Postnatal weight gain induced by overfeeding pups and maternal high-fat diet during the lactation period modulates glucose metabolism and the production of pancreatic and gastrointestinal peptides

Du, Qinwen; Hosoda, Hiroshi; Umekawa, Takashi; Kinouchi, Toshi; Ito, Natsuki; Miyazato, Minoru; Kangawa, Kenji; Ikeda, Tomoaki

doi:10.1016/j.peptides.2015.05.003

Cited by 31 publications

(36 citation statements)

References 44 publications

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“…Our data confirm previous findings showing that maternal HFD feeding during lactation in rodents results in metabolic alterations in the offspring (5, 6, 8, 43). From postnatal d 1 to 21, offspring from HFD‐fed mothers gained 23% more body weight than those from CD‐fed dams (Fig.…”

Section: Resultssupporting

confidence: 92%

“…Maternal obesity results in multiple alterations, most of them unknown, in milk composition, including changes in the lipid profile and in hormone and cytokine levels. Milk from obese humans and rodents has a higher content of long‐chain saturated FA and higher levels of insulin and leptin (3, 7, 8, 46, 59–62). PRL is an important regulator of milk composition; it promotes the expression of β‐casein (63), whey acidic protein (64), lactoglobulin (65), and α‐lactalbumin (66), leading, in turn, to increased lactose biosynthesis and milk volume (likely through enhanced production of lactose) (52, 67).…”

Section: Discussionmentioning

confidence: 99%

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Impaired prolactin actions mediate altered offspring metabolism induced by maternal high‐fat feeding during lactation

et al. 2018

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Maternal diet during lactation affects offspring metabolic health throughout life. Prolactin (PRL) is present in high quantities in maternal milk; however, the effects of milk PRL on the offspring remain poorly characterized. In this study, we evaluated whether feeding a high-fat diet (HFD) to rats during lactation alters PRL, both in the mother's serum and in milk, and whether this factor contributes to HFD-induced metabolic dysfunction in the offspring. Maternal HFD resulted in decreased PRL levels in milk (but not in serum), reduced mammary gland (MG) PRL receptor expression, and altered MG structure and function. Offspring from HFD-fed dams had increased body weight and adiposity, and developed fatty liver, hyperinsulinemia, and insulin resistance at weaning. Increasing PRL levels in the HFD-fed mothers by subcutaneous osmotic minipumps releasing PRL normalized MG function and PRL levels in milk. Moreover, PRL treatment in HFD-fed mothers, or directly in their pups via oral PRL administration, increased liver STAT5 phosphorylation, reduced visceral adiposity, ameliorated fatty liver, and improved insulin sensitivity in offspring. Our results show that HFD impairs PRL actions during lactation to negatively affect MG physiology and directly impair offspring metabolism.-De los Ríos, E. A., Ruiz-Herrera, X., Tinoco-Pantoja, V., López-Barrera, F., Martínez de la Escalera, G., Clapp, C., Macotela, Y. Impaired prolactin actions mediate altered offspring metabolism induced by maternal high-fat feeding during lactation.

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Section: Resultssupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Impaired prolactin actions mediate altered offspring metabolism induced by maternal high‐fat feeding during lactation

et al. 2018

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“…Pups cross-fostered to dams fed a high fat diet during lactation develop symptoms of metabolic disease including hypertension, 89 diet-induced obesity, 90 and insulin resistance. 91 While the mechanisms underlying these findings are poorly understood, dietary-mediated changes to human milk composition likely represent a major contributing factor. Given the significant association between microbiome composition and metabolic disease outcomes, 92 maternal dietary influence on offspring disease outcomes may be partially explained by the dietary modulation of human milk components impacting the offspring gut microbiome.…”

