Abstract

Recent reports indicated that nutrition in early infancy might influence later child health outcomes such as obesity and metabolic syndrome. Therefore, we examined the effects of maternal high fat diet (HFD) during lactation on the onset of a metabolic syndrome in their offspring. All offspring were cross-fostered by dams on the same or opposite diet to yield 4 groups: offspring from HFD-fed dams suckled by HFD-fed dams (OHH) and by control diet (CD)-fed dams (OHC) and CD-fed dams suckled by HFD-fed dams (OCH) and by CD-fed dams (OCC) mice. We examined several metabolic syndrome-related factors including body weight, blood pressure, glucose tolerance and adipocytokines. Mean body weights of OHH and OCH mice were significantly higher than those of OHC and OCC mice, respectively, with elevated systolic blood pressure. Moreover, OHH and OCH mice revealed significantly worse glucose tolerance compared with the OHC and OCC mice, respectively. Triglyceride and leptin levels were significantly increased and adiponectin levels were significantly reduced by the maternal HFD during lactation, with similar changes in leptin and adiponectin mRNA expression but without histone modifications in adipose tissues. In addition, maternal obesity induced by HFD during lactation increased and prolonged the leptin surge in the offspring and the gender differences of leptin surge were observed. Our data suggested that maternal HFD during lactation might have an additive effect on the onset of the metabolic syndrome in the offspring, irrespective of the nutritional status in utero through the modified leptin surge.

Highlights

  • Maternal obesity in human pregnancy often results in fetal overgrowth [1,2]

  • We examined whether and how maternal high fat diet (HFD) during pregnancy and lactation affects the onset of a metabolic syndrome-like phenomenon in the male and female offspring

  • Body weights of mice nursed by HFD-fed dams were significantly higher than those of mice nursed by dams on the control diet (CD), while OCH weighed less than OHC, suggesting that HFD during lactation had less but additive impact on the offspring weights compared with that during gestation

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Summary

Introduction

Maternal obesity in human pregnancy often results in fetal overgrowth [1,2] This increases the risk of the offspring developing obesity and metabolic syndrome later in life, thereby contributing to the incidence of type 2 diabetes [3,4,5]. Adipose tissue is a highly specialized endocrine and paracrine tissue that produces an array of adipocytokines such as leptin, tumor necrosis factor-a and adiponectin. It elicits cellmediated effects via proinflammatory and anti-inflammatory cells producing various cytokines and chemokines [9]. Leptin plays an important role in modulating satiety and energy homeostasis [13,14]

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