Relevant bibliographies by topics / Insulin role in lactation

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Academic literature on the topic 'Insulin role in lactation'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Insulin role in lactation"

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.
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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.
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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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Dissertations / Theses on the topic "Insulin role in lactation"

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Jones, R. G. "The role of insulin in short-term regulation of mammary-gland lipogenesis : Its relevance to substrate partitioning during lactation." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382547.

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Deleo, Domenica. "Structure and function of the insulin receptor: its role during lactation and foetal development." Curtin University of Technology, School of Biomedical Sciences, 1994. http://espace.library.curtin.edu.au:80/R/?func=dbin-jump-full&object_id=14833.

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Prior to the commencement of this study in 1990, a number of reports had appeared in the literature describing the importance of insulin action during lactation in mammals (see Chapter 1). These studies investigated the changes in circulating insulin and glucagon concentrations during lactation, the relative numbers of insulin receptors in insulin-sensitive tissues, and glucose utilisation by these tissues. However, at that time, no information was available on the structure of the mammary insulin receptor. The rationale for undertaking this study was to characterise the structure of the rat mammary insulin receptor as a means of furthering our understanding of the role insulin plays during lactation.An initial requirement of this study was the development of a method for the convenient and inexpensive preparation of A14-tyrosyl[125I]iodoinsulin. A14-tyrosyl[125I]iodoinsulin displays binding characteristics which are virtually indistinguishable from the native hormone, which is a necessary requirement for tracers which are to be used in binding studies. In Chapter 2, I describe a method for the purification of A14-tyrosyl[125I]iodoinsulin from a mixture of iodinated insulin molecules which are produced following oxidation by chloramine-T in the presence of Na125iodine. In this method I employed disposable cartridges packed with a C18 support matrix to which the iodinated insulin molecules are readily adsorbed when in an aqueous solution.A 14-tyrosyl[125I]iodoinsulin absorbed most strongly to the C18 matrix and unwanted products were removed through a sequence of washes prior to the elution of the A14-tyrosyl[125I]iodoinsulin derivative using a buffer containing 50% (v/v) acetonitrile. This prodct was unambiguously shown to be A14-tyrosyl[125I]iodoinsulin by N-terminal amino acid sequencing. The quality of this radiolabel compared favourably with commercially ++
available A14-tyrosyl[125I]iodoinsulin preparations both in terms of specific activity and stability upon storage at -20C. Furthermore, a modified method based on this protocol has been used in our and other laboratories for the isolation of other iodinated peptides with highly satisfactory results.I have established that the size of the a-subunit of the rat mammary insulin receptor is significantly diminished compared with the liver insulin receptor (125 kDa versus 130 kDa). This difference in size was present throughout all stages of lactation and was not due to proteolysis of a larger form. Furthermore, I demonstrated that both the mammary and liver insulin receptor a-subunits migrated equally on PAGE following treatment with neuraminidase, indicating that the apparent size difference may be accounted for by a variation in the extent of receptor sialation. Treatment of the mammary insulin receptor a-subunit with glycopeptidase F demonstrated that the size of the aglycoreceptor (100 kDa) was similar to that described for insulin receptors from other insulin-sensitive tissues.I characterised the distribution of mRNA encoding the two, naturally-occurring insulin receptor isoforms in mammary tissue throughout all stages of pregnancy and lactation. These insulin receptor isoforms differ due to the absence (IR-A) or presence (IR-B) of a 12 amino acid peptide, encoded by exon 11 of the insulin receptor gene, and located near the C-terminus of the insulin receptor a-subunit. Mammary tissue predominantly expressed IR-A mRNA in contrast to liver tissue, which almost exclusively expressed IRB mRNA. Furthermore, the ratio of IR-A to IR-B mRNA in mammary tissue changed significantly during the first week post-partum whilst the distribution of IR-A and IR-B mRNA in the liver remained constant throughout pregnancy and lactation. This difference in insulin receptor isoform ++
expression between mammary and liver tissue also contributed to the estimated size difference between the insulin receptor a-subunits from these two tissues. In addition, I characterised the expression of IR-A and IR-B mRNA in several different tissues obtained from rats on day 14 of gestation through to 7 days post partum. I established that the splicing mechanism is functional at least as early as day 14 of gestation, suggesting a possible role for the preferential expression of a particular insulin receptor isoform during organogenesis. I observed that IR-A mRNA was the predominant isoform in all foetal tissue studied, and the proportion of this isoform declined as the animal matured. These changes were significant in cardiac muscle, kidney and most dramatic in the liver where the expression of IR-A mRNA changed from 53% in the 21 day old foetus (the day before parturition) to 13% in the 1 day old neonate. These results suggest that the splicing mechanism which generates the receptor isoforms is subject to acute hormonal and/or metabolic control.The current literature suggests that the carbohydrate moieties of the insulin receptor affects its affinity for insulin. Furthermore, the IR-A and IR-B isoforms have been shown to display a 2-fold difference in their insulin binding affinity when expressed in heterologous cell lines such at CHO cells or Rat-1 fibroblasts. Since both glycosylational and isoform distribution differences were evident between mammary and liver tissues, the insulin binding affinities of these receptors were compared. Estimates of the binding affinity parameters were performed at both 4 C and 37 C. At both temperatures the equilibrium binding constants for mammary and liver tissues were not significantly different suggesting that structural variations of the mammary insulin receptor had no effect on the insulin binding affinity under the ++
conditions described in this study. Comparison of the 4 C and 37 C binding data showed that the mammary insulin receptor exhibited complex, temperature-dependent binding characteristics, similar to those previously described for the liver insulin receptor, and entirely consistent with the presence of a temperature-dependent regulatory protein that affects insulin binding.
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Metcalf, J. A. "The effect of insulin on glucose metabolism during lactation in the ewe." Thesis, University of Newcastle Upon Tyne, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378850.

