title: Resistance to insulin-stimulated-glucose uptake in patients with hypertension.
abstract: Plasma glucose and insulin responses to a glucose challenge and insulin-stimulated glucose uptake were measured in 24 age-, weight-, and sex-matched Chinese men (8 with normal blood pressure, 8 with untreated hypertension, and 8 patients with hypertension treated with thiazide and beta-adrenergic antagonist drugs). Plasma glucose and insulin responses were determined by measuring plasma glucose and insulin concentrations before and at 30-min intervals for 2 h after a 75-g oral glucose dose. Insulin-stimulated glucose uptake was estimated by measuring the steady state plasma glucose (SSPG) and insulin (SSPI) concentrations achieved during the last 60 min of a 180-min continuous infusion of somatostatin, insulin, and glucose (insulin suppression test). Under these conditions endogenous insulin secretion was suppressed, and similar SSPI concentrations were achieved in all men; thus, the differences in the resultant SSPG concentrations allowed direct comparison of insulin's ability to stimulate disposal of an identical glucose load in different individuals. The results indicated that the men with hypertension, whether treated or untreated, had significantly elevated plasma glucose (P less than 0.001) and insulin (P less than 0.001) responses to the oral glucose dose compared to the normal men. Mean (+/- SE) SSPG concentrations were also higher (P less than 0.001) in the men with either untreated hypertension [219 +/- 9 mg/dL (12.2 +/- 0.5 mmol/L)] or treated hypertension [211 +/- 18 mg/dL (11.7 +/- 1.0 mmol/L)] than in the normal men [134 +/- 13 mg/dL (7.4 +/- 0.7 mmol/L)]. Since the mean SSPI concentrations were similar in the 3 groups [approximately 70 microU/mL (502 pmol/L)], insulin was less effective in promoting glucose disposal in both groups with hypertension. These results document the fact that patients with hypertension, whether treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic compared to a well-matched control group.
authors.affiliation: Department of Medicine, Stanford University School of Medicine, California 94304.
authors.forename: D C
authors.initials: DC
authors.lastname: Shen
authors.forename: S M
authors.initials: SM
authors.lastname: Shieh
authors.forename: M M
authors.initials: MM
authors.lastname: Fuh
authors.forename: D A
authors.initials: DA
authors.lastname: Wu
authors.forename: Y D
authors.initials: YD
authors.lastname: Chen
authors.forename: G M
authors.initials: GM
authors.lastname: Reaven
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D006801:Humans; D006946:Hyperinsulinism / Q000097:blood; D006973:Hypertension / Q000097:blood*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged
chemical_list: D001786:Blood Glucose