance in the offspring. Those findings demonstrate that maternal Ca deficiency during pregnancy may affect the epigenetic regulation of gene expression and thereby induce different metabolic phenotypes. We aim to address the need for Ca during pregnancy and propose the scaling-up of clinical and public health approaches that improved pregnancy outcomes.
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Block, SS, WR Butler, RA Ehrhardt, AW Bell, ME Van Amburgh, and YR Boisclair. "Decreased concentration of plasma leptin in periparturient dairy cows is caused by negative energy balance." Journal of Endocrinology 171, no. 2 (November 1, 2001): 339–48. http://dx.doi.org/10.1677/joe.0.1710339.
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Dairy cows suffer from an intense energy deficit at parturition due to the onset of copious milk synthesis and depressed appetite. Despite this deficit, maternal metabolism is almost completely devoted to the support of mammary metabolism. Evidence from rodents suggests that, during periods of nutritional insufficiency, a reduction in plasma leptin serves to co-ordinate energy metabolism. As an initial step to determine if leptin plays this role in periparturient dairy cows, changes in the plasma concentration of leptin were measured during the period from 35 days before to 56 days after parturition. The plasma concentration of leptin was reduced by approximately 50% after parturition and remained depressed during lactation despite a gradual improvement in energy balance; corresponding changes occurred in the abundance of leptin mRNA in white adipose tissue. To determine whether negative energy balance caused this reduction in circulating leptin, cows were either milked or not milked after parturition. Absence of milk removal eliminated the energy deficit of early lactation, and doubled the plasma concentration of leptin. The plasma concentration of leptin was positively correlated with plasma concentrations of insulin and glucose, and negatively correlated with plasma concentrations of growth hormone and non-esterified fatty acids. In conclusion, the energy deficit of periparturient cows causes a sustained reduction in plasma leptin. This reduction could benefit early lactating dairy cows by promoting a faster increase in feed intake and by diverting energy from non-vital functions such as reproduction.