Affiliation:
1. Division of Diabetes and Hypertension, and the Division of Nephrology, Department of Medicine, and the Department of Physiology and Biophysics, University of Southern California Medical School Los Angeles, California
Abstract
We used intravenous glucose tolerance tests in vivo and 3-O-methylglucose transport into skeletal muscle in vitro to assess glucose tolerance, pancreatic β-cell function, and insulin action in 9- to 11-wk-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar Kyoto rats (WKY). Body weight was slightly higher in the WKY (P < 0.001), while blood pressure was elevated in the SHR (P < 0.001). Insulin responses to intravenous glucose after 4 or 12 h of fasting in SHR were 2–3 times the responses of WKY rats (P < 0.001). The greater insulin responses in SHR were associated with accelerated glucose disappearance P < 0.001 vs. WKY rats). A direct correlation (r = 0.49, P < 0.05) between the peak plasma insulin responses to glucose and Kg values in SHR suggested that the exaggerated insulin responses contributed to the accelerated glucose disappearance in that group. 3-O-methylglucose transport rates into epitrochlearis muscles in vitro did not differ significantly between SHR and WKY groups in the absence of insulin (P < 0.2) or in the presence of insulin at physiological (600 pM, P > 0.4) or pharmacological (120,000 pM, P > 0.9) concentrations. Thus, compared with WKY rats, SHR had exaggerated insulin responses to glucose, similar insulin-mediated glucose transport into skeletal muscle, and enhanced glucose tolerance. Our findings indicate that young, hypertensive SHR have hyperfunction of pancreatic β-cells that is unrelated to insulin resistance. The resultant nutrient-stimulated hyperinsulinemia could play a role in the development or maintenance of elevated blood pressure in SHR.
Publisher
American Diabetes Association
Subject
Endocrinology, Diabetes and Metabolism,Internal Medicine
Cited by
28 articles.
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