WHOLE-BODY GLUCOSE-METABOLISM IN OBESE PATIENTS WITH TYPE-2 DIABETES-MELLITUS - THE IMPACT OF HYPERTENSION AND STRICT BLOOD-GLUCOSE CONTROL

Citation
H. Vestergaard et al., WHOLE-BODY GLUCOSE-METABOLISM IN OBESE PATIENTS WITH TYPE-2 DIABETES-MELLITUS - THE IMPACT OF HYPERTENSION AND STRICT BLOOD-GLUCOSE CONTROL, Diabetic medicine, 12(2), 1995, pp. 156-163
Citations number
NO
Categorie Soggetti
Endocrynology & Metabolism","Medicine, General & Internal
Journal title
ISSN journal
07423071
Volume
12
Issue
2
Year of publication
1995
Pages
156 - 163
Database
ISI
SICI code
0742-3071(1995)12:2<156:WGIOPW>2.0.ZU;2-1
Abstract
We have examined the impact of hypertension and blood glucose control on insulin sensitivity in obese Type 2 (non-insulin-dependent) diabeti c patients. Glucose metabolism in the basal state and in response to i nsulin was examined using the euglycaemic, hyperinsulinaemic (2 mU kg( -1) min(-1)) clamp technique in combination with 3-[H-3]-glucose infus ion and indirect calorimetry in 60 obese Type 2 diabetic patients (30 normotensive patients and 30 hypertensive patients on antihypertensive treatment) and 10 obese normotensive control subjects. In the basal s tate and during hyperinsulinaemia, glucose disposal rates (total, oxid ative, and nonoxidative) were similar in Type 2 diabetic patients with or without hypertension (230 +/- 83 vs 270 +/- 114 mg m(-2) min(-1) ( NS), 83 +/- 28 vs 95 +/- 7 mg m(-2) min(-1) (NS), 148 +/- 70 vs 180 +/ - 89 mg m(-2) min(-1) (NS), treated hypertensive vs normotensive subje cts, respectively). However, compared to obese control subjects (403 /- 65 mg m(-2) min(-1)) both groups of diabetic patients had significa ntly decreased insulin-stimulated glucose disposal rates (p < 0.005). Even in a subset of Type 2 diabetic patients with long-term (> 6 month s) near normal blood glucose control (HbA(1c) < 6.1 %) significant def ects were detectable in whole-body glucose and lipid metabolism when c ompared to control subjects. These results indicate that treated hyper tension does not significantly aggravate the insulin insensitivity tha t is already present in Type 2 diabetes mellitus. Furthermore, Type 2 diabetic patients with long-term good metabolic control continue to de monstrate insulin insensitivity in peripheral tissues.