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• W2079150486 abstract "Gestational diabetes is one of the most common complications of pregnancy occurring in up to 10% of women in the Western world. The short-term risks of gestational diabetes to both mother and child, including preeclampsia, preterm delivery, and increased perinatal mortality, are well established (1). However, there is now strong evidence from both human and animal models that exposure to a diabetic environment during fetal life has substantial long-term health consequences for the child, including increased risk of type 2 diabetes and obesity (2). Much research effort has therefore been directed toward understanding the mechanisms by which such metabolic programming arises. In this issue of Endocrinology, Steculorum and Bouret demonstrate that maternal diabetes leads to impaired neonatal leptin signaling and structural disorganization of hypothalamic feeding pathways in the offspring. This is associated with leptin resistance in adulthood resulting in increased food intake and increased risk of metabolic disease (3). The concept of metabolic programming has been recognized for many years (reviewed in Ref. 4). Although initial focus was directed toward the long-term detrimental effects of fetal undernutrition and low birth weight (5), in light of the global epidemic of obesity and diabetes in women of child-bearing age, recent attention has shifted toward fetal overnutrition and high birth weight (6). Both ends of the birth weight spectrum have been associated with increased risk of type 2 diabetes and other features of the metabolic syndrome that may indicate common mechanistic pathways (7). Low birth weight is often followed by accelerated postnatal growth (frequently referred to as “catch-up growth”) and this has been shown to be particularly detrimental in terms of later obesity risk, highlighting the neonatal period as a critical time window for establishment of long-term regulation of energy balance (8). It is therefore possible that accelerated early postnatal growth may represent a commonality between animal models of low birth weight followed by catch-up growth (9) and models of maternal diabetes/obesity where suckling by such dams leads to increased weight gain during the lactation period (3, 10). The hypothalamus plays a central role in regulation of energy balance and has therefore been a major focus of experiments aimed at dissecting the mechanisms underlying the programming of obesity. Early experiments that manipulated neonatal growth and nutrient intake by variation of litter size showed programmed changes in crude measures of hypothalamic function and structure, including RNA content (11) and neuronal density (12). However, as understanding of the molecular mechanisms underlying hypothalamic regulation of energy balance has increased, more detailed information on programmed changes in the hypothalamus has emerged. These include programmed changes in neuropeptide expression (13–15) that could result from altered epigenetic regulation of gene transcription (15). A common phenotypic outcome that has been reported in a number of programming models, including those of neonatal overfeeding (16, 17), intrauterine undernutrition (18), maternal high fat feeding (19), and maternal diet-induced obesity (13), is resistance to leptin in adulthood in relation to inhibition of food intake. However, there has been less focus on whether leptin resistance during the very early stages of life, at a time when leptin has no effect on food intake (20, 21), plays a mechanistic role in metabolic programming (13, 17)." @default.
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• W2079150486 date "2011-11-01" @default.
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• W2079150486 title "Sugaring Appetite Development: Mechanisms of Neuroendocrine Programming" @default.
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• W2079150486 doi "https://doi.org/10.1210/en.2011-1659" @default.
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