clenbuterol increases insulin sensitivity. A ketogenic diet, of which on of the main purposes is to reduce blood insulin levels, is uneccessary and may be detrimental.
here is a little animal abstract- though the anabolism does not translate to humans(at least not significantly and seems to be limited to certain tissues)
Effects of clenbuterol on insulin resistance in conscious obese zucker rats. Pan, Shujia J., Joe Hancock, Zhenping Ding, Donovan Fogt, Mancheong Lee, and John L. Ivy. Exercise Physiology and Metabolism Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin, Austin, Texas 78712
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APStracts 7:0257E, 2000.
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The present study was conducted to determine the effect of chronic administration of the long-acting ß2-adrenergic agonist clenbuterol on rats that are genetically prone to insulin resistance and impaired glucose tolerance. Obese Zucker rats (fa/fa) were given 1 mg/kg of clenbuterol by oral intubation daily for 5 wk. Controls received an equivalent volume of water according to the same schedule. At the end of the treatment, rats were catheterized for euglycemic-hyperinsulinemic (15 mU insulin•kg«minus»1•min«minus»1) clamping. Clenbuterol did not change body weight compared with the control group but caused a redistribution of body weight: leg muscle weights increased, and abdominal fat weight decreased. The glucose infusion rate needed to maintain euglycemia and the rate of glucose disappearance were greater in the clenbuterol-treated rats. Furthermore, plasma insulin levels were decreased, and the rate of glucose uptake into hindlimb muscles and abdominal fat was increased in the clenbuterol-treated rats. This increased rate of glucose uptake was accompanied by a parallel increase in the rate of glycogen synthesis. The increase in muscle glucose uptake could not be ascribed to an increase in the glucose transport protein GLUT-4 in clenbuterol-treated rats. We conclude that chronic clenbuterol treatment reduces the insulin resistance of the obese Zucker rat by increasing insulin-stimulated muscle and adipose tissue glucose uptake. The improvements noted may be related to the repartitioning of body weight between tissues.
Received 11 August 2000; accepted in final form 4 December 2000
APS Manuscript Number E372-0.
Article publication pending Am J Physiol Endocrinol Metab
ISSN 1080-4757 Copyright 2000 The American Physiological Society.
Published in APStracts on 28 December 2000
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