Abstract
Obesity, a serious and growing health threat, is associated with low-grade inflammation that plays a role in mediating its adverse consequences. Previously, we have discovered a role for neural cholinergic signaling in controlling inflammation, and demonstrated that the cholinergic agent galantamine suppresses excessive proinflammatory cytokine release. The main objective of this study was to examine the efficacy of galantamine, a clinically-approved drug, in alleviating obesity-related inflammation and associated complications. After 8 wks on a high-fat diet, C57BL/6J mice were treated with either galantamine (4 mg/kg, intraperitoneally [i.p.]) or saline for 4 wks in parallel with mice on a low-fat diet and treated with saline. Galantamine treatment of obese mice significantly reduced body weight, food intake, abdominal adiposity, plasma cytokine and adipokine levels, and significantly improved blood glucose, insulin resistance and hepatic steatosis. In addition, galantamine alleviated impaired insulin sensitivity and glucose intolerance significantly. These results indicate a previously unrecognized potential of galantamine in alleviating obesity, inflammation and other obesity-related complications in mice. These findings are of interest for studying the efficacy of this clinically-approved drug in the context of human obesity and metabolic syndrome.
Highlights
Obesity, a global epidemic, represents a major public health threat [1]
Mice (5–6 months old, Jackson Lab, Bar Harbor, ME, USA) were performed in accordance with the National Institutes of Health (NIH) Guidelines under protocols approved by the Institutional Animal Care and Use Committee (IACUC) of the Feinstein Institute for Medical Research, North Shore-Long Island Jewish (LIJ) Health System, Manhasset, New York, United States of America
Galantamine treatment was associated with additional suppression of food intake in the high-fat diet and treated with galantamine (HFD-G) group as compared with the high-fat diet and treated with saline (HFD-S) group
Summary
Obesity is complicated by hyperinsulinemia, hyperglycemia, dyslipidemia, elevated blood pressure, low-grade systemic inflammation and fatty liver. This clustering of components, under the rubric of “the metabolic syndrome,” affects more than 50 million people in the United States alone [2,3,4]. Current pharmacological options for the treatment of the metabolic syndrome are limited [3], and it would be useful to target a common pathophysiological mechanism for the treatment of this complex disorder. Experimental evidence indicates that inflammation is an important contributor to the development of insulin resistance and other pathophysiological conditions underlying the metabolic syndrome [2,9,10,11,12]
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