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  • Author: Folke Lindgärde x
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Kerstin Landin, Folke Lindgärde and Bengt Saltin


Body composition calculated from total body potassium and skeletal muscle potassium were studied in middle-aged obese men and women with normal and impaired glucose tolerance as well as Type II diabetes before and after advice on calorie reduction during twelve months. The subjects were compared with healthy lean men and women. Mean weight loss was 6.6 kg (P< 0.05). Lean body mass and body fat decreased 2.0 kg (P< 0.05) and 4.6 kg (P< 0.05), respectively. Total body potassium decreased by a mean of 146 ± 49 mmol (P< 0.01). Obese men with Type II diabetes and impaired glucose tolerance had lower total body potassium and muscle potassium levels than obese healthy men. After dieting, the obese men and women increased their muscle potassium levels with a mean of 2.8 mmol/100 g fat-free dry weight to 42.6 ± 2.6 mmol/100 g fat-free dry weight (P< 0.05), but they were still below the levels of the lean controls, 44.4 ± 1.3 mmol/100 g fat-free dry weight, (P< 0.01). Increase in skeletal muscle potassium was correlated to decrease in body weight, r = 0.55 (P< 0.01) and to decrease in fasting blood glucose, r = 0.42 (P< 0.05).

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Jörgen Malmquist, Folke Lindgärde, Karl-Fredrik Eriksson and Elisabet Johansson


The relation between glucose homeostasis and insulin secretion (immunoreactive insulin and C-peptide) was studied in middle-aged males matched for age and body weight. Subjects with mild type II diabetes mellitus were compared to normals and to individuals with impaired glucose tolerance (IGT). In addition, the diabetics were subdivided according to duration, some of the subjects having recently deteriorated from IGT status.

In the IGT individuals, there were no indications of a reduction in basal or glucose-induced insulin output. On the contrary, data indicate somewhat higher than normal secretion. Within the type II diabetics, those of short duration were largely similar to normals, whereas diabetes of longer duration was associated with some diminution in indices of B cell secretion.

The data support the notion that a deficient insulin output is not a primary pathophysiological event in the development of type II diabetes.