EFFECT OF CHRONIC ACE INHIBITION ON GLUCOSE TOLERANCE AND INSULIN SENSITIVITY IN HYPERTENSIVE TYPE 2 DIABETIC PATIENTS
Chinese Medical Sciences JournalIssue 1, (1994)
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EFFECT OF CHRONIC ACE INHIBITION ON GLUCOSE TOLERANCE AND INSULIN SENSITIVITY IN HYPERTENSIVE TYPE 2 DIABETIC PATIENTS
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CLC:R363
Published:1994
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[1]尹卫东.EFFECT OF CHRONIC ACE INHIBITIONONGLUCOSE TOLERANCE AND INSULIN SENSITIVITY IN HYPERTENSIVE TYPE 2 DIABETIC PATIENTS[J].Chinese Medical Sciences Journal,1994(01):29-33.
EFFECT OF CHRONIC ACE INHIBITION ON GLUCOSE TOLERANCE AND INSULIN SENSITIVITY IN HYPERTENSIVE TYPE 2 DIABETIC PATIENTS[J]. Chinese medical sciences journal, 1994, (1).
[1]尹卫东.EFFECT OF CHRONIC ACE INHIBITIONONGLUCOSE TOLERANCE AND INSULIN SENSITIVITY IN HYPERTENSIVE TYPE 2 DIABETIC PATIENTS[J].Chinese Medical Sciences Journal,1994(01):29-33.DOI:
EFFECT OF CHRONIC ACE INHIBITION ON GLUCOSE TOLERANCE AND INSULIN SENSITIVITY IN HYPERTENSIVE TYPE 2 DIABETIC PATIENTS[J]. Chinese medical sciences journal, 1994, (1).DOI:
EFFECT OF CHRONIC ACE INHIBITION ON GLUCOSE TOLERANCE AND INSULIN SENSITIVITY IN HYPERTENSIVE TYPE 2 DIABETIC PATIENTS
We studied 14 moderately overweight Typo 2 diabetic patients with essential hypertension in stable metabolic control after a run-in period
and again after 3 months of antihypertensive treatment with the angiotensin-converting enzyme (ACF) inhibitor captopril. Glucose tolerance was tested with a 75g oral glucose load (OGTT) and insulin sensitivity was measured by the insulin suppression test (IST) while dietary and drug treatment of the hyperglycemia was maintained constant. In the whole group. mean blood pressure (MBP) fell progressively over 3months from a baseline value of 123± 3 mmHg (1 mmHg= 0. 133 kpa) to a final value of 115± 2 mmHg(P<0. 005). After treatment
fasting plasma glucose
insulin
free fatty acid (FFA). potassium
and glycosylated hemoglobin concentrations were unchanged from baseline. There were no significant differences in glucose tolerance and insulin sensitivity between pre- and post-trearment values. Neither endogenous (oral glucose) nor exogenous (IST) insulin caused any change in plasma potassium concentration. This resistance to the hypokalemic action of insulin was not affected by captopril.