Journal articles: 'Lactogenesis'

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Neville, Margaret C., Jane Morton, and Shinobu Umemura. "Lactogenesis." Pediatric Clinics of North America 48, no. 1 (February 2001): 35–52. http://dx.doi.org/10.1016/s0031-3955(05)70284-4.

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Huang, Li, Shangzhi Xu, Xi Chen, Qian Li, Lixia Lin, Yu Zhang, Duan Gao, et al. "Delayed Lactogenesis Is Associated with Suboptimal Breastfeeding Practices: A Prospective Cohort Study." Journal of Nutrition 150, no. 4 (December 25, 2019): 894–900. http://dx.doi.org/10.1093/jn/nxz311.

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ABSTRACT Background Breastfeeding has many established health benefits to both babies and mothers. There is limited evidence on the association between delayed lactogenesis and breastfeeding practices. Objective We assessed the association between delayed lactogenesis and breastfeeding practices in women initiating breastfeeding. Design We used data from a prospective cohort study in Wuhan, China, which enrolled pregnant women at 8–16 weeks of gestation and followed up to postpartum. Women were included who had a singleton live birth, initiated breastfeeding, and provided information on infant feeding. Maternal lactogenesis status was assessed by face-to-face interview at day 4 postpartum. Breastfeeding practices (full breastfeeding and/or any breastfeeding) were queried by telephone interview at 3, 6, and 12 mo postpartum. Poisson regression and Cox regression were used to identify the association between delayed lactogenesis and breastfeeding practices. Results Delayed lactogenesis was reported by 17.9% of the 2877 participants. After adjusting for potential confounders, when compared with timely lactogenesis, delayed lactogenesis was significantly associated with higher risk of inability to sustain full breastfeeding at 3 mo postpartum (RR: 1.24, 95% CI: 1.10, 1.39) and 6 mo postpartum (RR: 1.14, 95% CI: 1.04, 1.24). Delayed lactogenesis was also significantly associated with early termination of any breastfeeding (HR: 1.15, 95% CI: 1.01, 1.30) in the adjusted model. In a combined analysis, women with higher gestational weight gain (GWG, ≥16 kg for underweight and normal weight, 15 kg for overweight/obesity) and who subsequently experienced delayed lactogenesis had the highest risk of ending any breastfeeding earlier (adjusted HR: 1.32, 95% CI: 1.11, 1.55) compared with those who gained less GWG and experienced timely lactogenesis. Conclusions This study shows that delayed lactogenesis was associated with low rate of full breastfeeding and shorter duration of any breastfeeding. Greater efforts to promote breastfeeding should be targeted towards women with delayed lactogenesis.

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Preusting, Irma, Jessica Brumley, Linda Odibo, Diane L. Spatz, and Judette M. Louis. "Obesity as a Predictor of Delayed Lactogenesis II." Journal of Human Lactation 33, no. 4 (September 1, 2017): 684–91. http://dx.doi.org/10.1177/0890334417727716.

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Background: Lactogenesis II is the onset of copious milk production. A delay in this has been associated with an increased risk of formula supplementation and early cessation of breastfeeding. Prepregnancy obesity has also been associated with decreased breastfeeding rates and early cessation. Research aim: This study aimed to evaluate the effect of prepregnancy obesity on self-reported delayed lactogenesis II. Methods: We conducted a prospective observational cohort study of 216 women with a singleton pregnancy and who planned to breastfeed. We compared the onset of lactogenesis II between women with a body mass index (BMI) < 30 kg/m2 and women with a BMI ≥ 30 kg/m2. Using multivariate logistic regression analyses, we assessed the relationship between maternal BMI and delay of lactogenesis II. Results: The prevalence of delayed lactogenesis II among women with prepregnancy BMI < 30 kg/m2 and BMI ≥ 30 kg/m2 was 46.4% and 57.9%, respectively. Delayed lactogenesis II occurred more frequently among women who were obese at the time of delivery ( p < .05). After controlling for the covariates, age, prepregnancy BMI, and gestational weight gain were positively associated with delayed lactogenesis II. Conclusion: Prepregnancy obesity and excessive gestational weight gain are associated with an increased risk of delayed lactogenesis II. Women who are at risk for delay in lactogenesis II and early breastfeeding cessation will need targeted interventions and support for them to achieve their personal breastfeeding goals.

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Holmes, Mark A., and Peter E. Hartmann. "Concentration of citrate in the mammary secretion of sows during lactogenesis II and established lactation." Journal of Dairy Research 60, no. 3 (August 1993): 319–26. http://dx.doi.org/10.1017/s0022029900027667.

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SummaryThe functional significance of citrate in the mammary secretion of six sows was investigated during the second stage of lactogenesis (lactogenesis II) and established lactation. The changes in the concentrations of progesterone and lactose in the maternal blood, and lactose, Na and K in the mammary secretion, suggested that lactogenesis II began during the final day of pregnancy. The concentration of citrate in the mammary secretion of the sows during lactogenesis II was high and varied from 5·4 (SEM 0·5) mai at day 0·5 post partum to 6·8 (SEM 0·4) mM at day 1·5 post partum. There was a decline of ˜ 30% in the concentration of citrate in the milk of sows during the first week of lactation. These findings suggest that, in contrast to all other species studied previously, milk citrate is not a harbinger of lactogenesis II in the sow. However, the changes in the concentration of citrate in the mammary secretion of sows may reflect changes in the rate ofde novosynthesis of fatty acids that take place in the mammary glands of sows during lactogenesis II and established lactation.

