An early fish oil-enriched diet reverses biochemical, liver and adipose tissue alterations in male offspring from maternal protein restriction in mice

Maternal protein restriction (MPR) during pregnancy impaired the reproduction of male offspring. We investigated, during the first wave of spermatogenesis, whether MPR exerts deleterious effects on germ cell proliferation and differentiation, as well as androgen receptor (AR) protein expression, which was used as a marker for Sertoli cell (SC) maturation. At the beginning of pregnancy (day 0), dams were fed a control diet (C: 20% casein) or a restricted isocaloric diet (R: 10% casein). After birth, four groups were established: CC, RR, CR and RC (first letter diet during pregnancy and second during lactation). Male offspring were studied at postnatal days 14, 21 and 36. At birth, pup body weight was unchanged. Body weight and testis weight were reduced in RR and CR groups at all ages evaluated. MPR delayed the germinal epithelium development at all ages evaluated. On performing Western blot and immunohistochemistry, AR expression was found to be lower in the three restricted groups. The results suggest that MPR during pregnancy and/or lactation delays SC maturation and germ cell differentiation, and affects intratubular organization. These changes might be responsible for the lower fertility rate at older ages.

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Maternal green tea polyphenol intake during lactation attenuates kidney injury in high-fat-diet-fed male offspring programmed by maternal protein restriction in rats

The Journal of Nutritional Biochemistry ◽

10.1016/j.jnutbio.2018.01.012 ◽

2018 ◽

Vol 56 ◽

pp. 99-108 ◽

Cited By ~ 9

Author(s):

Saori Kataoka ◽

Toshio Norikura ◽

Shin Sato

Keyword(s):

Green Tea ◽

High Fat Diet ◽

Kidney Injury ◽

Protein Restriction ◽

Male Offspring ◽

Tea Polyphenol ◽

High Fat ◽

Maternal Protein Restriction ◽

Green Tea Polyphenol ◽

Polyphenol Intake

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Long-Term Effects of Maternal Low-Protein Diet and Post-weaning High-Fat Feeding on Glucose Metabolism and Hypothalamic POMC Promoter Methylation in Offspring Mice

Frontiers in Nutrition ◽

10.3389/fnut.2021.657848 ◽

2021 ◽

Vol 8 ◽

Author(s):

Jia Zheng ◽

Ling Zhang ◽

Jiayi Liu ◽

Yanli Li ◽

Junqing Zhang

Keyword(s):

Glucose Metabolism ◽

Critical Role ◽

Protein Restriction ◽

Male Offspring ◽

Melanocortin Receptor ◽

High Fat ◽

Altered Expression ◽

Low Protein ◽

Maternal Protein Restriction ◽

Fat Feeding

Substantial evidence indicated that maternal malnutrition could increase the susceptibility to obesity, insulin resistance, and type 2 diabetes in adulthood. It is increasingly apparent that the brain, especially the hypothalamus, plays a critical role in glucose homeostasis. However, little information is known about the mechanisms linking maternal protein restriction combined with post-weaning high-fat (HF) feeding with altered expression of brain neurotransmitters, and investigations into the epigenetic modifications of hypothalamus in offspring have not been fully elucidated. Our objective was to explore the effects of maternal protein restriction combined with post-weaning HF feeding on glucose metabolism and hypothalamic POMC methylation in male offspring mice. C57/BL6 mice were fed on either low-protein (LP) or normal chow (NC) diet throughout gestation and lactation. Then, the male offspring were randomly weaned to either NC or high-fat (HF) diet until 32 weeks of age. Gene expressions and DNA methylation of hypothalamic proopiomelanocortin (POMC) and melanocortin receptor 4 (MC4R) were determined in male offspring. The results showed that birth weights and body weights at weaning were both significantly lower in male offspring mice of the dams fed with a LP diet. Maternal protein restriction combined with post-weaning high-fat feeding, predisposes higher body weight, persistent glucose intolerance (from weaning to 32 weeks of age), hyperinsulinemia, and hyperleptinemia in male offspring mice. POMC and MC4R expressions were significantly increased in offspring mice fed with maternal LP and postnatal high-fat diet (P < 0.05). Furthermore, maternal protein restriction combined with post-weaning high-fat feeding induced hypomethylation of POMC promoter in the hypothalamus (P < 0.05) and POMC-specific methylation (%) was negatively correlated with the glucose response to a glucose load in male offspring mice (r = −0.42, P = 0.039). In conclusion, maternal LP diet combined with post-weaning high-fat feeding predisposed the male offspring to impaired glucose metabolism and hypothalamic POMC hypomethylation. These findings can advance our thinking about hypothalamic POMC gene methylation between maternal LP diet combined with post-weaning high-fat feeding and metabolic health in offspring.

