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ACE-inhibition increases hepatic and extrahepatic sensitivity to insulin in patients with Type 2 (non-insulin-dependent) diabetes mellitus and arterial hypertension

✍ Scribed by E. Torlone; A. M. Rambotti; G. Perriello; G. Botta; F. Santeusanio; P. Brunetti; G. B. Bolli


Publisher
Springer
Year
1991
Tongue
English
Weight
873 KB
Volume
34
Category
Article
ISSN
0012-186X

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✦ Synopsis


To assess the effects of ACE-inhibition on insulin action in Type 2 (non-insulin-dependent) diabetes mellitus associated with essential hypertension, 12 patients with Type 2 diabetes (on diet and oral hypoglycaemic agents) and arterial hypertension were examined on two occasions, in a single blind, cross-over study after two days of treatment with either captopril or a placebo. The study consisted of a euglycaemic-hyperinsulinaemic clamp (two sequential steps of insulin infusion at the rates of 0.25 mU.kg-1.min-1 and 1 mU.kg-1.min-1, 2 h each step), combined with an infusion of 3-3H-glucose to measure the rate of hepatic glucose production and that of peripheral glucose utilization. The results show that blood pressure was lower after captopril (sitting, systolic 148 +/- 5 mm Hg, diastolic 89 +/- 2 mm Hg) compared to placebo (155 +/- 6 and 94 +/- 2 mm Hg) (p less than 0.05). Captopril treatment resulted in a more suppressed hepatic glucose production (2.7 +/- 0.4 vs 4.94 +/- 0.55 mumol.kg-1.min-1), and a lower plasma non-esterified fatty acid concentration (0.143 +/- 0.05 vs 0.200 +/- 0.05 mmol/l) (captopril vs placebo, p less than 0.05) at the end of the first step of insulin infusion (estimated portal plasma insulin concentration 305 +/- 28 pmol/l); and in a greater glucose utilization (36.5 +/- 5.1 vs 28 +/- 3.6 mumol.kg-1.min-1, p less than 0.001) at the end of the second step of insulin infusion (arterial plasma insulin concentration of 604 +/- 33 pmol/l).(ABSTRACT TRUNCATED AT 250 WORDS)


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Type 2 (non-insulin dependent) diabetes mellitus may be inherited along the maternal line and a variety of mitochondrial DNA (mtDNA) variants have been implicated in the pathogenesis. We have previously reported mutations in five regions of the mitochondrial genome which encompass 11 of the 22 tRNA