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Rocha, Beatriz de Oliveira, Marcia Penido Machado, Livia Lima Bastos, Livia Barbosa Silva, Ana Paula Santos, Luana Caroline Santos, and Maria Candida Ferrarez Bouzada. "Risk Factors for Delayed Onset of Lactogenesis II Among Primiparous Mothers from a Brazilian Baby-Friendly Hospital." Journal of Human Lactation 36, no. 1 (March 22, 2019): 146–56. http://dx.doi.org/10.1177/0890334419835174.

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Background: Low milk supply is frequently reported as a reason for exclusive breastfeeding cessation. Research aims: To determine the occurrence of, and the risk factors associated with, delayed onset of lactogenesis II among primiparas seen at a Baby-Friendly Hospital in Brazil. Method: We conducted a prospective longitudinal observational cohort study of 224 primiparas who had a singleton delivery. Data were first collected at the hospital. We assessed the onset of lactogenesis on day four postpartum, based on maternal reports of changes in breast fullness. Breastfeeding practices and Edinburgh Postnatal Depression Scale were evaluated on day seven postpartum. Using Poisson regression, we assessed significant factors associated with delayed onset of lactogenesis II. Results: Delayed lactogenesis II occurred in 18.8% ( n = 42) of participants and was significantly associated with alcohol drinking during pregnancy (IRR = 2.710, 95% CI [1.469, 4.996]); Edinburgh Postnatal Depression Scale scores ≥ 10 (IRR = 2.092, 95% CI [1.118, 3.916]), and the age of the mother (IRR: 1.081, 95% CI [1.039, 1.125]). Conclusion: Postpartum depression and alcohol ingestion during pregnancy may be associated with lactogenesis II delay, but more research is needed to elucidate the directionality of these relationships. Older mothers are at risk of delayed lactogenesis II onset. The frequency of delayed lactogenesis in this population is similar to the rates seen in previous Latin America studies and much lower than the ranges seen in North America, possibly because of the low proportion of obesity and severe gestational diabetes in this sample.

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Mellenberger, R. W., D. E. Bauman, and D. R. Nelson. "Metabolic Adaptations During Lactogenesis." Journal of Mammary Gland Biology and Neoplasia 14, no. 3 (August 4, 2009): 261–68. http://dx.doi.org/10.1007/s10911-009-9140-x.

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Plath, A., R. Einspanier, F. Peters, F. Sinowatz, and D. Schams. "Expression of transforming growth factors alpha and beta-1 messenger RNA in the bovine mammary gland during different stages of development and lactation." Journal of Endocrinology 155, no. 3 (December 1, 1997): 501–11. http://dx.doi.org/10.1677/joe.0.1550501.

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It is now widely accepted that the mammary gland is under interconnected hormonal and local control. Growth factors are involved in the intercellular signalling of the gland. Our aim was the detection of transforming growth factors alpha (TGF-alpha) and beta 1 (TGF-beta 1) messenger RNA during mammogenesis, lactogenesis, galactopoiesis and involution in the bovine mammary gland (total n = 27). During these stages the RNA was assessed by means of ribonuclease protection assay and reverse transcription-polymerase chain reaction (RT-PCR). To study possible influences of oestrogen, progesterone and prolactin on growth factor expression, mammary RNA was obtained from heifers after induced mammogenesis and lactogenesis, with and without additional prolactin inhibition (total n = 20). Very low levels of TGF-alpha and TGF-beta 1 expression were detected during lactogenesis and galactopoiesis, increasing levels during mammogenesis of primigravid heifers, and highest levels during mammogenesis of virgin heifers and during involution. TGF-alpha expression after induced mammogenesis was greater than after induced lactogenesis or physiological mammogenesis during pregnancy. Furthermore, TGF-alpha mRNA contents increased after prolactin inhibition. TGF-beta 1 expression was almost equal after induced mammogenesis and lactogenesis, but greater than during the physiological mammogenesis and lactogenesis. In conclusion, it can be assumed that growth promoting TGF-alpha and growth inhibiting TGF-beta 1 are co-expressed in the bovine mammary gland. Higher mRNA contents of both factors during mammogenesis and involution may indicate autocrine or paracrine functions for these growth factors during proliferation and reorganisation of the mammary tissue.

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Casey, Theresa, Hui Sun, Helen J. Burgess, Jennifer Crodian, Shelley Dowden, Shelby Cummings, Karen Plaut, David Haas, Lingsong Zhang, and Azza Ahmed. "Delayed Lactogenesis II is Associated With Lower Sleep Efficiency and Greater Variation in Nightly Sleep Duration in the Third Trimester." Journal of Human Lactation 35, no. 4 (March 28, 2019): 713–24. http://dx.doi.org/10.1177/0890334419830991.

