Maternal Overweight Programs Insulin and Adiponectin Signaling in the Offspring

Shankar, Kartik; Kang, Pengde; Harrell, Amanda; Zhang, Ying; Marecki, John C.; Ronis, Martin J. J.; Badger, Thomas M.

doi:10.1210/jcem.95.5.9987

Cited by 12 publications

(17 citation statements)

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“…PGC-1␣ levels and phosphorylation (activation)/acetylation (inactivation) appear to be regulated by the energy and/or nutritional status of the cells and are regulated by PPARs, myocyte enhancer factor 2, forkhead box O, cAMP response element-binding protein, estrogen-related receptors, the adiponectin receptors (adipoR1/ R2), AMPK, and sirtuin (15,25,27,71). Results from the current studies parallel studies in which pregnant females were overfed in that offspring of overfed mothers had reduced adipoR1/R2 expression and AMPK activity (7,57), which can lead to less expression and activation of PGC-1␣ (27,71).…”

Section: Discussionsupporting

confidence: 52%

Multiparity leads to obesity and inflammation in mothers and obesity in male offspring

Rebholz

Jones

Burke

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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DA, Woollett LA. Multiparity leads to obesity and inflammation in mothers and obesity in male offspring. Am J Physiol Endocrinol Metab 302: E449 -E457, 2012. First published November 29, 2011; doi:10.1152/ajpendo.00487.2011.-Multiparity is an independent risk factor for obesity in parous females. In addition to being a health issue for the mother, offspring of multiparous females may also be at risk for obesity later in life. The aim of the current study was to establish a mouse model that mimics the human pathology of multiparity and determine the effects of multiparity-induced obesity (MIO) on offspring in adulthood. C57BL/6 mice were mated and studied when primiparous (1st pregnancy) or multiparous (4th pregnancy). Dams became obese with multiparity, an effect that was independent of the age of the dam. Multiparous dams also had increased markers of inflammation (JNK activation, cytokine expression) in adipose tissue and liver that was greater than inflammation in nulliparous females made obese with a high-fat diet. Placental inflammation was prevalent in multiparous vs. primiparous dams as well. Male offspring of the multiparous dams developed increased adiposity by 24 wk of age relative to the progeny of primiparous dams, although food consumption was similar in both groups. Lipid metabolism was altered in liver and fat in that mRNA levels of regulatory genes (PGC-1␣) as well as metabolic genes (CPT I) and Akt phosphorylation were decreased in offspring of multiparous dams. Thus, in mice, as in humans, multiparity increases adiposity and is associated with hepatic and placental inflammation and abnormal glucose tolerance. Importantly, MIO leads to increased body fat and metabolic dysfunction in the offspring, suggesting a role in the propagation of obesity. developmental programming; diabetes; peroxisome proliferator-activated receptor-␥ coactivator-1␣ OBESITY HAS BECOME AN EPIDEMIC in developed countries and is on the rise in underdeveloped countries. Consequently, a significant number of women in their reproductive years, including those that are pregnant, are obese or overweight (30, 31). Obesity during gestation poses a significant clinical problem since it is linked to a spectrum of maternal complications, including gestational diabetes, exaggerated inflammation, hypertension, thromboembolism, preeclamplsia, and delivery complications (26,31,55,62,69).Multiparity is a cause of weight gain in women during their reproductive years and is in fact an independent predictor of obesity (12,20). The increase in multiparity-induced obesity (MIO) has followed overall trends in obesity, since gestational weight gain is additive to prepregnancy weight and the inability to loose weight gained postpartum (51,53,54). Moreover, overweight women are more likely than leaner women to retain the weight gained during pregnancy (19). Thus, as the population becomes heavier, the effect of multiparity on body weight is amplified. Similar to obesity, pregnancy has been described as an inflammatory state, with the placenta cont...

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Section: Discussionsupporting

confidence: 52%

Multiparity leads to obesity and inflammation in mothers and obesity in male offspring

Rebholz

Jones

Burke

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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“…Liver and adipose tissue are differently affected by HF-fed mothers, leading to upregulated hepatic lipogenesis coupled with blunted lipolysis in white adipose tissue. Critical points of regulation in the respective pathways are associated with a high expression of SREBP-1c and downstream genes involved in hepatic lipid biosynthesis concomitant with reduced expression of PPAR-alpha and related genes involved in fatty acid oxidation (Shankar et al, 2010), which agrees with our results. However, the steatosis observed in F2, probably was favored hepatic lipogenesis through enhanced PPAR-gamma expression.…”

