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高能饮食对大鼠白色和棕色脂肪中腺苷酸环化酶抑制途径的修饰存在差异。

Adenylyl cyclase inhibitory pathway is differentially modified in rat white and brown fat by high-energy diets.

作者信息

Kenan Y, Levinson M, Pines M, Naim M

机构信息

Institute of Biochemistry, Food Sciences and Nutrition, Hebrew University of Jerusalem, Rehovot, Israel.

出版信息

Am J Physiol. 1997 Jun;272(6 Pt 1):E1043-9. doi: 10.1152/ajpendo.1997.272.6.E1043.

DOI:10.1152/ajpendo.1997.272.6.E1043
PMID:9227450
Abstract

Incubation of white adipose tissue (WAT) adipocytes from rats fed a high-energy diet (Exp group) with antilipolytic Gi-coupled adenylyl cyclase inhibitory agonists, nicotinic acid (Nic) and N8-(L-2-phenylisopropyl)adenosine (PIA), resulted in lower cellular adenosine 3',5'-cyclic monophosphate (cAMP) levels than in stimulated adipocytes from rats fed a nutritionally balanced diet (Con group). In contrast to WAT, incubation of brown adipose tissue (BAT) adipocytes with Nic yielded higher cAMP levels in the Exp vs. Con rats. In both WAT and BAT adipocytes, pertussis toxin treatment abolished the differences in Nic- and PIA-inhibited cAMP formation between Exp and Con animals. Immunoblotting of adipocyte membranes indicated a lower content of Gi alpha but not Gs alpha in BAT membranes of Exp vs. Con animals after 6 and 10 wk of feeding. No such differences were found in the Gs alpha or Gi alpha contents of WAT membranes. Thus the inhibitory pathway of adenylyl cyclase is proposed to be sensitized in WAT and desensitized in BAT of rats fed high-energy diets. These modifications in sensitivity are in line with reduced cAMP and lipolysis in WAT and increased cAMP and thermogenesis in BAT during obesity.

摘要

将高能量饮食喂养的大鼠(实验组)的白色脂肪组织(WAT)脂肪细胞与抗脂解的Gi偶联腺苷酸环化酶抑制激动剂烟酸(Nic)和N8-(L-2-苯异丙基)腺苷(PIA)一起孵育,结果显示,与营养均衡饮食喂养的大鼠(对照组)的受刺激脂肪细胞相比,其细胞内3',5'-环磷酸腺苷(cAMP)水平更低。与白色脂肪组织相反,将棕色脂肪组织(BAT)脂肪细胞与Nic一起孵育时,实验组大鼠的cAMP水平高于对照组。在白色脂肪组织和棕色脂肪组织的脂肪细胞中,百日咳毒素处理消除了实验组和对照组动物之间Nic和PIA抑制的cAMP形成的差异。脂肪细胞膜的免疫印迹表明,喂养6周和10周后,实验组动物棕色脂肪细胞膜中Giα的含量较低,但Gsα的含量没有差异。在白色脂肪组织膜的Gsα或Giα含量中未发现此类差异。因此,有人提出,在高能量饮食喂养的大鼠中,腺苷酸环化酶的抑制途径在白色脂肪组织中被致敏,而在棕色脂肪组织中被脱敏。这些敏感性的改变与肥胖期间白色脂肪组织中cAMP和脂肪分解减少以及棕色脂肪组织中cAMP和产热增加一致。

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