Maternal Protein Restriction in Rats Alters Postnatal Growth and Brain Lipid Sensing in Female Offspring

Abstract

Perinatal nutrition is a key player in the susceptibility to developing metabolic diseases in adulthood, leading to the concept of “metabolic programming”. The aim of this study was to assess the impact of maternal protein restriction during gestation and lactation on glucose homeostasis and eating behaviour in female offspring. Pregnant rats were fed a normal or protein-restricted (PR) diet and followed throughout gestation and lactation. Body weight, glucose homeostasis, and eating behaviour were evaluated in offspring, especially in females. Body weight gain was lower in PR dams during lactation only, despite different food and water intakes throughout gestation and lactation. Plasma concentration of leptin, adiponectin and triglycerides increased drastically before delivery in PR dams in relation to fat deposits. Although all pups had identical birth body weight, PR offspring body weight differed from control offspring around postnatal day 10 and remained lower until adulthood. Offspring glucose homeostasis was mildly impacted by maternal PR, although insulin secretion was reduced for PR rats at adulthood. Food intake, satiety response, and cerebral activation were examined after a lipid preload and demonstrated some differences between the two groups of rats. Maternal PR during gestation and lactation does induce extrauterine growth restriction, accompanied by alterations in maternal plasma leptin and adiponectin levels, which may be involved in programming the alterations in eating behaviour observed in females at adulthood.

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“…These studies are consistent with the authors' in the context of the overall goal, but do not agree on the results, since V.S. Moullé et al (2023) fed the study group a limited level of protein, and the authors of the presented studies did not bring the level of protein to a deficiency in any of the groups, but its origin was different.…”

“…V.S. Moullé et al (2023) experimentally demonstrated that groups with lower protein content during pregnancy and lactation were characterized by lower weight parameters compared to groups with a balanced diet. These studies are consistent with the authors' in the context of the overall goal, but do not agree on the results, since V.S.…”

Unraveling the Molecular Mechanisms of the Neurodevelopmental Consequences of Fetal Protein Deficiency: Insights From Rodent Models and Public Health Implications

“…Gestational protein restriction disrupts this process of neurogenesis and cell fate determination ( 75 , 76 ), leading to fewer NPY neurons and attenuated projections from the arcuate nucleus to the paraventricular nucleus ( 77 , 78 , 79 ). This is manifested in hyperinsulinemia, increased body weight, hyperleptinemia, and altered leptin responsiveness, which are hallmarks of metabolic syndrome, in adult offspring ( 78 , 80 , 81 ). Another study found that altered expression of genes encoding NPY, POMC, and leptin receptor isoforms was evident in the protein-deprived fetal brain as early as G12 ( 82 ).…”