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Background: Metabolic and hormonal disturbances are associated with sleep disturbances and delayed onset of lactogenesis II. Research aims: The aim of this study was to measure sleep using wrist actigraphy during gestation weeks 22 and 32 to determine if sleep characteristics were associated with blood glucose, body mass index, gestational related disease, delayed onset of lactogenesis II, or work schedule. Methods: Demographic data were collected at study intake from primiparous women who wore a wrist actigraph during gestation weeks 22 ( n = 50) and 32 ( n = 44). Start and end sleep time, total nighttime sleep, sleep efficiency, wake after sleep onset, and sleep fragmentation were measured. Night to night variability was assessed with the root mean square of successive difference. Blood glucose levels, body mass index, and gestational disease data were abstracted from medical charts. Timing of lactogenesis II was determined by survey. Results: Between gestation week 22 and 32, sleep efficiency decreased and fragmentation increased ( p < .05). During gestation week 32, blood glucose was negatively correlated with sleep duration, and positively related to fragmentation ( p < .05). Women who experienced delayed lactogenesis II had lower sleep efficiency and greater fragmentation ( p < .05), and greater night-to-night variability in sleep start and end time, efficiency, and duration during gestation week 32 ( p < .05). Conclusion: Women with better sleep efficiency and more stable nightly sleep time are less likely to experience delayed onset of lactogenesis II. Interventions to improve sleep may improve maternal health and breastfeeding adequacy.

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Rasmussen, Kathleen M., Julie A. Hilson, and Chris L. Kjolhede. "Obesity May Impair Lactogenesis II." Journal of Nutrition 131, no. 11 (November 1, 2001): 3009S—3011S. http://dx.doi.org/10.1093/jn/131.11.3009s.

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Barbalinardo, Laurie H. "Allergic Response to Lactogenesis 2?" Breastfeeding Medicine 7, no. 2 (April 2012): 128. http://dx.doi.org/10.1089/bfm.2012.9992.

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Taylor, Barbara. "Retained Placenta and Suppressed Lactogenesis?" Journal of Human Lactation 11, no. 4 (December 1995): 261. http://dx.doi.org/10.1177/089033449501100403.

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Rassie, Kate, Aya Mousa, Anju Joham, and Helena J. Teede. "Metabolic Conditions Including Obesity, Diabetes, and Polycystic Ovary Syndrome: Implications for Breastfeeding and Breastmilk Composition." Seminars in Reproductive Medicine 39, no. 03/04 (July 2021): 111–32. http://dx.doi.org/10.1055/s-0041-1732365.

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AbstractBreastfeeding is internationally recognized as the recommended standard for infant nutrition, informed by evidence of its multiple benefits for both mother and baby. In the context of common metabolic conditions such as polycystic ovary syndrome, diabetes (type 1, type 2, and gestational), and obesity, breastfeeding may be particularly beneficial for both mother and infant. However, there is evidence of delayed lactogenesis and reduced breastfeeding rates and duration in women with these conditions, and the effects of altered maternal metabolic environments on breastmilk composition (and potentially infant outcomes) are incompletely understood. In this review, we explore the relationships between maternal metabolic conditions, lactogenesis, breastfeeding, and breastmilk composition. We examine relevant potential mechanisms, including the central role of insulin both in lactogenesis and as a milk-borne hormone. We also describe the bioactive and hormonal components of breastmilk and how these may link maternal and infant health.

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Mullen, Amber J., Deborah L. O’Connor, Anthony J. Hanley, Giovanni Piedimonte, Maeve Wallace, and Sylvia H. Ley. "Associations of Metabolic and Obstetric Risk Parameters with Timing of Lactogenesis II." Nutrients 14, no. 4 (February 19, 2022): 876. http://dx.doi.org/10.3390/nu14040876.

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Lactogenesis II is the onset of copious milk production following parturition. Delayed onset of lactogenesis II (DLII) often contributes to poorer lactation performance, which may adversely affect maternal and child health. The present study aims to identify the metabolic and obstetric risk factors for DLII in a secondary analysis of a prospective cohort study following pregnant women through postpartum. We defined the onset of lactogenesis II as delayed if it occurred ≥72 h postpartum. Multiple logistic regression analyses were conducted to evaluate the associations of metabolic and obstetric variables with DLII. Median onset of lactogenesis II was 72.4 h (IQR 60.4–91.6) postpartum, and 55.4% (98 of 177) of women experienced DLII. Time to first breast contact ≥ 2 h postpartum compared to ≤1 h postpartum was associated with DLII (OR 2.71 95% CI 1.12–6.53) with adjustment for age, race, pregravid BMI, primiparity, and mode of delivery, while metabolic variables were not significantly associated with DLII. In this comprehensive examination of potential metabolic and obstetric parameters, earlier timing of putting the infant to the breast remained significantly associated with earlier onset of milk coming in after consideration of the other potential risk factors. Obstetrical practices, including putting the baby to the breast later, may have an important impact on the timing of lactation, and interventions are needed to address this concern.

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Noble, L. M. "Delayed Lactogenesis II Decreases Breastfeeding Success." AAP Grand Rounds 28, no. 3 (August 31, 2012): 26. http://dx.doi.org/10.1542/gr.28-3-26.

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Haldeman, Wendy. "Can Magnesium Sulfate Therapy Impact Lactogenesis?" Journal of Human Lactation 9, no. 4 (December 1993): 249–52. http://dx.doi.org/10.1177/089033449300900426.

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Nguyen, DA, AF Parlow, and MC Neville. "Hormonal regulation of tight junction closure in the mouse mammary epithelium during the transition from pregnancy to lactation." Journal of Endocrinology 170, no. 2 (August 1, 2001): 347–56. http://dx.doi.org/10.1677/joe.0.1700347.

