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Parathyroid hormone decreases in vivo insulin effect on glucose utilization.

作者信息

Saxe A W, Gibson G, Gingerich R L, Levy J

机构信息

DeRoy Surgical Research Laboratory, Department of Surgery, Sinai Hospital, Detroit, Michigan 48235, USA.

出版信息

Calcif Tissue Int. 1995 Aug;57(2):127-32. doi: 10.1007/BF00298433.

DOI:10.1007/BF00298433
PMID:7584873
Abstract

Hyperparathyroidism is associated with impaired glucose tolerance, and parathyroidectomy may improve carbohydrate homeostasis. It has been suggested that parathyroid hormone (PTH) suppresses insulin secretion but it is unclear whether it also interferes with the peripheral action of insulin. To evaluate in vivo effects of PTH on insulin-mediated glucose utilization, 15 male Sprague Dawley rats were continuously infused with rat PTH (1-34) using an Alzet miniosmotic pump at a rate of 0.03 nm/hour. Controls were infused with the vehicle alone. Following 5 days of PTH infusion, plasma calcium (Ca) levels were higher in the PTH-infused rats (12.3 +/- 0.2 versus 9.9 +/- 0.1 mg/dl, P < 0.01). On the 5th day, glucose (700 mg/kg) and insulin (0.175 U/kg) were given as a bolus infusion through the left femoral vein, blood samples were obtained from the right femoral vein, and plasma glucose and insulin were measured at basal (0 minutes) and at 2, 5, 10, and 20 minutes postinfusion. Basal, nonfasting glucose levels were higher (166 +/- 4 versus 155 +/- 4 mg/dL, P < 0.04) in the PTH-infused rats but their insulin levels were similar to those of controls (6.5 +/- 0.6 versus 5.6 +/- 0.5 ng/ml). Postinfusions and maximal (2 minutes) glucose and insulin levels were similar in both groups. However, although insulin levels were similar in both groups at all measured time points, glucose levels at 20 minutes were higher in the PTH-treated rats (205 +/- 13 versus 173 +/- 9; P < 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

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本文引用的文献

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Limitations of the application of fourfold table analysis to hospital data.四格表分析在医院数据应用中的局限性。
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Primary hyperparathyroidism is associated with decreased insulin receptor binding and glucose intolerance.原发性甲状旁腺功能亢进与胰岛素受体结合减少及葡萄糖耐量异常有关。
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Peripheral insulin resistance in primary hyperparathyroidism.
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