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Maternal protein restriction during pregnancy and lactation in rats imprints long-term reduction in hepatic lipid content selectively in the male offspring

Nutrition Research ◽

10.1016/j.nutres.2010.05.008 ◽

2010 ◽

Vol 30 (6) ◽

pp. 410-417 ◽

Cited By ~ 26

Author(s):

Rani J. Qasem ◽

Ganesh Cherala ◽

Anil P. D'mello

Keyword(s):

Lipid Content ◽

Protein Restriction ◽

Male Offspring ◽

Hepatic Lipid ◽

Maternal Protein Restriction ◽

Pregnancy And Lactation ◽

Hepatic Lipid Content

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Maternal Protein Restriction Altered Insulin Resistance and Inflammation-Associated Gene Expression in Adipose Tissue of Young Adult Mouse Offspring in Response to a High-Fat Diet

Nutrients ◽

10.3390/nu12041103 ◽

2020 ◽

Vol 12 (4) ◽

pp. 1103 ◽

Cited By ~ 2

Author(s):

Juhae Kim ◽

Alee Choi ◽

Young Hye Kwon

Keyword(s):

Gene Expression ◽

Insulin Resistance ◽

Adipose Tissue ◽

Serum Insulin ◽

Protein Restriction ◽

Epididymal Adipose Tissue ◽

Model Assessment ◽

High Fat ◽

Maternal Protein Restriction ◽

Increased Risk

Maternal protein restriction is associated with increased risk of insulin resistance and inflammation in adulthood offspring. Here, we investigated whether maternal protein restriction could alter the risk of metabolic syndrome in postweaning high-fat (HF)-diet-challenged offspring, with focus on epididymal adipose tissue gene expression profile. Female ICR mice were fed a control (C) or a low-protein (LP) diet for two weeks before mating and throughout gestation and lactation, and their male offspring were fed an HF diet for 22 weeks (C/HF and LP/HF groups). A subset of offspring of control dams was fed a low-fat control diet (C/C group). In response to postweaning HF diet, serum insulin level and the homeostasis model assessment of insulin resistance (HOMA-IR) were increased in control offspring. Maternal LP diet decreased HOMA-IR and adipose tissue inflammation, and increased serum adiponectin level in the HF-diet-challenged offspring. Accordingly, functional analysis revealed that differentially expressed genes (DEGs) enriched in cytokine production were downregulated in the LP/HF group compared to the C/HF group. We also observed the several annotated gene ontology terms associated with innate immunity and phagocytosis in down-regulated DEGs between LP/HF and C/C groups. In conclusion, maternal protein restriction alleviated insulin resistance and inflammation in young offspring mice fed a HF diet but may impair development of immune system in offspring.

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Maternal protein restriction in mice causes adverse metabolic and hypothalamic effects in the F1 and F2 generations

British Journal Of Nutrition ◽

10.1017/s0007114511001735 ◽

2011 ◽

Vol 106 (9) ◽

pp. 1364-1373 ◽

Cited By ~ 28

Author(s):

Nayara Peixoto-Silva ◽

Eliete Dalla Corte Frantz ◽

Carlos Alberto Mandarim-de-Lacerda ◽

Alessandra Pinheiro-Mulder

Keyword(s):

Leptin Receptor ◽

Protein Restriction ◽

Metabolic Programming ◽

Male Offspring ◽

Leptin Resistance ◽

Altered Expression ◽

Leptin Sensitivity ◽

Maternal Protein Restriction ◽

Group 5 ◽

F2 Generation

Maternal protein restriction causes metabolic alterations associated with hypothalamic dysfunction. Because the consequences of metabolic programming can be passed transgenerationally, the present study aimed to assess whether maternal protein restriction alters the expression of hypothalamic neuropeptides in offspring and to evaluate hormonal and metabolic changes in male offspring from the F1 and F2 generations. Female Swiss mice (F0) were mated and fed either a normal-protein (NP group; 19 % protein) or a low-protein (LP group; 5 % protein) diet throughout gestation of the F1 generation (NP1 and LP1). At 3 months of age, F1 females were mated to produce the F2 generation (NP2 and LP2). Animals from all groups were evaluated at 16 weeks of age. LP1 offspring had significantly lower weights and shorter lengths than NP1 offspring at birth, but they underwent a phase of rapid catch-up growth. Conversely, the LP2 offspring were not significantly different from the NP2 offspring in either weight or length. At 16 weeks, no differences were found in body mass among any of the groups, although LP1 and LP2 offspring showed hypercholesterolaemia, hypertriacylglycerolaemia, hyperglycaemia, glucose intolerance, insulin resistance, increased levels of insulin, leptin and resistin, decreased endogenous leptin sensitivity, increased adiposity with elevated leptin levels and leptin resistance characterised by altered expression of neuropeptide Y and pro-opiomelanocortin without any changes in the leptin receptor Ob-Rb. We conclude that severe maternal protein restriction promotes metabolic programming in F1 and F2 male offspring due to a dysregulation of the adipoinsular axis and a state of hypothalamic leptin resistance.

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