@article{3145592,
    title = "Rates of lipid fluxes in adipose tissue in vivo after a mixed meal in
morbid obesity",
    author = "Mitrou, P. and Boutati, E. and Lambadiari, V. and Maratou, E. and and Komesidou, V. and Papakonstantinou, A. and Sidossis, L. and Tountas, N. and and Katsilambros, N. and Economopoulos, T. and Raptis, S. A. and and Dimitriadis, G.",
    journal = "International Journal of Obesity Supplements",
    year = "2010",
    volume = "34",
    number = "4",
    pages = "770-774",
    publisher = "Nature Publishing Group",
    issn = "2046-2166, 2046-2174",
    doi = "10.1038/ijo.2009.293",
    keywords = "insulin action; triglycerides; non-esterified fatty acids; lipid fluxes;
adipose tissue; morbid obesity",
    abstract = "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 +/- 1 years,
body mass index 46 +/- 1 kg m(-2)) and 11 non-obese women (age 38 +/- 2
years, 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 Xe-133.
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. International
Journal of Obesity (2010) 34, 770-774; doi: 10.1038/ijo.2009.293;
published online 19 January 2010"
}