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Knights, Penelope Anne. "Magnesium status in normal and diabetic pregnancy : pregnancy outcome and lactation." Thesis, University of Wolverhampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263332.

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Kim, Tae-gyu. "Effects of #beta#-casomorphins on metabolism of dairy cows." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301620.

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Tavare, J. M. "The insulin receptor and insulin stimulated protein kinase : Their role in insulin action." Thesis, University of Bristol, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370675.

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Almutairi, Mohammed Mashari. "Role of Bumetanide on Insulin Secretion." Wright State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=wright1408377608.

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Denis, Raphaël Georges Philippe. "Role of the leptin-hypothalmic axis in the hyperphagia of lactation." Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268899.

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Basson, Annelie. "Circulating glucose responses in early lactation dairy cows to dietary restriction and rbST treatment." Diss., University of Pretoria, 2008. http://hdl.handle.net/2263/28939.

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Galactopoietic effects of somatotropin are the result of IGF-I and require high-quality nutrient intake. This study investigated short-term partitioning effects during recombinant bovine somatotropin (bST) administration in high yielding early lactation dairy cows. Administration of recombinant bST has been shown generally to alter results of metabolic tests in the face of unchanged basal glucose and insulin concentrations. Ten multiparous Holstein cows were subjected to rbST (Lactotropin®) and/or feed intake restriction to 80% of predicted ME requirement (80% ME). Responses to insulin challenge (0.1 IU porcine insulin/kg BW. 210 min) and hyperglycaemic clamp (+50 mg/dL whole blood, 120 min) were tested during weeks 8 (control), 9 (rbST ), 11 (80% ME) and 12 (rbST + 80% ME) postpartum. Plasma and whole blood samples were assayed for glucose concentrations. The rbST treatment decreased fasting whole-blood glucose concentration by 9.4% (P<0.0001), which was likely a remnant of control hyperglycaemia. Maximum glucose response was 4.0 mg/dL (21.7%) lower (P<0.0038) and took 6.5 minutes longer to attain (P<0.0037). Steady-state glucose infusion rate (SSGIR) decreased by 8.1 % (P<0.0001). The 80% ME treatment decreased glucose availability by 5 to 6% (P<0.0100), while no glucose responses were affected. Restricted energy intake during treatment with rbST resulted in plasma glucose increase by 5.5% (P<0.0001). Peripheral uptake and utilization of glucose increased by 5.1 % (P<0.0005). Compared to energy restriction, 80%ME + rbST did not alter effects of nutrient restriction on responses to exogenous insulin challenge. Effects were small and inconsistent. SSGIR decreased by 5.0% in the 80% ME + rbST compared to the 80% ME period (P<0.0004) and the change in the hyperglycaemic clamp in the absence of an effect in the insulin challenge may be due to differences in endogenous insulin secretion. The conclusion was that rbST treatment resulted in altered glucose metabolic responses, even with restricted energy intake.
Dissertation (MSc(Agric))--University of Pretoria, 2008.
Animal and Wildlife Sciences
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Hoppa, Michael Blake. "The role of calcium in Insulin exocytosis." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510976.

