Beck B, Max J P
INSERM U.59, Unité de Nutrition et Diététique, Nancy, France.
Horm Metab Res. 1988 Jan;20(1):24-7. doi: 10.1055/s-2007-1010740.
To determine the mechanism by which gastric inhibitory polypeptide (GIP) and insulin stimulate the in vitro fatty acid incorporation into adipose tissue (FIAT), we measured the cyclic AMP variations and FIAT in epididymal fat pads of lean Fa/-- and obese fa/fa Zucker rats. GIP was used at 1, 2 and 4 ng/ml and insulin at a concentration of 100 microU/ml. There was no significant variation of cAMP when FIAT was stimulated either by GIP, either by insulin or by both hormones. There was no correlation at all between FIAT increases and cAMP levels. We conclude that GIP and insulin act through cAMP independent mechanisms in adipose tissue. The modification by GIP of insulin binding to adipocytes or an easier passage of fatty acids through the membrane could constitute alternative solutions for such mechanisms.
为了确定胃抑制多肽(GIP)和胰岛素刺激体外脂肪酸掺入脂肪组织(FIAT)的机制,我们测量了瘦型Fa/–和肥胖型fa/fa Zucker大鼠附睾脂肪垫中的环磷酸腺苷(cAMP)变化和FIAT。GIP的使用浓度为1、2和4 ng/ml,胰岛素的浓度为100微单位/ml。当FIAT由GIP、胰岛素或两种激素共同刺激时,cAMP没有显著变化。FIAT增加与cAMP水平之间完全没有相关性。我们得出结论,GIP和胰岛素在脂肪组织中通过不依赖cAMP的机制发挥作用。GIP对胰岛素与脂肪细胞结合的修饰或脂肪酸更容易通过细胞膜可能构成这些机制的替代解决方案。