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Conférences Desjardins

Conférence Desjardins le 07 December 2006
Consumption of a high fat diet during pregnancy causes development of
widespread metabolic disorders in offspring

( Tous )
Par: Kevin L Grove
 De12:00 à 13:00
Lieu : Visio-conférence HL, CHUM, CHUL, CHUS - Y2260 Pavillon d'Youville HL
Québec, Québec(Canada)
The long-term health risks associated with early onset obesity has raised serious questions about the contribution of maternal health and diet. In humans gestational diabetes dramatically increases the risk of early onset obesity and diabetes in children; however, an increased risk has also been suggested for maternal diet and obesity independent of diabetes, but remains to be fully tested. To begin to address this critical health issue we have developed a non-human primate model of diet induced obesity and insulin resistance. The purpose of these studies is to determine the combined effects of chronic maternal high fat/calorie consumption, obesity and severe insulin resistance on the development of metabolic systems in the offspring, including the liver, muscle, pancreas and the hypothalamic circuitry that controls appetite and energy expenditure. To date we have observed widespread developmental abnormalities in all of these tissues that would greatly increase the risk of the offspring becoming obese and diabetic. Within the liver we have demonstrated that fetal offspring of animals chronically consuming a high fat/calorie diet have significantly elevated liver triglycerides, evidence of steatosis, increased oxidative stress and damage, and overexpression of transcription factors and enzymes involved in gluconeogenesis, all early signs of nonalcoholic fatty liver disease (NAFLD). Importantly, the increased fetal liver triglycerides and steatosis were not dependent maternal obesity, insulin sensitivity. These results suggest that predisposition to pediatric NAFLD and obesity may arise as a consequence of early exposure to excess dietary fat, and identify maternal dietary fat as a previously unrecognized link contributing to the risk for the infant of developing metabolic syndrome later in life. Acknowledgements: NIH grants DK060685, HD14643, HD18185 and RR00163.

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