Perinatal Hyperinsulinism and Perinatal Obesity as Risk Factors for Hyperinsulinaemia in Later Life

Kohlhoff, R; Dörner, G

doi:10.1055/s-0029-1210995

Cited by 12 publications

(4 citation statements)

References 4 publications

(6 reference statements)

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“…It has been shown that offspring of women with gestational diabetes have high insulin levels perinatally which continue into adult life (Kohlhoff & Dorner 1990, Dorner & Plagemann 1994. Similarly, rats reared in smaller litters also display hyperinsulinemia in early postnatal life (Kohlhoff & Dorner 1990, Dorner & Plagemann 1994, Plagemann et al 1999b. Our earlier studies showed that HF fetal islets displayed a hypersecretory capacity which probably contributed to the observed fetal hyperinsulinemia (Srinivasan et al 2006).…”

Section: Discussionmentioning

confidence: 88%

Hypothalamic alterations in fetuses of high fat diet-fed obese female rats

Gupta¹,

Srinivasan²,

Thamadilok³

et al. 2008

Journal of Endocrinology

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The offspring of high fat (HF) diet-fed rats display increased body weight during adulthood. However, it is not known whether the changes in appetite regulation in these animals occur in utero or postnatally. We investigated the effects of maternal obesity induced by a HF diet prior to and during pregnancy on leptin and insulin signaling and the expression of orexigenic and anorexigenic peptides in term fetal hypothalami. The consumption of a HF diet prior to and during pregnancy resulted in obesity in HF female rats; additionally, HF female rats exhibited hyperinsulinemia and hyperleptinemia which were exaggerated in late gestation compared with control female rats that were fed a standard rodent laboratory chow (LC). Term fetuses of HF female rats (FHF) also had significantly higher serum leptin and insulin levels compared with control fetuses (FLC) while there was no difference in average fetal weight between the two groups.FHF hypothalami showed elevated levels of mRNA and proteins for leptin long receptor and insulin receptor bsubunit. However, the protein levels of signal transducers and activators of transcription-3 and insulin receptor substrate-2, the downstream signaling components of leptin and insulin signaling respectively were decreased. Also, FHF hypothalami had increased mRNA levels of neuropeptide Y and agoutirelated polypeptide indicating that orexigenic neuropeptides in HF progeny are already upregulated by term fetal stage. Additionally, the mRNA levels of pro-opiatemelanocortin and melanocortin receptor-4 were also increased in the HF fetal hypothalami. These findings indicate potential programming effects of an altered intrauterine environment induced by HF diet consumption on appetite-regulating neuropeptides and leptin and insulin signaling in the late fetal period.

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Section: Discussionmentioning

confidence: 88%

Hypothalamic alterations in fetuses of high fat diet-fed obese female rats

Gupta¹,

Srinivasan²,

Thamadilok³

et al. 2008

Journal of Endocrinology

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“…Later retrospective studies of infants of T1DM mothers vs. those from mothers with gestational diabetes showed both increased birth weight and a higher incidence of overweight from 1–4 years of age [33]. Furthermore, maternal obesity and/or diabetes have been associated with increased birth weight and often an increase in body weight gain and obesity in their offspring [34; 35; 36] [37; 38; 39]. However, it is important to note that evidence linking increased birth weight, often thought to predispose to adult obesity, is controversial [40] and the association of intrauterine growth retardation to adverse outcomes in adulthood are not fully consistent across all studies [41].…”

Section: Introductionmentioning

confidence: 99%

Developmental gene×environment interactions affecting systems regulating energy homeostasis and obesity

Levin

2010

Frontiers in Neuroendocrinology

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Most human obesity is inherited as a polygenic trait which is largely refractory to medical therapy because obese individuals avidly defend their elevated body weight set-point. This set-point is mediated by an integrated neural network that controls energy homeostasis. Epidemiological studies suggest that perinatal and pre-pubertal environmental factors can promote offspring obesity. Rodent studies demonstrate the important interactions between genetic predisposition and environmental factors in promoting obesity. This review covers issues of development and function of neural systems involved in the regulation of energy homeostasis and the roles of leptin and insulin in these processes, the ways in which interventions at various phases from gestation, lactation and prepubertal stages of development can favorably and unfavorably alter the development of obesity n offspring. These studies suggest that early identification of obesityprone humans and of the factors that can prevent them from becoming obese could provide an effective strategy for preventing the world wide epidemic of obesity.

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“…Some clinical investigations during childhood indicated elevated frequency of impaired glucose tolerance (IGT) in the offspring of mothers with diabetes during pregnancy (16). Some authors also reported alterations of insulin secretion, such as hyperinsulinemia, which is known to play a key role in the development of metabolic and cardiovascular disturbances in adults (16–19).…”

mentioning

confidence: 99%