EFFECTS OF NITRENDIPINE ON GLUCOSE-TOLERANCE AND SERUM-INSULIN AND DEHYDROEPIANDROSTERONE SULFATE LEVELS IN INSULIN-RESISTANT OBESE AND HYPERTENSIVE MEN

被引:53
作者
BEER, NA
JAKUBOWICZ, DJ
BEER, RM
AROCHA, IR
NESTLER, JE
机构
[1] VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA,DEPT INTERNAL MED, DIV ENDOCRINOL & METAB,MCV STN, RICHMOND, VA 23298 USA
[2] FDN CARDIOVASC CONGRESO NATL, HOSP CLIN CARACAS, DEPT INTERNAL MED, CARACAS, VENEZUELA
关键词
D O I
10.1210/jc.76.1.178
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
To determine whether the calcium channel blocker nitrendipine improves glucose tolerance, lowers circulating insulin, and raises serum dehydroepiandrosterone sulfate (DHEA-8) levels in insulin-resistant men, a total of 15 obese and hypertensive men were enrolled in a single blind, placebo-controlled study. A nitrendipine group (n = 8) and a placebo group (n = 7) were studied before and after treatment with either nitrendipine (10 mg) or a placebo capsule, twice daily for 7 days, by determining serum insulin, glucose, and DHEA-S levels in the fasting state and during an oral glucose tolerance test. Nitrendipine treatment 1) lowered fasting serum insulin from 265 +/- 24 to 194 +/- 22 pmol/L (P < 0.01) without changing fasting serum glucose, 2) reduced both the area under the curve for glucose (from 1246 +/- 31 to 1091 +/- 26 mmol/L . min; P < 0.005) and the area under the curve for insulin (from 123.6 +/- 9.4 to 82.9 +/- 10.0 nmol/L . min; P < 0.015) during the oral glucose tolerance test, and 3) increased fasting serum DHEA-S by 63% from 4.21 +/- 0.17 to 6.84 +/- 0.21 mumol/L (P = 0.0001). No change was noted in the placebo group. We conclude that nitrendipine treatment is associated with improved glucose tolerance, reduced fasting and glucose-stimulated serum insulin levels, and increased circulating DHEA-S levels.
引用
收藏
页码:178 / 183
页数:6
相关论文
共 39 条
[1]   DEHYDROEPIANDROSTERONE FEEDING PREVENTS AORTIC FATTY STREAK FORMATION AND CHOLESTEROL ACCUMULATION IN CHOLESTEROL-FED RABBIT [J].
ARAD, Y ;
BADIMON, JJ ;
BADIMON, L ;
HEMBREE, WC ;
GINSBERG, HN .
ARTERIOSCLEROSIS, 1989, 9 (02) :159-166
[2]   RATES AND TISSUE SITES OF NON-INSULIN-MEDIATED AND INSULIN-MEDIATED GLUCOSE-UPTAKE IN HUMANS [J].
BARON, AD ;
BRECHTEL, G ;
WALLACE, P ;
EDELMAN, SV .
AMERICAN JOURNAL OF PHYSIOLOGY, 1988, 255 (06) :E769-E774
[3]   A PROSPECTIVE-STUDY OF DEHYDROEPIANDROSTERONE SULFATE, MORTALITY, AND CARDIOVASCULAR-DISEASE [J].
BARRETTCONNOR, E ;
KHAW, KT ;
YEN, SSC .
NEW ENGLAND JOURNAL OF MEDICINE, 1986, 315 (24) :1519-1524
[4]   MODULATION BY CALCIUM OF INSULIN ACTION AND OF INSULIN-LIKE EFFECT OF OCYTOCIN ON ISOLATED RAT LIPOCYTES [J].
BONNE, D ;
BELHADJ, O ;
COHEN, P .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1977, 75 (01) :101-105
[5]   CLINICAL REVIEW .26. INSULIN RESISTANCE IN OBESE AND NONOBESE MAN [J].
CARO, JF .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1991, 73 (04) :691-695
[6]   INSULIN RESISTANCE - A MULTIFACETED SYNDROME RESPONSIBLE FOR NIDDM, OBESITY, HYPERTENSION, DYSLIPIDEMIA, AND ATHEROSCLEROTIC CARDIOVASCULAR-DISEASE [J].
DEFRONZO, RA ;
FERRANNINI, E .
DIABETES CARE, 1991, 14 (03) :173-194
[7]   EFFECT OF ACUTE PHYSIOLOGICAL ELEVATIONS OF INSULIN ON CIRCULATING ANDROGEN LEVELS IN NONOBESE WOMEN [J].
DIAMOND, MP ;
GRAINGER, DA ;
LAUDANO, AJ ;
STARICKZYCH, K ;
DEFRONZO, RA .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1991, 72 (04) :883-887
[8]   POSSIBLE ROLE OF CYTOSOLIC FREE CALCIUM CONCENTRATIONS IN MEDIATING INSULIN RESISTANCE OF OBESITY AND HYPERINSULINEMIA [J].
DRAZNIN, B ;
SUSSMAN, KE ;
ECKEL, RH ;
KAO, M ;
YOST, T ;
SHERMAN, NA .
JOURNAL OF CLINICAL INVESTIGATION, 1988, 82 (06) :1848-1852
[9]  
DRAZNIN B, 1987, J BIOL CHEM, V262, P14385
[10]  
EICH DM, 1990, CLIN RES, V38, pA2