Suppr超能文献

恒河猴胰岛素诱导低血糖期间胰高血糖素分泌的自主调节

Autonomic mediation of glucagon secretion during insulin-induced hypoglycemia in rhesus monkeys.

作者信息

Havel P J, Valverde C

机构信息

Department of Nutrition, University of California, Davis 95626, USA.

出版信息

Diabetes. 1996 Jul;45(7):960-6. doi: 10.2337/diab.45.7.960.

Abstract

Autonomic activation mediates the majority of the increase of glucagon secretion during insulin-induced hypoglycemia in several species including dogs, mice, and rats. However, the role of the autonomic nervous system to increase glucagon during hypoglycemia in humans remains controversial, and investigations in nonhuman primates have not been previously conducted. The autonomic contribution to glucagon secretion during hypoglycemia in a nonhuman primate was examined by two independent pharmacological approaches. Glucagon responses to clamped insulin-induced hypoglycemia were compared in conscious rhesus monkeys in the presence or absence of ganglionic blockade with trimethaphan, or during combined muscarinic and adrenergic receptor blockade with atropine, propranolol, and tolazoline. Insulin-induced hypoglycemia (plasma glucose = 1.9 +/- 0.1 mmol/l) activated parasympathetic nerves to the pancreas as assessed by increased plasma pancreatic polypeptide (PP) levels (delta = 135.0 +/- 36.8 pmol/l, P < 0.01), produced sympathoadrenal activation as assessed by elevations of plasma epinephrine (EPI) (delta = 22.3 +/- 2.95 nmol/l, P < 0.0005) and norepinephrine (NE) (delta = 3.72 +/- 0.77 mmol/l, P < 0.0025) and increased plasma immunoreactive glucagon (IRG) (delta = 920 +/- 294 ng/l, P < 0.025). Nicotinic ganglionic blockade with trimethaphan prevented parasympathetic (deltaPP = 16.5 +/- 16.3 pmol/l, P < 0.01 vs. control) and sympathoadrenal (deltaEPI = 1.52 +/- 0.98 nmol/l; deltaNE = -0.62 +/- 0.24 mmol/l, both P < 0.0025 vs. control) activation during hypoglycemia and inhibited the IRG response by 70% (delta = 278 +/- 67 ng/l, P < 0.025 vs. control). Combined muscarinic and adrenergic receptor blockade reduced parasympathetic activation (deltaPP = 48.3 +/- 16.3 pmol/l, P < 0.01 vs. control) and inhibited the IRG response by a similar degree to ganglionic blockade (deltaIRG = 284 +/- 60 ng/l, P < 0.025 vs. control). These results demonstrate by two independent pharmacological approaches that autonomic activation makes a substantial contribution to increased glucagon secretion during hypoglycemia of approximately 2.0 mmol/l in a species of nonhuman primate.

摘要

在包括狗、小鼠和大鼠在内的几种物种中,自主神经激活介导了胰岛素诱导的低血糖期间胰高血糖素分泌增加的大部分过程。然而,自主神经系统在人类低血糖期间增加胰高血糖素分泌的作用仍存在争议,此前尚未在非人类灵长类动物中进行过研究。通过两种独立的药理学方法研究了非人类灵长类动物低血糖期间自主神经对胰高血糖素分泌的作用。在清醒的恒河猴中,比较了在存在或不存在用三甲噻方进行神经节阻滞的情况下,或在联合使用阿托品、普萘洛尔和妥拉唑啉进行毒蕈碱和肾上腺素能受体阻滞期间,胰高血糖素对钳夹胰岛素诱导的低血糖的反应。胰岛素诱导的低血糖(血浆葡萄糖 = 1.9±0.1 mmol/l)激活了胰腺的副交感神经,这可通过血浆胰多肽(PP)水平升高来评估(δ = 135.0±36.8 pmol/l,P < 0.01),产生了交感肾上腺激活,这可通过血浆肾上腺素(EPI)升高来评估(δ = 22.3±2.95 nmol/l,P < 0.0005)和去甲肾上腺素(NE)升高来评估(δ = 3.72±0.77 mmol/l,P < 0.0025),并增加了血浆免疫反应性胰高血糖素(IRG)(δ = 920±294 ng/l,P < 0.025)。用三甲噻方进行烟碱样神经节阻滞可防止低血糖期间的副交感神经(δPP = 16.5±16.3 pmol/l,与对照组相比P < 0.01)和交感肾上腺(δEPI = 1.52±0.98 nmol/l;δNE = -0.62±0.24 mmol/l,两者与对照组相比P < 0.0025)激活,并使IRG反应抑制70%(δ = 278±67 ng/l,与对照组相比P < 0.025)。联合毒蕈碱和肾上腺素能受体阻滞可降低副交感神经激活(δPP = 48.3±16.3 pmol/l,与对照组相比P < 0.01),并使IRG反应的抑制程度与神经节阻滞相似(δIRG = 284±60 ng/l,与对照组相比P < 0.025)。这些结果通过两种独立的药理学方法证明,在一种非人类灵长类动物中,自主神经激活对约2.0 mmol/l低血糖期间胰高血糖素分泌增加有重大贡献。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验