Rates of lipid fluxes in adipose tissue in vivo after a mixed meal in morbid obesity

Objective: Although insulin resistance in obesity is established, information on insulin action on lipid fluxes, in morbid obesity, is limited. This study was undertaken in morbidly obese women to investigate insulin action on triacylglycerol fluxes and lipolysis across adipose tissue. Subjects and...

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Published in:International Journal of Obesity Vol. 34; no. 4; pp. 770 - 774
Main Authors: Mitrou, P, Boutati, E, Lambadiari, V, Maratou, E, Komesidou, V, Papakonstantinou, A, Sidossis, L, Tountas, N, Katsilambros, N, Economopoulos, T, Raptis, S.A, Dimitriadis, G
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 01-04-2010
Nature Publishing Group
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Summary:Objective: Although insulin resistance in obesity is established, information on insulin action on lipid fluxes, in morbid obesity, is limited. This study was undertaken in morbidly obese women to investigate insulin action on triacylglycerol fluxes and lipolysis across adipose tissue. Subjects and Design: A meal was given to 26 obese (age 35±1years, body mass index 46±1 kg m–2) and 11 non-obese women (age 38±2years, body mass index 24±1 kg m–2). Plasma samples for glucose, insulin, triglycerides and non-esterified fatty acids (NEFAs) were taken for 360 min from a vein draining the abdominal subcutaneous adipose tissue and from the radial artery. Adipose tissue blood flow was measured with 133Xe. Results: In obese vs non-obese: (1) Arterial glucose was similar, but insulin was increased (P=0.0001). (2) Adipose tissue blood flow was decreased (P=0.0001). (3) Arterial triglycerides (P=0.0001) and NEFAs (P=0.01) were increased. (4) Lipoprotein lipase was decreased (P=0.0009), although the arteriovenous triglyceride differences were similar. (5) Veno-arterial NEFA differences across the adipose tissue were similar. (6) NEFA fluxes and hormone-sensitive lipase-derived glycerol output from 100 g adipose tissue were not different. (7) Total adipose tissue NEFA release was increased (P=0.02). Conclusions: In morbid obesity: (a) hypertriglycerinemia could be attributed to a defect in the postprandial dynamic adjustment of triglyceride clearance across the adipose tissue, partly caused by blunted BF; and (b) postprandially, there is an impairment of adipose tissue to buffer NEFA excess, despite hyperinsulinemia.
Bibliography:http://dx.doi.org/10.1038/ijo.2009.293
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ISSN:0307-0565
1476-5497
DOI:10.1038/ijo.2009.293