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Closure of the tight junctions of the mammary epithelium has been shown to accompany the onset of copious milk secretion or lactogenesis, stage 2, in both goats and humans. Here we use injection of [(14)C]sucrose and FITC-albumin (fluorescein isothiocyanate-albumin) into the mammary duct to follow the course of tight junction closure during lactogenesis in mice. To examine the hormonal changes responsible, we ovariectomized day 16 or 17 pregnant mice and found that closure followed ovariectomy with a mean delay of 13.6+/-1.5 (s.e.m. ) h. That progesterone withdrawal is the trigger for closure was shown by the finding that injection of progesterone within 4 h of ovariectomy delayed closure and that closure occurred after injection of the progesterone antagonist RU 486 in intact late pregnant mice. Endocrine ablation studies showed that low to moderate concentrations of corticosterone and either placental lactogen or prolactin are necessary for tight junction closure triggered by progesterone withdrawal. Thus the hormonal requirements for tight junction closure are similar to those shown by other investigators to promote lactogenesis, stage 2. Further, the tight temporal control of tight junction permeability suggests that ovariectomy of the late pregnant mouse may be a good model for molecular studies of the lactogenic switch.

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Pramaningtyas, Miranti Dewi. "Delayed lactogenesis II and unsuccessful exclusive breastfeeding." Jurnal Kedokteran dan Kesehatan Indonesia 10, no. 2 (August 30, 2019): 107–9. http://dx.doi.org/10.20885/jkki.vol10.iss2.art2.

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Livingstone, Verity. "Retained Placenta and Suppressed Lactogenesis: Author's Reply." Journal of Human Lactation 11, no. 4 (December 1995): 261. http://dx.doi.org/10.1177/089033449501100404.

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Morrison, Bethanie, and Mary Lou Cutler. "The contribution of adhesion signaling to lactogenesis." Journal of Cell Communication and Signaling 4, no. 3 (September 15, 2010): 131–39. http://dx.doi.org/10.1007/s12079-010-0099-6.

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Anderson, Ann M. "Disruption of Lactogenesis by Retained Placental Fragments." Journal of Human Lactation 17, no. 2 (May 2001): 142–44. http://dx.doi.org/10.1177/089033440101700210.

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Tao, Xing-Yong, Kun Huang, Shuang-Qin Yan, A.-Zhu Zuo, Rui-Wen Tao, Hui Cao, Chun-Li Gu, and Fang-Biao Tao. "Pre-pregnancy BMI, gestational weight gain and breast-feeding: a cohort study in China." Public Health Nutrition 20, no. 6 (December 7, 2016): 1001–8. http://dx.doi.org/10.1017/s1368980016003165.

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AbstractObjectiveThe purpose of the present study was to examine the influence of maternal pre-pregnancy BMI and gestational weight gain (GWG) on initiation and duration of infant breast-feeding in a prospective birth cohort study.DesignBreast-feeding information was collected at 1, 3, 6 and 12 months postpartum. The association of pre-pregnancy BMI and GWG with delayed lactogenesis II and termination of exclusive breast-feeding was assessed with logistic regression analysis. The risk of early termination of any breast-feeding during the first year postpartum was assessed with Cox proportional hazards models.SettingUrban city in China.SubjectsWomen with infants from the Ma’anshan Birth Cohort Study (n 3196).ResultsThe median duration of any breast-feeding in this cohort was 7·0 months. Pre-pregnancy obese women had higher risks of delayed lactogenesis II (risk ratio=1·89; 95 % CI 1·04, 3·43) and early termination of any breast-feeding (hazard ratio=1·38; 95 % CI 1·09, 1·75) adjusted for potential maternal and infant confounders, when compared with normal-weight women. No differences in breast-feeding initiation or duration of exclusive breast-feeding according to pre-pregnancy BMI were found. Moreover, GWG was not associated with any poor breast-feeding outcomes.ConclusionsThe present study indicated that pre-pregnancy obesity increases the risks of delayed lactogenesis II and early termination of any breast-feeding in Chinese women.

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Chen, Qiong, Feng-Qi Zhao, Yifei Ren, Jialiang Han, Jianxin Liu, Yang Li, and Hongyun Liu. "Parenterally Delivered Methionyl-Methionine Dipeptide During Pregnancy Enhances Mammogenesis and Lactation Performance Over Free Methionine by Activating PI3K-AKT Signaling in Methionine-Deficient Mice." Journal of Nutrition 150, no. 5 (January 31, 2020): 1186–95. http://dx.doi.org/10.1093/jn/nxaa005.

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ABSTRACT Background Pregnancy-induced hypoaminoacidemia, l-methionine (Met) included, disturbs embryogenesis and may also affect breast function. Supplementation with the dipeptide l-methionyl-Met (Met-Met) may improve lactation performance. Objective We compared the effects of supplemental Met or Met-Met during pregnancy on mammogenesis and lactogenesis and investigated underlying mechanisms. Methods In experiment 1, 9-wk-old ICR mice (n = 72, ∼30 g) were divided into 3 groups. During the first 17 days of pregnancy (DP), the Control group was fed a diet with Met (8.2 g/kg) and saline was intraperitoneally injected, the Met group was fed a Met-devoid diet and 35% of the Met (92-mmo l Met) as contained in the Control diet was intraperitoneally injected, and the Met-Met group was fed the same diet and 70-mmo l Met plus 11-mmo l Met-Met was intraperitoneally injected. All animals were fed the Control diet after DP17 and during lactation. Mammogenesis, lactogenesis, transcriptome at DP17, and milk performance during lactation were examined. In experiment 2, 9-wk-old ICR mice (n = 55, ∼30 g) at DP0 were injected through the teat with adeno-associated virus for overexpression/inhibition of phosphoinositide-3-kinase regulatory subunit 1 (Pik3r1), divided into the Control, Met, and Met-Met groups and received the same treatment as experiment 1 to examine mammogenesis and lactogenesis at DP17. Results In experiment 1, compared with the Met group, the Met-Met group showed higher (P < 0.05) mammary epithelium percentage (42%) and αS1-casein expression (84%) at DP17, milk yield (34%) and energy concentrations (8.7%) during lactation; transcriptomic analysis illustrated activated phosphatidylinositol-3 kinase (PI3K)/protein kinase B (AKT) signaling in the mammary glands of the Met-Met group (P-adj < 0.001). In experiment 2, overexpression of Pik3r1 enhanced (P < 0.05) the protective effect of Met-Met over Met on mammogenesis and β-casein expression. Conclusion Met-Met is more effective than Met in promoting mammogenesis and lactogenesis mainly by activation of PI3K-AKT signaling in Met-deficient mice.

