Public release date: 1-Apr-2012 [ | E-mail | Share ] <\/p>\n
Contact: Bonnie Prescott bprescot@bidmc.harvard.edu<\/a> 617-667-7306 Beth Israel Deaconess Medical Center<\/p>\n BOSTON -- In a finding that may challenge popular notions of body fat and health, researchers at Beth Israel Deaconess Medical Center (BIDMC) have shown how fat cells can protect the body against diabetes. The results may lead to a new therapeutic strategy for preventing and treating type 2 diabetes and obesity-related metabolic diseases, the authors say. <\/p>\n In the last decade, several research groups have shown that fat cells in people play a major role in controlling healthy blood sugar and insulin levels throughout the body. To do this crucial job, fat cells need a small portion of the sugars derived from food. Obesity often reduces the dedicated sugar transport molecules on fat cells, blocking the glucose from entering fat cells. As a result, the whole body becomes insulin resistant, and blood sugar rises, leading to diabetes. <\/p>\n The new study shows why glucose is so important to fat cells. The team discovered a new version of a gene inside fat cells that responds to sugar with a powerful systemic effect. <\/p>\n \"If we change that one gene, that makes the animal more prone to or more protected from diabetes,\" said senior author Barbara Kahn MD, the George R. Minot Professor of Medicine at Harvard Medical School and Vice Chair of the Department of Medicine at BIDMC. \"Many foods get converted into sugar, so there is no need to eat more sugar.\" <\/p>\n The paper is published online April 1 in the journal Nature. In the study, the BIDMC researchers pinpointed the fat gene and its effect in mouse models of human obesity and insulin resistance and reported supporting evidence from fat tissue samples from both lean and obese people. <\/p>\n \"Two things were surprising first, that a lone gene could shift the metabolism of the fat cell so dramatically and then, that turning on this master switch selectively in adipose tissue is beneficial to the whole body,\" Kahn said. Twelve years ago, Kahn first demonstrated that fat cells are a master regulator of healthy levels of glucose and insulin in mice and require sugar to do the job. <\/p>\n \"The general concept of fat as all bad is not true,\" said first author Mark Herman MD, an investigator in the Division of Endocrinology, Diabetes and Metabolism at BIDMC and Instructor of Medicine at Harvard Medical School (HMS). \"Obesity is commonly associated with metabolic dysfunction that puts people at higher risk for diabetes, stroke and heart disease, but there is a large percentage of obese people who are metabolically healthy. We started with a mouse model that disassociates obesity from its adverse effects.\" <\/p>\n In the latest study, evidence suggests the newfound gene also may account for the protective effect of glucose uptake in human fat. German collaborators found more gene activity in people with greater insulin sensitivity, based on 123 adipose tissue samples from non-diabetic, glucose tolerant people. The fat gene activity also correlated highly with insulin sensitivity in obese, non-diabetic people, as measured in 38 fat samples by another pair of co-authors based in St. Louis. <\/p>\n<\/p>\n Continue reading here: Public release date: 1-Apr-2012 [ | E-mail | Share ] Contact: Bonnie Prescott bprescot@bidmc.harvard.edu<\/a> 617-667-7306 Beth Israel Deaconess Medical Center BOSTON -- In a finding that may challenge popular notions of body fat and health, researchers at Beth Israel Deaconess Medical Center (BIDMC) have shown how fat cells can protect the body against diabetes. The results may lead to a new therapeutic strategy for preventing and treating type 2 diabetes and obesity-related metabolic diseases, the authors say. In the last decade, several research groups have shown that fat cells in people play a major role in controlling healthy blood sugar and insulin levels throughout the body. Continue reading
\nStudy finds protective gene in fat cells<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"