Day‐restricted feeding during pregnancy and lactation programs glucose intolerance and impaired insulin secretion in male rat offspring

Faria, Juliana de Almeida; Araújo, Thiago Matos Ferreira de; Mancuso, Rubia Isler; Meulman, Jessica; Ferreira, Danilo da Silva; Batista, Thiago M.; Vettorazzi, Jean Franciesco; Silva, P. M. R. da; Rodrigues, Sandra; Kinote, Andrezza Pinheiro Bezerra de Menezes; Carneiro, Everardo M.; Bordin, Silvana; Anhê, Gabriel Forato

doi:10.1111/apha.12684

Cited by 16 publications

(14 citation statements)

References 38 publications

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“…In agreement with our fetal data, maternal obesogenic diet during pregnancy and lactation resulted in reduced abundance of both IRS1 and the p110β subunit of PI3K in adult rodent offspring skeletal muscle (32) and adipose tissue (33). Further, IRS1-PI3K activity, but not IRS1 phosphorylation, was reduced in fetal muscle in offspring of obese sheep (34); although, these measures in fetal sheep were made in fasted, and not insulin-stimulated tissues, it provides additional evidence that IRS1-PI3K may be a critical node regulated by maternal obesity in the fetal muscle.…”

Section: Discussionsupporting

confidence: 92%

Maternal Obesity and Western-style Diet Impair Fetal and Juvenile Offspring Skeletal Muscle Insulin-Stimulated Glucose Transport in Nonhuman Primates

Campodonico-Burnett

Hetrick

Wesolowski³

et al. 2019

Preprint

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AbstractInfants born to mothers with obesity have a greater risk for childhood obesity and metabolic diseases; however, the underlying biological mechanisms remain poorly understood. We used a nonhuman primate model to investigate whether maternal obesity combined with a western-style diet (WSD) impairs offspring muscle insulin action. Briefly, adult females were fed a control (CON) or WSD prior to and during pregnancy and lactation. Offspring were weaned to a CON or WSD. Muscle glucose uptake and insulin signaling were measured ex vivo in fetal and juvenile offspring. In vivo signaling was evaluated before and after an intravenous insulin bolus just prior to weaning. We find that fetal muscle exposed to maternal WSD had reduced insulin-stimulated glucose uptake and impaired insulin signaling. In juvenile offspring, insulin-stimulated glucose uptake was similarly reduced by both maternal and post-weaning WSD. Analysis of insulin signaling activation revealed distinct changes between fetal and post-weaning WSD exposure. We conclude that maternal WSD leads to a persistent decrease in insulin-stimulated glucose uptake in juvenile offspring even in the absence of increased offspring adiposity or markers of systemic insulin resistance. Switching offspring to a healthy diet did not ameliorate the effects of maternal WSD suggesting earlier interventions may be necessary.

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Section: Discussionsupporting

confidence: 92%

Maternal Obesity and Western-style Diet Impair Fetal and Juvenile Offspring Skeletal Muscle Insulin-Stimulated Glucose Transport in Nonhuman Primates

Campodonico-Burnett

Hetrick

Wesolowski³

et al. 2019

Preprint

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“…This proposition is corroborated by studies showing that forced physical activity (swimming) during the light phase fails to modulate nocturnal melatonin production in rats [42]. We and others have also previously shown that light phase-restricted feeding with standard chow fail to reduce melatonin metabolite in the urine or melatonin circulating levels during the dark phase [43,44]. On the other hand, the daytime consumption of carbohydrates by rodents seems to be particularly relevant to yield reductions in nocturnal melatonin production.…”

Section: Discussionsupporting

confidence: 59%

Metabolic Impact of Light Phase-Restricted Fructose Consumption Is Linked to Changes in Hypothalamic AMPK Phosphorylation and Melatonin Production in Rats

et al. 2017

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Recent studies show that the metabolic effects of fructose may vary depending on the phase of its consumption along with the light/dark cycle. Here, we investigated the metabolic outcomes of fructose consumption by rats during either the light (LPF) or the dark (DPF) phases of the light/dark cycle. This experimental approach was combined with other interventions, including restriction of chow availability to the dark phase, melatonin administration or intracerebroventricular inhibition of adenosine monophosphate-activated protein kinase (AMPK) with Compound C. LPF, but not DPF rats, exhibited increased hypothalamic AMPK phosphorylation, glucose intolerance, reduced urinary 6-sulfatoxymelatonin (6-S-Mel) (a metabolite of melatonin) and increased corticosterone levels. LPF, but not DPF rats, also exhibited increased chow ingestion during the light phase. The mentioned changes were blunted by Compound C. LPF rats subjected to dark phase-restricted feeding still exhibited increased hypothalamic AMPK phosphorylation but failed to develop the endocrine and metabolic changes. Moreover, melatonin administration to LPF rats reduced corticosterone and prevented glucose intolerance. Altogether, the present data suggests that consumption of fructose during the light phase results in out-of-phase feeding due to increased hypothalamic AMPK phosphorylation. This shift in spontaneous chow ingestion is responsible for the reduction of 6-S-Mel and glucose intolerance.

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“…It was therefore of interest to discover that restricting food availability of pregnant rats to the inactive day period can impair metabolic outcomes in progeny (3). Exposure of rat dams to a day-restricted feeding protocol through gestation and lactation programmed poor glucose tolerance and reduced glucose stimulated insulin secretion of pancreatic islets in the male offspring (3).…”

Section: Maternal Chronodisruption and Progeny Metabolic Healthmentioning

confidence: 99%

Maternal circadian rhythms and the programming of adult health and disease

Varcoe

Gatford

Kennaway

2018

American Journal of Physiology-Regulatory, Integrative and Comp

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The in utero environment is inherently rhythmic, with the fetus subjected to circadian changes in temperature, substrates, and various maternal hormones. Meanwhile, the fetus is developing an endogenous circadian timing system, preparing for life in an external environment where light, food availability, and other environmental factors change predictably and repeatedly every 24 h. In humans, there are many situations that can disrupt circadian rhythms, including shift work, international travel, insomnias, and circadian rhythm disorders (e.g., advanced/delayed sleep phase disorder), with a growing consensus that this chronodisruption can have deleterious consequences for an individual's health and well-being. However, the impact of chronodisruption during pregnancy on the health of both the mother and fetus is not well understood. In this review, we outline circadian timing system ontogeny in mammals and examine emerging research from animal models demonstrating long-term negative implications for progeny health following maternal chronodisruption during pregnancy.

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Day‐restricted feeding during pregnancy and lactation programs glucose intolerance and impaired insulin secretion in male rat offspring

Abstract: We conclude that out-of-phase feeding during pregnancy and lactation can lead to glucose intolerance in male offspring, which is caused by a disruption in insulin secretion capacity. This metabolic programming is possibly caused by mechanisms dependent on miRNA modulation of syntaxin 1a.

Cited by 16 publications

References 38 publications

Maternal Obesity and Western-style Diet Impair Fetal and Juvenile Offspring Skeletal Muscle Insulin-Stimulated Glucose Transport in Nonhuman Primates

Maternal Obesity and Western-style Diet Impair Fetal and Juvenile Offspring Skeletal Muscle Insulin-Stimulated Glucose Transport in Nonhuman Primates

Metabolic Impact of Light Phase-Restricted Fructose Consumption Is Linked to Changes in Hypothalamic AMPK Phosphorylation and Melatonin Production in Rats

Maternal circadian rhythms and the programming of adult health and disease

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