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Nephrol Dial Transplant (1999) 14: 2282-2285
© 1999 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Insulin-mediated sympathoexcitation in obesity and type 2 diabetes

Martin S. Muntzel

Department of Biological Sciences, Lehman College, Bronx, NY, USA

Correspondence and offprint requests to: Martin S. Muntzel PhD, Lehman College, Department of Biological Sciences, 250 Bedford Park Boulevard West, Bronx, NY 10468-1589, USA.

Keywords: diabetes; hypertension; insulin; obesity; sympathetic nervous system

Introduction

Obesity and type 2 diabetes mellitus represent major health problems in industrialized societies [1]. The insulin resistance characterizing these conditions frequently results in a compensatory and sustained hyperinsulinaemia. It has been recently recognized that hyperinsulinaemia, apart from stimulating glucose uptake in skeletal muscle, also exerts important and potentially pathophysiological effects on the cardiovascular system. For instance, research over the last decade has demonstrated that insulin promotes vascular smooth-muscle proliferation, renal sodium retention, elevations in blood pressure (BP), and increases in sympathetic nerve activity (SNA) [2].

Insulin causes sympathetic activation

Of these actions, an effect of insulin to increase SNA has been very consistent and the most well documented. In humans, acute insulin infusion during euglycaemic clamp generates elevations in muscle SNA, accompanied by increases in plasma noradrenaline levels. Similar infusion failed to increase SNA to skin, indicating preferential sympathoexcitation to skeletal muscle vasculature [2,3]. Although epidemiology . . . [Full Text of this Article]

Hyperinsulinaemia and cardiovascular complications

Mechanisms of insulin-mediated sympathoexcitation

Interactions with the renin–angiotensin system

Conclusions

Acknowledgments

References


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