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Books on the topic "Insulin role in lactation"

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Mahood, I. Kim. Glycated insulin and its role in the pathogenesis of diabetics. [S.l: The Author], 2003.

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Khan, Frances Rosemary. The role of insulin and the insulin-like growth factors in the proliferation of the rat thymic lymphocyte. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1989.

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Willetts, Alison. The role of cytoskeletal proteins in the mechanism of insulin release. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1988.

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Farese, Robert V. The role of protein kinase C in insulin action, resistence and secretion. Austin: R.G. Landes, 1994.

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Playford, Martin P. The role of the type 1 insulin-like growth factor receptor in cancer biology. Oxford: Oxford Brookes University, 2000.

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Cho, Charles Young. Role of oxidative stress in two models of insulin resistance within primary rat adipocytes. Ottawa: National Library of Canada, 1999.

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Belbrahem, Atika. Characterisation of protein Kinase C in chick embryo tissues and hepatocytes: Role in insulin signalling. Manchester: University of Manchester, 1994.

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Smulker, Simon R. Determination and characterization of the functional role nitric oxide in the regulation of insulin release. Ottawa: National Library of Canada, 2002.

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Miller, Stella-Maria. The expression and putative role of the insulin-like growth factor genes in human ovary. Manchester: University of Manchester, 1996.

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Dahl, Douglas Middleton. The hormonal and humoral regulators of myocardial protein metabolism: The in vivo measurement of the physiologic role of insulin and amino acids in cardiac protein kinetics. [s.l: s.n.], 1992.

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Book chapters on the topic "Insulin role in lactation"

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Rushakoff, R. J., R. A. Liddle, J. A. Williams, and I. D. Goldfine. "The Role of Cholecystokinin and Other Gut Peptides on Regulation of Postprandial Glucose and Insulin Levels." In Insulin, 125–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_7.

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Garg, Abhimanyu. "The Role of Body Fat Distribution in Insulin Resistance." In Insulin Resistance, 83–96. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_5.

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Radziuk, Jerry, and Susan Pye. "The Role of the Liver in Insulin Action and Resistance." In Insulin Resistance, 197–231. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_11.

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Ogawa, Wataru, Takashi Matozaki, and Masato Kasuga. "Role of binding proteins to IRS-1 in insulin signalling." In Insulin Action, 13–22. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5647-3_2.

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Drake, Paul G., and Barry I. Posner. "Insulin receptor-associated protein tyrosine phosphatase(s): Role in insulin action." In Insulin Action, 79–89. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5647-3_9.

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Bremel, Robert D. "α-Lactalbumin Regulation and Its Role in Lactation." In Intercellular Signalling in the Mammary Gland, 121–29. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_28.

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Salehi, Marzieh. "The Role of Incretins in Insulin Secretion." In Principles of Diabetes Mellitus, 57–69. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-18741-9_4.

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Schroeder, Brock E., and Orville Kolterman. "The Role of Incretins in Insulin Secretion." In Principles of Diabetes Mellitus, 57–74. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-09841-8_4.