Section: Discussionsupporting

confidence: 92%

Both Hepatic Lipogenesis and Beta-Oxidation are Altered in Offspring of Mothers Fed a High-Fat Diet in the First Two Generations (F1 and F2)

et al. 2015

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SUMMARY:The high fat (HF) fed mothers may program susceptibility in offspring to chronic diseases and affect subsequent generations. The present study evaluated the liver structure in adulthood, focusing on the F1 and F2 generations. Females C57BL/6 (F0) were fed standard chow (SC) or HF diet (8 weeks) prior to mating and during the gestation and lactation to provide the F1 generation (SC-F1 and HF-F1). All other mothers and offspring fed SC. At 3 months old, F1 females were mated to produce the F2 generation (SC-F2 and HF-F2). The liver was kept in several fragments and prepared for histological analysis or frozen for biochemical and molecular analyzes. The F1 and F2 offspring were studied at 3 months old. HF-F1 had higher body mass (BM) compared to SC-F1 (P= 0.001), but not HF-F2 compared to SC-F2. HF-F1 had glucose intolerance when compared to SC-F1, but not HF-F2 compared to SC-F2. HF-F1 (P= 0.009) and HF-F2 (P= 0.03) showed hyperinsulinemia compared to their counterparts. Both groups HF-F1 and HF-F2 showed more steatosis than the SC counterparts (F1 and F2, P<0.0001). HF-F1 showed increased expression of PPAR-gamma and SREBP1-c compared to SC-F1 (P= 0.01). HF-F2 showed increased PPAR-gamma expression compared to SC-F2 (P= 0.04). In conclusion, HF-fed mother impairs both lipogenesis and beta-oxidation pathways in F1 through upregulation of PPAR-gamma and downregulation of PPAR-alpha. In F2, the only lipogenesis is enhanced, but it causes a disrupted PPAR balance, favoring the hepatic lipid accumulation and impaired metabolism in these animals that were not directly exposed to the maternal HF intake.

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“…On the other hand, Shankar and cols. (13) reported that the number of newborns, the (26) and later effects in adults (14) as results of a possible fetal programming (13).…”

Section: Discussionmentioning

confidence: 99%

Maternal obesity and late effects on offspring metabolism

Vido

Nejm

Ribeiro-Silva

et al. 2014

Arq Bras Endocrinol Metab

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Objective: The aim of this study was to evaluate the late effects of maternal obesity induced by lesion of the ventromedial hypothalamus on offspring metabolism. Materials and methods: Thirty days after the bilateral lesion of the ventromedial hypothalamus, female rats were mated and divided into 2 groups of pregnant animals: Control (C) -false lesion (sham) and Obese (OB) -lesion. Three months after that, with the groups of mothers, offspring were divided into control and obese animals that received a normocaloric diet (C-N and OB-N), and control and obese animals that received a hypercaloric diet (C-H and OB-H). At 120 days of age, the animals were euthanized and their carcasses, feces and food were submitted to calorimetric analysis to determine energy balance and body composition. Results: During the growth period, offspring from obese mothers showed higher values of body weight and food intake than controls. Obese animals showed higher body weight gain and gross food efficiency than control animals in adulthood. The hypercaloric diet led to increased metabolizable energy intake, percentage of absorbed energy and energy expenditure in both groups. Body composition was only affected by the association of hypercaloric diet and maternal obesity that led to increased body fat. Conclusions: Maternal obesity has led to the development of later overweight in offspring, suggesting fetal programming. According to the trend presented, it is believed that the prolonged intake of hypercaloric diets in adult animals may, as an additional effect, induce worsening of the overweight induced by maternal obesity. Arq Bras Endocrinol Metab. 2014;58(3):301-7 Keywords Fetal programming; obesity; energy metabolism; body composition; hypercaloric diet RESUMO Objetivo: Avaliar os efeitos tardios da obesidade materna induzida por lesão do núcleo ventromedial do hipotálamo sobre o metabolismo da prole. Materiais e métodos: Trinta dias após a lesão bilateral do hipotálamo ventromedial, ratos fêmeas foram colocadas para acasalar e divididas em dois grupos de animais gestantes: Controle (C) -falsa lesão e Obeso (OB) -lesionados. Três meses após o nascimento, de acordo com os grupos das mães, os filhotes foram divididos em animais controle e obesos que recebiam dieta normocalórica (C-N and OB-N) e animais controle e obesos que recebiam dieta hipercalórica (C-H and OB-H). Aos 120 dias de idade, os animais foram eutanasiados e as carcaças, fezes e ração foram submetidas à análise calorimétrica para determinação do balanço energético e composição corporal. Resultados: Durante o período de crescimento, os filhos de mães obesas mostraram maiores valores de peso corporal e ingestão alimentar que animais controle. Os animais obesos apresentaram maiores valores de ganho de peso corporal e eficiência metabólica que os animais controle quando adultos. A dieta hipercalórica levou ao aumento da energia metabolizável, percentagem de energia absorvida e gasto energético para ambos os grupos. A composição corporal foi somente afetada pela assoc...

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Maternal Overweight Programs Insulin and Adiponectin Signaling in the Offspring

Cited by 12 publications

References 0 publications

Multiparity leads to obesity and inflammation in mothers and obesity in male offspring

Multiparity leads to obesity and inflammation in mothers and obesity in male offspring

Both Hepatic Lipogenesis and Beta-Oxidation are Altered in Offspring of Mothers Fed a High-Fat Diet in the First Two Generations (F1 and F2)

Maternal obesity and late effects on offspring metabolism

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