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U.S.A."],"published-print":{"date-parts":[[2016,1,12]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    The G protein G\n                    <jats:sub>s<\/jats:sub>\n                    \u03b1 mediates the activation of lipolysis in white and brown adipose tissue (WAT and BAT) and thermogenesis in BAT by sympathetic nerves. In this study we show that G\n                    <jats:sub>s<\/jats:sub>\n                    \u03b1 deficiency in BAT and WAT leads to cold intolerance and inactive BAT in mice, as expected, but does not alter body weight or energy balance, associated with a reduction in both lipolysis and lipogenesis. Despite having similar adiposity, these mice had improved insulin sensitivity and glucose metabolism, possibly secondary to reduced release of free fatty acids and fatty acid binding protein 4 from adipose tissue. These findings show that G\n                    <jats:sub>s<\/jats:sub>\n                    \u03b1 in adipocytes is not required to maintain energy balance but still has an important effect on glucose metabolism.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1517142113","type":"journal-article","created":{"date-parts":[[2015,12,28]],"date-time":"2015-12-28T22:34:01Z","timestamp":1451342041000},"page":"446-451","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":35,"title":["G\n                    <sub>s<\/sub>\n                    \u03b1 deficiency in adipose tissue improves glucose metabolism and insulin sensitivity without an effect on body weight"],"prefix":"10.1073","volume":"113","author":[{"given":"Yong-Qi","family":"Li","sequence":"first","affiliation":[{"name":"Metabolic Diseases Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yogendra B.","family":"Shrestha","sequence":"additional","affiliation":[{"name":"Metabolic Diseases Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min","family":"Chen","sequence":"additional","affiliation":[{"name":"Metabolic Diseases Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatyana","family":"Chanturiya","sequence":"additional","affiliation":[{"name":"Mouse Metabolism Core Laboratory, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oksana","family":"Gavrilova","sequence":"additional","affiliation":[{"name":"Mouse Metabolism Core Laboratory, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lee S.","family":"Weinstein","sequence":"additional","affiliation":[{"name":"Metabolic Diseases Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2015,12,28]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2013.12.021"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2008.12.014"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.44.101802.121659"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1139\/y91-276"},{"key":"e_1_3_3_5_2","first-page":"R979","article-title":"Dietary obesity and neonatal sympathectomy. 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