Les stratégies nutritionnelles visant coute que coute à controller l'insuline sont-elles mal fondées ?
1: Am J Physiol Endocrinol Metab. 2009 Feb 3. [Epub ahead of print]
Amino acid-sensing mTOR signaling is involved in modulation of lipolysis by chronic insulin treatment in adipocytes.
Zhang C, Yoon MS, Chen J.
Univ. Ill-Urbana.
Chronically high insulin levels and increased circulating free fatty acids
released from adipose tissue through lipolysis are two features associated with
insulin resistance. The relationship between chronic insulin exposure and
adipocyte lipolysis has been unclear. In the present study we found that chronic
insulin exposure in 3T3-L1 adipocytes, as well as in mouse primary adipocytes,
increased basal lipolysis rates. This effect of insulin on lipolysis was only
observed when the mammalian target of rapamycin (mTOR) pathway was inhibited by
rapamycin in the adipocytes. The synergistic effect of insulin and rapamycin was
confirmed by the effect of insulin in cells with mTOR levels reduced by RNAi. In
addition, amino acid deprivation in adipocytes phenocopied the effect of
rapamycin or mTOR knockdown in permitting the stimulation of lipolysis by chronic
insulin exposure. Furthermore, we found that triacylglycerol hydrolase (TGH)
activity was required for the stimulation of lipolysis by the combined exposure
to insulin and rapamycin. Therefore, we propose that nutrient sufficiency,
mediated by an mTOR pathway, suppresses TGH-dependent lipolysis stimulated by
chronic insulin exposure in adipocytes. Key words: Insulin resistance, 3T3-L1
cells, nutrient sufficiency, triacylglycerol hydrolase.
