Vincent Frering

Lyon Ortho Clinic-Clinique de la Sauvegarde, Lyons, Rhône-Alpes, France

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Publications (2)6.64 Total impact

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    Hind Ray · Claudie Pinteur · Vincent Frering · Michel Beylot · Valérie Large ·
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    ABSTRACT: Mainly dependent on hormone-sensitive lipase, lipolysis is differently impaired between fat depots in human obesity. Perilipin A expression is a critical element in adipocyte lipolysis. The present study aimed at comparing expression and subcellular distribution of perilipin and hormone-sensitive lipase in two abdominal adipose tissues of lean and obese women. We examined whether regional differences in perilipin expression contribute to impaired lipolytic rates. Abdominal subcutaneous and omental adipose tissues were obtained from six lean and ten obese women. We measured total protein content and relative distribution of hormone-sensitive lipase and perilipin proteins between lipid and non-lipid fractions in tissue homogenates. Hormone-sensitive lipase and perilipin mRNA levels, adipocyte size, basal (non-stimulated) and noradrenaline-stimulated lipolysis in isolated adipocytes were determined. Adipocytes were significantly larger in the obese versus the lean women and in subcutaneous versus omental fat. Expressed as a function of cell number, basal lipolysis and noradrenaline responsiveness were higher in subcutaneous versus omental adipocytes from the obese women (P < 0.05). Despite higher or identical mRNA levels in the lean and the obese subjects and in subcutaneous and omental tissues, perilipin protein expression was lower in both depots in the obese versus the lean women, and in subcutaneous versus omental in both lean and obese women (P < 0.05). Perilipin was mostly (above 80%) present in the lipid fraction in both depots from the obese patients and the value decreased to 60% in the lean subjects (P < 0.05). Perilipin protein expression was inversely correlated to adipocyte size and basal lipolysis in both depots. Despite higher mRNA levels, hormone-sensitive lipase protein expression decreased in both depots of the obese women. Regional difference for hormone-sensitive lipase was reported in lipid fraction of subcutaneous fat of the obese subjects: hormone-sensitive lipase content was twice as low as in omental adipose tissue. In both fat depots, a reduced perilipin protein expression was observed in women obesity. Perilipin protein level may contribute to differences in basal lipolysis and in adipocyte size between fat depots and may regulate lipid accumulation in adipocytes. Differences in hormone-sensitive lipase subcellular distribution were reported between fat depots in the obese women.
    Lipids in Health and Disease 12/2009; 8(1):58. DOI:10.1186/1476-511X-8-58 · 2.22 Impact Factor
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    ABSTRACT: Lipogenesis is considered less active in human than in rat adipose tissue. This could be explained by different nutritional conditions, namely high-carbohydrate (HCHO) diet in rats and high-fat (HF) diet in humans. Adipose tissue was sampled (postabsorptive state) in rats and humans receiving HCHO or HF diets, ad libitum fed humans, and obese subjects. We measured 1) mRNA concentrations of fatty acid synthase (FAS), acetyl-CoA carboxylase 1 (ACC1), sterol regulatory element binding protein 1c (SREBP-1c), and carbohydrate response element binding protein (ChREBP), 2) SREBP-1c protein, and 3) FAS activity. FAS, ACC1, ChREBP, and SREBP1-c mRNA concentrations were unaffected by diet in humans or in rats. FAS and ACC1 mRNA levels were lower in humans than in rats (P < 0.05). FAS activity was unaffected by diet and was lower in humans (P < 0.05). SREBP-1c mRNA concentrations were similar in rats and humans, but the precursor and mature forms of SREBP-1c protein were less abundant in humans (P < 0.05). ChREBP mRNA concentrations were lower in humans than in rats. In conclusion, the lipogenic capacity of adipose tissue is lower in humans than in rats. This is not related to differences in diet and is probably explained by lower abundance of SREBP-1c protein. A decreased expression of ChREBP could also play a role.
    The Journal of Lipid Research 11/2003; 44(11):2127-34. DOI:10.1194/jlr.M300235-JLR200 · 4.42 Impact Factor