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López-Fontana, Constanza M., María E. Maselli, Ana M. Salicioni, and Rubén W. Carón. "The inhibitory effect of progesterone on lactogenesis during pregnancy is already evident by mid- to late gestation in rodents." Reproduction, Fertility and Development 24, no. 5 (2012): 704. http://dx.doi.org/10.1071/rd11160.

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Lactogenesis is a very complex process highly dependent on hormonal regulation. In the present study the time-course of the inhibitory actions of progesterone on prolactin secretion, mammary gland morphology and lactogenesis from mid- to late gestation in rodents was investigated. Groups of pregnant rats were luteectomised or administered with mifepristone on Day 10, 13, 15 or 17 of gestation and decapitated 28 or 48 h later. Whole-blood samples and the inguinal mammary glands were taken for determinations of hormone levels and for measurement of mammary content of casein and lactose and for tissue morphology analyses, respectively. Luteectomy or mifepristone evoked prolactin increases only after Day 17 of gestation. Mammary content of casein was increased by both treatments regardless of timing or duration. Mifepristone was less effective than luteectomy in inducing lactose production and the effect was only observed after Day 15 of gestation. Analysis of mammary gland morphology confirmed the observed effect of progesterone on lactogenesis. Both treatments triggered remarkable secretory activity in the mammary gland, even without a parallel epithelial proliferation, demonstrating that the mammary epithelium is able to synthesise milk compounds long before its full lobulo–alveolar development is achieved, provided that progesterone action is abolished. Thus, the present study demonstrates that progesterone is a potent hormonal switch for the prolactin and prolactin-like effects on mammary gland development and its milk-synthesising capacity during pregnancy, and that its inhibitory action is already evident by mid-pregnancy in rodents.

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Mizoguchi, Yasushi. "Regulation of Prolactin Receptor Gene Expression at Lactogenesis." Journal of animal genetics 26, no. 1 (1998): 26–30. http://dx.doi.org/10.5924/abgri1993.26.26.

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Rasmussen, A., M. Nielsen, A. H. Tauson, and D. Blache. "Leptin and lactogenesis in the periparturient dairy goat." Journal of Animal and Feed Sciences 13, Suppl. 1 (August 30, 2004): 555–58. http://dx.doi.org/10.22358/jafs/74034/2004.

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Savona, V., V. Zanardo, C. Cadamuro, F. Cavallin, and D. Trevisanuto. "438 Effects of Elective Cesarean Section on Lactogenesis." Pediatric Research 68 (November 2010): 225. http://dx.doi.org/10.1203/00006450-201011001-00438.

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Gabrieli, C., R. Ciullo, L. Sansone, I. Gambina, F. Cavallin, D. Faggian, M. Santini, and V. Zanardo. "1681 Late-Preterm Delivery: Psychological Distress and Lactogenesis." Archives of Disease in Childhood 97, Suppl 2 (October 1, 2012): A475. http://dx.doi.org/10.1136/archdischild-2012-302724.1681.

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Neville, Margaret C., and Jane Morton. "Physiology and Endocrine Changes Underlying Human Lactogenesis II." Journal of Nutrition 131, no. 11 (November 1, 2001): 3005S—3008S. http://dx.doi.org/10.1093/jn/131.11.3005s.

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Hildebrandt, H. Mark. "Maternal Perception of Lactogenesis Time: A Clinical Report." Journal of Human Lactation 15, no. 4 (December 1999): 317–23. http://dx.doi.org/10.1177/089033449901500409.

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Betzold, C. "Delayed lactogenesis II: a comparison of four cases." Journal of Midwifery & Women's Health 49, no. 2 (April 2004): 132–37. http://dx.doi.org/10.1016/s1526-9523(03)00537-3.

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Betzold, Christine M., Kathleen L. Hoover, and Cathy L. Snyder. "Delayed Lactogenesis II: A Comparison of Four Cases." Journal of Midwifery & Women's Health 49, no. 2 (March 4, 2004): 132–37. http://dx.doi.org/10.1016/j.jmwh.2003.12.008.

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Hurst, Nancy M. "Recognizing and Treating Delayed or Failed Lactogenesis II." Journal of Midwifery & Women's Health 52, no. 6 (November 12, 2007): 588–94. http://dx.doi.org/10.1016/j.jmwh.2007.05.005.

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Cowie, A. T., and W. R. Lyons. "Mammogenesis and lactogenesis in hypophysectomized, ovariectomized, adrenalectomized rats." Journal of Mammary Gland Biology and Neoplasia 14, no. 3 (August 5, 2009): 321–25. http://dx.doi.org/10.1007/s10911-009-9145-5.