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Frost, Susan C., and Robert Risch. "Role of Receptor Internalization in Insulin Signalling." In Advances in Experimental Medicine and Biology, 215–25. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5949-4_20.

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Varela, Isabel, Jose F. Alvarez, Jose Puerta, Rosa Clemente, Ana Guadaño, Matias Avila, Francisco Estevez, Susana Alemany, and Jose M. Mato. "Role of Glycosyl-Phosphatidylinositols in Insulin Signalling." In Activation and Desensitization of Transducing Pathways, 167–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83618-3_10.

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Conference papers on the topic "Insulin role in lactation"

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Đokovic, Radojica, Marko Cincovic, Vladimir Kurćubic, Milun D. Petrovic, Miloš Ži Petrovic, Ljiljana Anđušic, and Biljana Anđelic. "HOMEORETSKA REGULACUJA METABOLIČKIH FUNKCIJA KOD KRAVA U PERIPARTALNOM PERIODU." In SAVETOVANJE o biotehnologiji sa međunarodnim učešćem. University of Kragujevac, Faculty of Agronomy, 2021. http://dx.doi.org/10.46793/sbt26.235dj.

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The aim of this paper is to describe complex homeoretic and homeostatic mechanisms in dairy cows during the peripartum period. The endocrine system has a key function in regulating the adaptation of metabolism during the peripartum period. Homeoresis represents the functioning of the endocrine system and metabolism in conditions when the organism must primarily provide certain physiological processes, such as fetal growth or lactation. Then the function of all tissues is adjusted to the new situation. Homeoretic hormones (growth hormone, prolactin, glucocorticosteroids, thyroid hormones, insulin, glucagon and leptin) in dairy cows in the peripartum period play a key role in maintaining high lactation and maintaining cow health.
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Guerra- Menéndez, L., S. Amor, B. Martín-Carro, D. González Hedström, A. Tejera, B. Oltra, R. Arriazu, G. Diéguez, AL García-Villalón, and M. Granado. "P20 Study of insulin cardiovascular resistance in an animal model of childhood obesity by over-feeding during lactation." In British Society for Cardiovascular Research, Autumn Meeting 2017 ‘Cardiac Metabolic Disorders and Mitochondrial Dysfunction’, 11–12 September 2017, University of Oxford. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bscr.25.

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Al-Jaber, Hend Sultan, Layla Jadea Al-Mansoori, and Mohamed Aghar Elrayess. "The Role of GATA3 in Adipogenesis & Insulin Resistance." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0143.

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Background: Impaired adipogenesis plays an important role in the development of obesityassociated insulin resistance and type 2 diabetes. Adipose tissue inflammation is a crucial mediator of this process. In hyperglycemia, immune system is activated partially through upregulation of GATA3, causing exacerbation of the inflammatory state associated with obesity. GATA3 also plays a role as a gatekeeper of terminal adipocyte differentiation. Here we are examining the impact of GATA3 inhibition in adipose tissue on restoring adipogenesis, reversing insulin resistance and potentially lowering the risk of type 2 diabetes. Results: GATA-3 expression was higher in insulin resistant obese individuals compared to their insulin sensitive counterparts. Targeting GATA-3 with GATA-3 specific inhibitors reversed impaired adipogenesis and induced changes in the expression of a number insulin signaling-related genes, including up-regulation of insulin sensitivity-related gene and down-regulation of insulin resistance-related genes. Conclusion: GATA3 expression is higher in differentiating adipocytes from obese insulin resistant. Inhibiting GATA3 improves adipocytes differentiation and rescues insulin sensitivity in insulin resistant cells
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Yee, D. "Abstract ES9-1: Role for IGF/Insulin signaling in breast cancer." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-es9-1.

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Oberg, DH, H. Zhang, and D. Yee. "Role of the insulin receptor in IGF-system signaling and biology." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-4055.

