Increased Plasma Adiponectin in Losartan-treated Type 1 Diabetic Patients. A Mediator of Improved Insulin Sensitivity?

Introduction

Adiponectin is a secretory protein derived from adipose tissue with potential insulin sensitizing, anti-inflammatory, and anti-atherogenic properties [1]. Reduced plasma adiponectin concentrations are found in obesity, type 2 diabetes, and coronary artery disease; low plasma levels predict the development of type 2 diabetes in Pima Indians [1]. Conversely, plasma adiponectin increases after weight loss. However, modification of insulin sensitivity without changes in body fat mass, such as chronic physical exercise training [2] and short-term (experimental) changes in plasma free fatty acids (FFA) [3], fail to alter circulating adiponectin concentrations. On the other hand, treatment with insulin-sensitizing thiazolidinediones increases plasma adiponectin in humans [4]. It has therefore been speculated that drugs targeted at increasing adiponectin production may also improve insulin sensitivity and potentially prevent development of type 2 diabetes and atherosclerosis. Treatment of insulin-resistant, essential hypertensive patients with angiotensin II receptor blockers has been shown to be associated with improved sensitivity to insulin mediated glucose metabolism [5] [6] and increased plasma adiponectin concentrations [6]. Recently, we reported improved basal and insulin-mediated glucose metabolism after six weeks of treatment with losartan 50 mg o. d. in a study of normotensive, normoalbuminuric type 1 diabetic men [7]. Here, we have examined whether the effects of losartan on glucose metabolism were associated with changes in plasma adiponectin.

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