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Morozova, N. A., A. B. Mamonov, E. A. Sirotina, and S. M. Kornienko. "The role of somatotropin in the lactogenesis process." International Journal of Gynecology & Obstetrics 70 (2000): A94. http://dx.doi.org/10.1016/s0020-7292(00)82811-8.

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Schams, D., S. Kohlenberg, W. Amselgruber, B. Berisha, MW Pfaffl, and F. Sinowatz. "Expression and localisation of oestrogen and progesterone receptors in the bovine mammary gland during development, function and involution." Journal of Endocrinology 177, no. 2 (May 1, 2003): 305–17. http://dx.doi.org/10.1677/joe.0.1770305.

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It is now well established that oestrogen and progesterone are absolutely essential for mammary gland development. Lactation can be induced in non-pregnant animals by sex steroid hormone treatment. Most of the genomic actions of oestrogens are mediated by two oestrogen receptors (ER)-alpha and ERbeta, and for gestagens in ruminants by the progesterone receptor (PR). Our aim was the evaluation of mRNA expression and protein (localisation and Western blotting) during mammogenesis, lactogenesis, galactopoiesis (early, middle and late) and involution (8, 24, 28, 96-108 h and 14-28 days after the end of milking) in the bovine mammary gland (total no. 53). During these stages, the mRNA was assessed by means of real-time RT-PCR (LightCycler). The protein for ERalpha, ERbeta and PR was localised by immunohistochemistry and Western blotting. The mRNA expression results indicated the existence of ERalpha, ERbeta and PR in bovine mammary gland. Both ERalpha and PR are expressed in fg/ micro g total RNA range. The highest mRNA expression was found for ERalpha and PR in the tIssue of non-pregnant heifers, followed by a significant decrease to a lower level at the time of lactogenesis with low concentrations remaining during lactation and the first 4 weeks of involution. In contrast, the expression of ERbeta was about 1000-fold lower (ag/ micro g total RNA) and showed no clear difference during the stages examined, with a significant increase only 2-4 weeks after the end of milking. Immunolocalisation for ERalpha revealed a strong positive staining in nuclei of lactocytes in non-pregnant heifers, became undetectable during pregnancy, lactogenesis and lactation, and was again detectable 14-28 days after the end of milking. In contrast, PR was localised in the nuclei of epithelial cells in the mammary tIssue of non-pregnant heifers, in primigravid animals, and during late lactation and involution. During lactogenesis, peak and mid lactation, fewer nuclei of epithelial cells were positive, but increased staining of the cytoplasm of epithelial cells was obvious. ERalpha and ERbeta protein was found in all mammary gland stages examined by Western blotting. In contrast to mRNA expression, the protein signal for ERalpha was weaker in the tIssue of non-pregnant heifers and during involution (4 weeks). ERbeta protein showed a stronger signal (two isoform bands) in non-pregnant heifers and 4 weeks after the end of milking. This correlated with the mRNA expression data. Three isoforms of PR (A, B and C) were found by Western blotting in the tIssue of non-pregnant heifers, but only isoform B remained during the following stages (lactogenesis, galactopoiesis and involution). In conclusion, the mRNA expression and protein data for ER and PR showed clear regulatory changes, suggesting involvement of these receptors in bovine mammary gland development and involution.

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Plath-Gabler, A., C. Gabler, F. Sinowatz, B. Berisha, and D. Schams. "The expression of the IGF family and GH receptor in the bovine mammary gland." Journal of Endocrinology 168, no. 1 (January 1, 2001): 39–48. http://dx.doi.org/10.1677/joe.0.1680039.

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To study the involvement of the IGFs in mammary development and lactation of the cow, the temporal expressions of IGF-I and -II, its receptor type 1 (IGFR-1), IGF-binding proteins (IGFBPs)-1 to -6 and GH receptor (GHR) mRNA were examined. This was carried out for different stages of mammogenesis, lactogenesis, galactopoiesis and involution in the bovine mammary gland of 26 animals. Furthermore, IGF-I was localised by immunohistochemistry. The highest mRNA concentrations for IGF-I were detected in the mammary tissue of late pregnant heifers (days 255-272) and significantly lower expression was detected during lactogenesis and galactopoiesis. Immunohistochemistry of IGF-I revealed only a weak staining in the epithelium of the ducts during mammogenesis. The epithelium of the alveoli were negative during mammogenesis, lactogenesis and galactopoiesis but displayed distinct IGF-I activity during involution. In the stroma a distinct staining of the cytoplasm of adipocytes and of vascular smooth muscle cells was observed. A certain percentage of fibroblasts (usually 20-30%) were also immunopositive. In contrast, highest expression for IGFR-1 was detected during galactopoiesis and involution. The lowest mRNA concentration for IGFR-1 was found during pregnancy (days 194-213). In general, the expression of IGF-II was not regulated during mammogenesis and lactation, but decreased during involution. The mRNA for the six binding proteins was detected in the bovine mammary gland. The dominant binding proteins were IGFBP-3 and -5. The highest expression of IGFBP-3 was observed during mid-pregnancy and the lowest during late lactation, involution and in non-pregnant heifers. The mRNA for IGFBP-5 increased during late mammogenesis and lactogenesis followed by a decrease thereafter. In general, the mRNA concentrations for IGFBP-2, -4 and -6 were barely detectable during all stages. In contrast, the expression for IGFBP-1 was upregulated in the mammary gland of virgin heifers and increased around the onset of lactation. mRNA for GHR was found during all stages examined without outstanding fluctuations. In conclusion, locally produced IGF-I and -II may mediate mammogenesis. The high mammary IGFR-1 mRNA during lactation suggests a role for peripheral IGF-I in maintenance of lactation. The role of IGFBPs in the mammary gland needs further evaluation.