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Huchem, Zamen Issea, and Kareem Hamed Ghali. "The role of CXCL9 and IFIH1 in insulin dependent diabetes mellitus." In INTERNATIONAL CONFERENCE OF NUMERICAL ANALYSIS AND APPLIED MATHEMATICS ICNAAM 2019. AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0027463.

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Abdullah Almuraikhy, Shamma, and Mohamed Elrayess. "Role Of Inflammatory Cells In Insulin Resistance-associated Impairment Of Preadipocytes Differentiation." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0194.

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Doyle, Suzanne L., Claire Donohoe, Joanne Lysaght, Fiona Lithander, Graham Pidgeon, and John V. Reynolds. "Abstract 2283: The role of insulin-like growth factor-1 and insulin like growth factor-1 receptor in obesity and oesophageal cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2283.

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Wilhelmi, I., T. Laeger, B. Eggen, M. Stadion, O. Kluth, and A. Schürmann. "The role of the GTPase ARFRP1 on insulin secretion from pancreatic β-cells." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641774.

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Kries, R. V., M. J. Shearer, P. T. McCarthy, M. Haug, and C. Harzer. "VITAMIN K1 IN HUMAN MILK." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643400.

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Fatal vitamin K deficiency haemorrhage has been observed in breast fed babies. Though the incidence of vitamin K deficiency haemorrhage seems to be low in exclusively breastfed babies in Germany, subclinical vitamin K deficiency is by far more common as demonstrated in recent studies. Vitamin K concentrations in human milk are lower than in cow's milk and infant formula, however, nothing is known about the factors determinating the vitamin K1 concentrations in human milk. Vitamin K1 concentrations in human milk were studied during the first five weeks of lactation with respect to a) stage of lactation, b) interindividual differences, c) relationship of vitamin K1 to other lipids, and d) influence of oral supplements of vitamin K1 given to the mother. Milk samples from 9 mothers were collected on day 1,3,5,22,29 and 36 of lactation using standarized techniques.a) Vitamin K1 concentrations in colostral milk, day 1-5 (median 1,8 ng/ml) were significanctly higher than in mature milk, day 22-36 (median 1,1 ng/ml) (Wilcoxon U-Test p< 0,01). These changes during the course of lactation must be considered for estimation of the vitamin K supply in breastfed babies.b) Vitamin K concentrations both for colostral and mature milk were found to vary widely: colostral milk 0,6-4,4 ng/ml, mature milk 0,4 - 2,8 ng/ml.c) For colostral milk regression analyses revealed good correlations of vitamin K1 to cholesterol but none to total lipid and phospholipids, whereas no correlation to either lipid was observed for mature milk. Cholesterol appears to have a role in vitamin K1 secretion into colostral milk.d) Vitamin K1 concentrations of maternal milk were influenced by oral supplements given to the mother. Even with a dose of 100 μ vitamin K1 (similar to the dose which may be ingested with a meal) a twofold increase of the vitamin K1. content of breast milk was observed. These data suggest that mutritional factors may influence the vitamin concentration in human milk. Vitamin K supplements for breastfeeding mothers on vitamin K1 poor diets could improve the vitamin K supply of these babies.
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Reports on the topic "Insulin role in lactation"

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Harbeson, Caroline E., and Steven A. Rosenzweig. The Role of Insulin-Like Growth Factor (IGF) in IGF-Mediated Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada432027.

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Olefsky, Jerrold. Role of Inflammation and Insulin Resistance in Mouse Models of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580520.

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Harbeson, Caroline E., and Steven A. Rosenzweig. The Role of Insulin-Like Growth Factor (IGF) Binding Proteins (IGFBPs) in IGF-Mediated Tumorigenicity. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada420331.

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Harbeson, Caroline E., and Steven A. Rosenzweig. The Role of the Insulin-Like Growth Factor (IGF) Binding Proteins (IGFBPs) in IGF-Mediated Tumorigenicity. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada409808.

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Weisberg, Tracey F. The Role of Growth Hormone and Insulin-Like Growth Factor-1 in Human Breast Cancer Growth in a Mouse Xenograft Model. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada391179.

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