The adaptation of maternal energy metabolism to lactation and its underlying mechanisms

Anhê, Gabriel Forato; Bordin, Silvana

doi:10.1016/j.mce.2022.111697

Cited by 6 publications

(7 citation statements)

References 235 publications

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“…Furthermore, lactation performance is influenced by the capacity to dissipate body heat, and prolactin may be a contributing factor in this process limiting thermogenesis by the downregulation of BAT UCP1. 133,135 Of note, prolactin-induced UCP1 decrease in female adult rats was not evidenced in male rats. 131 Interestingly, in many mammals circulating prolactin levels display seasonality 136 with the highest levels during summer and lowest during winter months 137,138 and this circannual rhythm appears to be involved in acclimatization to seasonal changes.…”

Section: Prolactin and Batmentioning

confidence: 95%

“…131,132 In lactating dams the expression levels of BAT thermogenic genes are decreased, 132,133 and in hamsters, BAT weight and activity decrease throughout pregnancy. 134 These data suggest a negative association between high prolactin and the thermogenic capacity of BAT during pregnancy and lactation, 135 when glucose and triglycerides should not be burned to produce heat because they are needed for the pregnant and lactating mother, and glucose for the developing fetus. Furthermore, lactation performance is influenced by the capacity to dissipate body heat, and prolactin may be a contributing factor in this process limiting thermogenesis by the downregulation of BAT UCP1.…”

Section: Prolactin and Batmentioning

confidence: 99%

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Neuroendocrine control of brown adipocyte function by prolactin and growth hormone

Winne

Pascual

Lopez‐Vicchi

et al. 2023

J Neuroendocrinology

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Growth hormone (GH) is fundamental for growth and glucose homeostasis, and prolactin for optimal pregnancy and lactation outcome, but additionally, both hormones have multiple functions that include a strong impact on energetic metabolism. In this respect, prolactin and GH receptors have been found in brown, and white adipocytes, as well as in hypothalamic centers regulating thermogenesis. This review describes the neuroendocrine control of the function and plasticity of brown and beige adipocytes, with a special focus on prolactin and GH actions. Most evidence points to a negative association between high prolactin levels and the thermogenic capacity of BAT, except in early development. During lactation and pregnancy, prolactin may be a contributing factor that limits unneeded thermogenesis, downregulating BAT UCP1. Furthermore, animal models of high serum prolactin have low BAT UCP1 levels and whitening of the tissue, while lack of Prlr induces beiging in WAT depots. These actions may involve hypothalamic nuclei, particularly the DMN, POA and ARN, brain centers that participate in thermogenesis. Studies on GH regulation of BAT function present some controversies. Most mouse models with GH excess or deficiency point to an inhibitory role of GH on BAT function. Even so, a stimulatory role of GH on WAT beiging has also been described, in accordance with whole‐genome microarrays that demonstrate divergent response signatures of BAT and WAT genes to the loss of GH signaling. Understanding the physiology of BAT and WAT beiging may contribute to the ongoing efforts to curtail obesity.

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Section: Prolactin and Batmentioning

confidence: 95%

Section: Prolactin and Batmentioning

confidence: 99%

Neuroendocrine control of brown adipocyte function by prolactin and growth hormone

Winne

Pascual

Lopez‐Vicchi

et al. 2023

J Neuroendocrinology

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“…Considering that we observed loss of p53 expression during lactation in the BL/6 NZB females (Fig. 2A) and lactation engages robust secretion that alters both ER-stress and mitochondria 34,35 , we tested whether the idiosyncrasies of lactation between genotypes also results in differential activation of stress pathways in the ER and mitochondria.…”

Section: Idiosyncrasy Of Lactation Leads To Differential Activation O...mentioning

confidence: 99%

Idiosyncratic nature of lactation reveals link to breast cancer risk.

Germain,

Chattopadhyay,

Jenkins

et al. 2024

Preprint

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Breastfeeding protects against breast cancer in some women but not others, however the mechanism remains elusive. Lactation requires intense secretory activity of the endoplasmic reticulum (ER) for the production of milk proteins and ER- mitochondria contacts for lipid synthesis. We show that in female mice that share the same nuclear genome (BL/6) but differ in mitochondrial genomes (C57 or NZB), the biological processes engaged during lactation are entirely different at the sub-cellular organization and transcriptional levels resulting in anti-tumorigenic lactation in BL/6C57 females and pro-tumorigenic lactation in BL/6NZB females. Single cell sequencing identified a sub-population of cells, uniquely amplified during lactation in BL/6NZB females, which shares the genetic signature that characterizes post-partum breast cancer (PPBC) in humans relative to matched breast cancers in never pregnant women. Our data indicate that differences in ER and mitochondrial-stress responses during lactation between genotypes inadvertently leads to loss of p53 tumor suppressor function in BL/6NZB females allowing the expansion of the PPBC-like sub-population of cells. Overall, our data reveals the unexpected idiosyncratic nature of lactation and its impacts on the risk of the development of PPBC.

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“…Moreover, lipolysis in white adipose tissue increases, while gluconeogenesis in the liver and thermogenesis in brown adipose tissue is reduced. Simultaneously with these adjustments, the endocrine pancreas undergoes plastic remodeling, resulting in a temporary loss of pancreatic beta cell mass gained during pregnancy as well as a reduction in insulin output [79]. Bearing in mind all these alterations, lactation's impact on adiposity, lipid, and glucose homeostasis seems significant, and various research studies have been conducted to prove it.…”

Section: Breastfeeding's Impact On the Meta-inflammatory Processmentioning

confidence: 99%

Influence of Breastfeeding on the State of Meta-Inflammation in Obesity—A Narrative Review

Mazur,

Satora,

Rekowska

et al. 2023

CIMB

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Obesity has become an emerging health issue worldwide that continues to grow in females of reproductive age as well. Obesity, as a multisystem and chronic disease, is associated with metabolic inflammation, which is defined as chronic low-grade systemic inflammation mediated by, i.a., adipose tissue macrophages. Lactation has been proven to have a beneficial influence on maternal health and could help restore metabolic balance, especially in the state of maternal obesity. In this review, we aimed to analyze the influence of breastfeeding on chronic low-grade meta-inflammation caused by obesity. We performed a comprehensive literature review using the PubMed, Science Direct, and Google Scholar electronic databases. For this purpose, we searched for “metabolic inflammation”; “meta-inflammation”; “obesity”; “breastfeeding”; “fetal programming”; “energy metabolism”; “postpartum”; “immunity”; “immune system”; and “inflammation” keyword combinations. While the clinical impact of breastfeeding on maternal and offspring health is currently well known, we decided to gain insight into more specific metabolic effects of adiposity, lipid, and glucose homeostasis, and immunological effects caused by the activity of cytokines, macrophages, and other immune system cells. Further research on the immunological and metabolic effects of breastfeeding in obese patients is key to understanding and potentially developing obesity therapeutic strategies.

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The adaptation of maternal energy metabolism to lactation and its underlying mechanisms

Cited by 6 publications

References 235 publications

Neuroendocrine control of brown adipocyte function by prolactin and growth hormone

Neuroendocrine control of brown adipocyte function by prolactin and growth hormone

Idiosyncratic nature of lactation reveals link to breast cancer risk.

Influence of Breastfeeding on the State of Meta-Inflammation in Obesity—A Narrative Review

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