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Am J Physiol Endocrinol Metab 282: E412-E418, 2002. First published October 2, 2001; doi:10.1152/ajpendo.00307.2001
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Vol. 282, Issue 2, E412-E418, February 2002

Resistance of adipose tissue lipoprotein lipase to insulin action in rats fed an obesity-promoting diet

Frédéric Picard, André Boivin, Josée Lalonde, and Yves Deshaies

Centre de Recherche de l'Hôpital Laval et Centre de Recherche sur le Métabolisme Énergétique, Département d'Anatomie et Physiologie, Faculté de Médecine, Université Laval, Quebec, Canada G1K 7P4

This study aimed to assess whether adipose lipoprotein lipase (LPL) becomes resistant to insulin in a nutritional model of resistance of glucose metabolism to insulin. Sprague-Dawley rats were fed for 4 wk chow or a purified high-sucrose, high-fat (HSHF) diet that induced overt insulin resistance. Rats were fasted for 24 h and then refed chow for 1, 3, or 6 h. The postprandial rise in insulinemia was similar in both dietary cohorts, whereas glycemia was higher in HSHF-fed than in chow-fed animals, indicating glucose intolerance and insulin resistance. In chow-fed rats, adipose LPL activity increased two- to fourfold postprandially, but only minimally (30%) in HSHF-fed rats. Muscle LPL decreased postprandially in HSHF-fed rats, suggesting intact sensitivity to insulin, but it increased in chow-fed animals. Peak postprandial triglyceridemia was higher (+70%) in insulin-resistant than in control rats. The postprandial rate of appearance of triglycerides in the circulation was similar in control and insulin-resistant rats, indicating that hypertriglyceridemia of the latter was the result of impaired clearance. These results demonstrate that adipose LPL becomes resistant to insulin in diet-induced IR and further suggest that, under certain nutritional conditions, modifications in adipose LPL modulation associated with insulin resistance, along with low muscle LPL, heightens postprandial hypertriglyceridemia through attenuated triglyceride clearance.

high-fat diet; insulin resistance; triglycerides


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