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Whole‐body Glucose Metabolism in Obese Patients with Type 2 Diabetes Mellitus: the Impact of Hypertension and Strict Blood Glucose Control
Author(s) -
Vestergaard H.,
Parving H.H.,
Hansen L.,
Pedersen O.
Publication year - 1995
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.1995.tb00447.x
Subject(s) - medicine , diabetes mellitus , type 2 diabetes mellitus , endocrinology , carbohydrate metabolism , metabolism , obesity , type 2 diabetes , metabolic control analysis
We have examined the impact of hypertension and blood glucose control on insulin sensitivity in obese Type 2 (non‐insulin‐dependent) diabetic patients. Glucose metabolism in the basal state and in response to insulin was examined using the euglycaemic, hyperinsulinaemic (2 mU kg −1 min −1 ) clamp technique in combination with 3‐[3H]‐glucose infusion 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 state and during hyperinsulinaemia, glucose disposal rates (total, oxidative, 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 subjects, respectively). However, compared to obese control subjects (403 ± 65 mg m −2 min −1 ) both groups of diabetic patients had significantly decreased insulin‐stimulated glucose disposal rates ( p < 0.005). Even in a subset of Type 2 diabetic patients with long‐term (> 6 months) near normal blood glucose control (HbA 1c < 6.1 %) significant defects were detectable in whole‐body glucose and lipid metabolism when compared to control subjects. These results indicate that treated hypertension does not significantly aggravate the insulin insensitivity that is already present in Type 2 diabeted mellitus. Furthermore, Type 2 diabetic patients with long‐term good metabolic control continue to demonstrate insulin insensitivity in peripheral tissues.