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O'Dowd, Rachael, Mary E. Wlodek, and Kevin R. Nicholas. "Uteroplacental insufficiency alters the mammary gland response to lactogenic hormones in vitro." Reproduction, Fertility and Development 20, no. 4 (2008): 460. http://dx.doi.org/10.1071/rd07228.

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Adequate mammary development and coordinated actions of lactogenic hormones are essential for the initiation of lactation. Pregnancies compromised by uteroplacental insufficiency impair mammary development and lactation, further slowing postnatal growth. It is not known whether the initiation of lactation or galactopoesis is compromised. Uteroplacental insufficiency induced in rats by bilateral uterine vessel ligation (Restricted) or sham surgery (Control) on Day 18 of gestation preceded collection of mammary tissue on Day 20 of pregnancy. Mammary explants were cultured with combinations of insulin, cortisol and prolactin and analysed for α-lactalbumin and β-casein gene expression. Mammary tissue from late pregnant Restricted rats had elevated α-lactalbumin, but not β-casein, mRNA, which is consistent with premature lactogenesis resulting from an early decline in peripheral maternal progesterone. Explants from Restricted rats were more responsive to hormone stimulation after 3 days in culture, indicating that compromised galactopoesis, not lactogenesis, most likely leads to the reduced growth of suckled pups.

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38

Buttle, H. L. "Role of the ovaries in inducing mammogenesis in pregnant pigs." Journal of Endocrinology 118, no. 1 (July 1988): 41–45. http://dx.doi.org/10.1677/joe.0.1180041.

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ABSTRACT Ovariectomy, but not removal of the corpora lutea, of gilts at mid-pregnancy delayed the onset of lobuloalveolar development in the mammary glands. Lactogenesis at the time of parturition was delayed by both ovariectomy and removal of the corpora lutea. J. Endocr. (1988) 118,41–45

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39

Flint, David J., Maureen T. Travers, Michael C. Barber, Nadine Binart, and Paul A. Kelly. "Diet-induced obesity impairs mammary development and lactogenesis in murine mammary gland." American Journal of Physiology-Endocrinology and Metabolism 288, no. 6 (June 2005): E1179—E1187. http://dx.doi.org/10.1152/ajpendo.00433.2004.

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We have developed a mouse model of diet-induced obesity that shows numerous abnormalities relating to mammary gland function. Animals ate ∼40% more calories when offered a high-fat diet and gained weight at three times the rate of controls. They exhibited reduced conception rates, increased peripartum pup mortality, and impaired lactogenesis. The impairment of lactogenesis involved lipid accumulation in the secretory epithelial cells indicative of an absence of copius milk secretion. Expression of mRNAs for β-casein, whey acid protein, and α-lactalbumin were all decreased immediately postpartum but recovered as lactation was established over 2–3 days. Expression of acetyl-CoA carboxylase (ACC)-α mRNA was also decreased at parturition as was the total enzyme activity, although there was a compensatory increase in the proportion in the active state. By day 10 of lactation, the proportion of ACC in the active state was also decreased in obese animals, indicative of suppression of de novo fatty acid synthesis resulting from the supply of preformed fatty acids in the diet. Although obese animals consumed more calories in the nonpregnant and early pregnant states, they showed a marked depression in fat intake around day 9 of pregnancy before food intake recovered in later pregnancy. Food intake increased dramatically in both lean and obese animals during lactation although total calories consumed were identical in both groups. Thus, despite access to high-energy diets, the obese animals mobilized even more adipose tissue during lactation than their lean counterparts. Obese animals also exhibited marked abnormalities in alveolar development of the mammary gland, which may partially explain the delay in differentiation evident during lactogenesis.

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Farah, Erin, Mary K. Barger, Carrie Klima, Beverly Rossman, and Patricia Hershberger. "Impaired Lactation: Review of Delayed Lactogenesis and Insufficient Lactation." Journal of Midwifery & Women's Health 66, no. 5 (September 2021): 631–40. http://dx.doi.org/10.1111/jmwh.13274.

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41

Neubauer, S. H., A. M. Ferris, C. G. Chase, J. Fanelli, C. A. Thompson, C. J. Lammi-Keefe, R. M. Clark, R. G. Jensen, R. B. Bendel, and K. W. Green. "Delayed lactogenesis in women with insulin-dependent diabetes mellitus." American Journal of Clinical Nutrition 58, no. 1 (July 1, 1993): 54–60. http://dx.doi.org/10.1093/ajcn/58.1.54.

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42

Pieh-Holder, Kelly L., James A. Scardo, and Deborah H. Costello. "Lactogenesis Failure Following Successful Delivery of Advanced Abdominal Pregnancy." Breastfeeding Medicine 7, no. 6 (December 2012): 543–46. http://dx.doi.org/10.1089/bfm.2011.0131.

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Thompson, Gordon E., Wendy A. Ratcliffe, and Anthony D. Care. "Onset of calcium secretion during lactogenesis in the goat." Journal of Dairy Research 62, no. 3 (August 1995): 539–42. http://dx.doi.org/10.1017/s002202990003123x.

