Insulin sensitivity, glucose metabolism, and membrane fluidity in hypertensive subjects.

Membrane Fluidity in Hypertensive Subjects To the Editor: We read with great interest the recent article by Dr Rheaume and colleagues1 dealing with a possible link between insulin sensitivity and carbohydrate metabolism in hypertensive subjects. The results of their study demonstrated that insulin sensitivity at rest was lower and not improved by exercise in hypertensive subjects. In addition, it was shown that glycogen contents in skeletal muscles were higher with a concomitant increase in total glycogen synthase in hypertensive subjects. The authors proposed that increased intramuscular glycogen storage and resynthesis in hypertension may be related to higher insulin levels and may represent compensatory mechanisms for the reduced insulin sensitivity in this condition. Numerous studies have already shown a relationship between insulin and glucose metabolism. It was demonstrated that metformin, an antihyperglycemic drug that improves insulin sensitivity, acts on the liver to suppress gluconeogenesis by potentiating the effect of insulin.2 On the other hand, glucose transport across the membranes may be strongly influenced by a variety of membrane functions, such as membrane fluidity.3 In a study presented earlier, we investigated a relationship between membrane fluidity of erythrocytes and insulin in hypertensive subjects by means of an electron paramagnetic resonance method.4 The membrane fluidity of erythrocytes was significantly lower in patients with essential hypertension than in normotensive subjects. We showed that the higher the plasma insulin level, the lower the membrane fluidity of erythrocytes. This might indicate that hyperinsulinemia could be involved in the regulation of membrane fluidity of erythrocytes in hypertensive subjects. Wiernsperger5 proposed that metformin corrects membrane fluidity in the diabetic state and restores the function regulating glucose transport and metabolism. In this context, we speculate that abnormal membrane fluidity associated with hyperinsulinemia might partially explain the increased intramuscular glycogen storage and resynthesis in hypertension. Therefore, we would like to know whether membrane fluidity and other related membrane physicochemical properties of skeletal muscles that the authors biopsied might be changed in hypertensive subjects compared with normotensive controls. It would be necessary to assess more precisely the relationship between membrane functions and insulin-sensitive glucose transport systems in hypertension.