Section: Impact Of Maternal Nutrition During Breastfeedingmentioning

confidence: 99%

Impact of maternal nutrition in pregnancy and lactation on offspring gut microbial composition and function

et al. 2016

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Evidence supporting the Developmental Origins of Health and Disease Hypothesis indicates that maternal nutrition in pregnancy has a significant impact on offspring disease risk later in life, likely by modulating developmental processes in utero. Gut microbiota have recently been explored as a potential mediating factor, as dietary components strongly influence microbiota abundance, function and its impact on host physiology. A growing body of evidence has additionally indicated that the intrauterine environment is not sterile as once presumed, indicating that maternal-fetal transmission of microbiota may occur during pregnancy. In this article, we will review the body of literature that supports this emerging hypothesis, as well as highlight the work in relevant animal models demonstrating associations with maternal gestational nutrition and the offspring gut microbiome that may influence offspring physiology and susceptibility to disease.

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“…Rodents raised in small litters (SLs) are consistently overfed during lactation and develop late-onset obesity, hepatic steatosis, insulin resistance, impaired glucose tolerance, and renal and cardiac metabolic alterations (10). The long-term metabolic derangements caused by neonatal overfeeding are likely due to a combination of disturbances in the CNS, which may alter food intake (11)(12)(13), and the peripheral tissues (14)(15)(16)(17).…”

mentioning

confidence: 99%

Epigenetic programming at the Mogat1 locus may link neonatal overnutrition with long‐term hepatic steatosis and insulin resistance

et al. 2018

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Postnatal overfeeding increases the risk of chronic diseases later in life, including obesity, insulin resistance, hepatic steatosis, and type 2 diabetes. Epigenetic mechanisms might underlie the long-lasting effects associated with early nutrition. Here we aimed to explore the molecular pathways involved in early development of insulin resistance and hepatic steatosis, and we examined the potential contribution of DNA methylation and histone modifications to long-term programming of metabolic disease. We used a well-characterized mouse model of neonatal overfeeding and early adiposity by litter size reduction. Neonatal overfeeding led to hepatic insulin resistance very early in life that persisted throughout adulthood despite normalizing food intake. Up-regulation of monoacylglycerol O-acyltransferase ( Mogat) 1 conceivably mediates hepatic steatosis and insulin resistance through increasing intracellular diacylglycerol content. Early and sustained deregulation of Mogat1 was associated with a combination of histone modifications that might favor Mogat1 expression. In sum, postnatal overfeeding causes extremely rapid derangements of hepatic insulin sensitivity that remain relatively stable until adulthood. Epigenetic mechanisms, particularly histone modifications, could contribute to such long-lasting effects. Our data suggest that targeting hepatic monoacylglycerol acyltransferase activity during early life might provide a novel strategy to improve hepatic insulin sensitivity and prevent late-onset insulin resistance and fatty liver disease.-Ramon-Krauel, M., Pentinat, T., Bloks, V. W., Cebrià, J., Ribo, S., Pérez-Wienese, R., Vilà, M., Palacios-Marin, I., Fernández-Pérez, A., Vallejo, M., Téllez, N., Rodríguez, M. À., Yanes, O., Lerin, C., Díaz, R., Plosch, T., Tietge, U. J. F., Jimenez-Chillaron, J. C. Epigenetic programming at the Mogat1 locus may link neonatal overnutrition with long-term hepatic steatosis and insulin resistance.

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Postnatal weight gain induced by overfeeding pups and maternal high-fat diet during the lactation period modulates glucose metabolism and the production of pancreatic and gastrointestinal peptides

Cited by 31 publications

References 44 publications

Impaired prolactin actions mediate altered offspring metabolism induced by maternal high‐fat feeding during lactation

Impaired prolactin actions mediate altered offspring metabolism induced by maternal high‐fat feeding during lactation

Impact of maternal nutrition in pregnancy and lactation on offspring gut microbial composition and function

Epigenetic programming at the Mogat1 locus may link neonatal overnutrition with long‐term hepatic steatosis and insulin resistance

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