Papel de CCL2 na adiposidade e intolerância à glicose induzidos em camundongos por dieta normocalórica/rica em carboidratos refinados

Abstract

Obesity is associated with chronic inflammation and represents the risk factor for diabetes and metabolic syndrome. The results of works about the role of CC chemokine ligand 2 (CCL2) in adiposity and metabolic diseases are controversial and not clean the real role of this chemokine in occurrence of metabolics changes associated with exacerbated expansion of adipose tissue. Our aim was to evaluate if the inhibition of CCL2 prodution in adipose tissue interferes in adiposity induced by HC diet, as well as in the occurence of glucose intolerance and inflammatory response in adipose tissue. For this, we used the experimental model of adiposity and increase of pro-inflammatory molecules, as CCL2 in adipose tissue induced by diet. We used C57BL/6 male mice. Mice were fed with control or HC diet associated or not with Bindarit (synthetic drug that inhibits the production of CCL2). The oral treatment of Bindarit was once a day (100mg/Kg of body weight) from fourth to tenth week or from eighth to tenth week. Test of glucose tolerance was made on the ninth week of diet intake. The group fed with HC diet and treated with the drug, although the inhibition of CCL2 production in adipose tissue, not presented improvement of glucose intolerance and/or profile changes in the secretion of adipokines linked to induction of insulin resistance. Then, we suggest that absence of CCL2 doesnt have role in adiposity and glucose intolerance induced by HC diet.