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Gurtcheff, Shawn E., David K. Turok, Greg Stoddard, Patricia A. Murphy, Mark Gibson, and Kirtly P. Jones. "Lactogenesis After Early Postpartum Use of the Contraceptive Implant." Obstetrics & Gynecology 117, no. 5 (May 2011): 1114–21. http://dx.doi.org/10.1097/aog.0b013e3182165ee8.

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45

Gallardo, María, Juan G. Cárcamo, Luis Arias-Darraz, and Carlos Alvear. "Effect of Diet and Type of Pregnancy on Transcriptional Expression of Selected Genes in Sheep Mammary Gland." Animals 9, no. 9 (August 21, 2019): 589. http://dx.doi.org/10.3390/ani9090589.

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These trials were carried out to determine firstly the effect of diet and type of pregnancy on the transcriptional expression of genes involved in angiogenesis and cell turnover/lactogenesis inside the sheep mammary gland from late gestation to late lactation. Eighteen Ile de France sheep, 8 twin- and 10 single-bearing ewes were alloted into two groups according to their diet, either based on ad libitum naturalized pasture or red clover hay plus lupine from day −45 pre-partum until day +60 post-partum. Samples from diets and mammary glands were collected at day −10 pre partum (time 1), day +30 (time 2) and day +60 post-partum (time 3) and analyzed by qRT-PCR. Additionally, samples from longissimus dorsi muscle were taken from lambs twice, at weaning and 45 days later, to determine the effect of the maternal treatment with regard to diet and type of pregnancy, on the mRNA expression of genes involved in lipid metabolism. The data was processed using the lme4 package for R, and SPSS Statistics 23.0 for Windows®. The results showed that the group of twin-bearing ewes fed red clover showed a higher expression of genes involved in angiogenesis before lambing and in cell turnover/lactogenesis during late lactation, explained by a lamb survival mechanism to delay apoptosis as a way to keep a secretory cells population and boosted by the diet quality, assuring a longer milk production potential during late lactation. Regarding lambs, apparently the maternal diet would influence the transcriptional expression of lipogenic enzymes in the longissimus dorsi muscle after weaning, but further studies are necessary to validate these results. In summary, Twin-bearing ewes fed red clover performed best at increasing the expression of genes associated with angiogenesis and cell turnover/lactogenesis in the mammary gland.

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Rosato, Roberto R., Maria S. Gimenez, and Graciela A. Jahn. "Effects of chronic thyroid hormone administration on pregnancy, lactogenesis and lactation in the rat." Acta Endocrinologica 127, no. 6 (December 1992): 547–54. http://dx.doi.org/10.1530/acta.0.1270547.

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We studied the effects of daily administration of 1 mg/kg thyroxine (T4) starting 10–15 days before mating, on parturition, maternal behavior and lactation in rats. Treated rats had elevated serum titers of T3 and T4, a greater number of fetuses and parturition was advanced approximately 12 h and lasted longer than in controls. None of the treated rats were able to lactate because of defects in maternal behavior and milk ejection; the litters died usually within 48 h postpartum. In rats sacrificed at 10.00 on day 21 of pregnancy, mammary gland content of total protein, phospholipids, casein and lactose were significantly increased, but total lipid was markedly reduced. Lipogenesis was also significantly increased, as well as the activity of the lipogenic enzymes glucose-6-phosphate dehydrogenase, fatty acid synthetase and isocytrate dehydrogenase. These results are indicative of normal albeit premature lactogenesis. The T4-treated rats also had advances in the prepartum fall in serum progesterone and the increase in prolactin as well as in the increase in mammary casein and lactose concentrations of approximately 12 h with respect to control pregnant rats. These results show that chronic T4 treatment induces an advance of approximately 12 h in luteolysis, which in turn advances lactogenesis and parturition in rats. Although the mammary gland was able to produce milk, lactation failed due to abnormal maternal behavior and milk ejection, the causes of which are still unknown. Other effects of hyperthyroidism were also present, such as a severe reduction in lipid content of the gland. The observed increases in lipogenesis and lipogenic enzyme activities could be due to a combination of the effects of hyperthyroidism per se as well as to the increase in lipogenesis that occurs during lactogenesis.

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Liu, X., G. W. Robinson, K. U. Wagner, L. Garrett, A. Wynshaw-Boris, and L. Hennighausen. "Stat5a is mandatory for adult mammary gland development and lactogenesis." Genes & Development 11, no. 2 (January 15, 1997): 179–86. http://dx.doi.org/10.1101/gad.11.2.179.

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Olshevskaya, H. "Clinical and hormonal parallels of lactogenesis in women with preeclampsia." International Journal of Gynecology & Obstetrics 70 (2000): B127. http://dx.doi.org/10.1016/s0020-7292(00)83102-1.

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Thompson, G. E. "Mammary extraction of plasma triglycerides in the cow during lactogenesis." Comparative Biochemistry and Physiology Part B: Comparative Biochemistry 94, no. 2 (January 1989): 411–13. http://dx.doi.org/10.1016/0305-0491(89)90365-9.

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Faraci-Orf, Elena, Catherine McFadden, and Wolfgang F. Vogel. "DDR1 signaling is essential to sustain Stat5 function during lactogenesis." Journal of Cellular Biochemistry 97, no. 1 (2005): 109–21. http://dx.doi.org/10.1002/jcb.20618.

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Journal articles on the topic 'Lactogenesis'

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