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高血糖沙地大鼠脂肪组织中脂解激素调节受损及体外腺苷干扰

Impaired hormonal regulation of lipolysis and the interference with adenosine in adipose tissue from hyperglycemic sand rats in vitro.

作者信息

Knospe S, Köhler E

出版信息

Horm Metab Res. 1984 Jul;16(7):349-53. doi: 10.1055/s-2007-1014788.

Abstract

Sand rats (Psammomys obesus) developed in response to different food intake various states of hyperglycemia and hyperinsulinism. 12 normo- and 10 hyperglycemic animals were selected by means of a weekly control of plasma glucose and plasma insulin over a period of 12 weeks after separation from the mother. During this time also the development of body weight gain was checked. In both groups of rats the hormonal regulation of glycerol release by incubated adipose tissue was investigated. In any case, the fat tissue from hyperglycemic sand rats showed a lower lipolytic responsiveness to noradrenaline stimulation than that of their normoglycemic controls. This correlates well with previous results in hyperglycemic sand rats in which the catecholamine-stimulated cAMP production was disturbed (Knospe and Köhler 1981). Degradation of released adenosine by addition of adenosine deaminase significantly enhanced the noradrenaline action on glycerol release in both groups of sand rats. Even though the noradrenaline-stimulated lipolytic activity of adipose tissue from normo- and hyperglycemic animals was enhanced in the presence of adenosine deaminase, the hormone resistance of adipose tissue from hyperglycemic sand rats was nevertheless not abolished. The theophylline-mediated adenosine receptor blockade gave further evidence that particularly endogenous adenosine released during incubation of adipose tissue from sand rats inhibited the noradrenaline action on lipolysis. The antilipolytic action of insulin on glycerol release is negligibly low in normoglycemic as well as hyperglycemic sand rats. The degradation of adenosine by adenosine deaminase failed to improve the insulin action. Adenosine addition completely blocked the stimulating effects of noradrenaline on glycerol release.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

沙鼠(肥尾心颅跳鼠)因食物摄入量不同而出现了各种高血糖和高胰岛素血症状态。在与母鼠分离后的12周内,通过每周检测血浆葡萄糖和血浆胰岛素,挑选出12只血糖正常和10只高血糖的动物。在此期间,还检查了体重增加的情况。对两组大鼠中经孵育的脂肪组织甘油释放的激素调节进行了研究。无论如何,高血糖沙鼠的脂肪组织对去甲肾上腺素刺激的脂解反应性低于血糖正常的对照沙鼠。这与之前高血糖沙鼠的研究结果很好地相关,在这些研究中,儿茶酚胺刺激的环磷酸腺苷(cAMP)产生受到了干扰(Knospe和Köhler,1981年)。添加腺苷脱氨酶降解释放的腺苷,显著增强了两组沙鼠中去甲肾上腺素对甘油释放的作用。尽管在腺苷脱氨酶存在的情况下,血糖正常和高血糖动物脂肪组织的去甲肾上腺素刺激的脂解活性有所增强,但高血糖沙鼠脂肪组织的激素抵抗性仍然没有消除。茶碱介导的腺苷受体阻断进一步证明,特别是在沙鼠脂肪组织孵育过程中释放的内源性腺苷抑制了去甲肾上腺素对脂解的作用。在血糖正常和高血糖的沙鼠中,胰岛素对甘油释放的抗脂解作用极低。腺苷脱氨酶对腺苷的降解未能改善胰岛素的作用。添加腺苷完全阻断了去甲肾上腺素对甘油释放的刺激作用。(摘要截断于250字)

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