{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T15:47:36Z","timestamp":1791042456353,"version":"4.1.0"},"reference-count":39,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2002,11,1]]},"abstract":"<jats:p>\n                    Group 1B phospholipase A\n                    <jats:sub>2<\/jats:sub>\n                    (PLA\n                    <jats:sub>2<\/jats:sub>\n                    ) is an abundant lipolytic enzyme that is well characterized biochemically and structurally. Because of its high level of expression in the pancreas, it has been presumed that PLA\n                    <jats:sub>2<\/jats:sub>\n                    plays a role in the digestion of dietary lipids, but in vivo data have been lacking to support this theory. Our initial study on mice lacking PLA\n                    <jats:sub>2<\/jats:sub>\n                    demonstrated no abnormalities in dietary lipid absorption in mice consuming a chow diet. However, the effects of PLA\n                    <jats:sub>2<\/jats:sub>\n                    deficiency on animals consuming a high-fat diet have not been studied. To investigate this, PLA\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>+\/+<\/jats:sup>\n                    and PLA\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice were fed a western diet for 16 wk. The results showed that PLA\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice were resistant to high-fat diet-induced obesity. This observed weight difference was due to decreased adiposity present in the PLA\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Compared with PLA\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>+\/+<\/jats:sup>\n                    mice, the PLA\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice had 60% lower plasma insulin and 72% lower plasma leptin levels after high-fat diet feeding. The PLA\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice also did not exhibit impaired glucose tolerance associated with the development of obesity-related insulin resistance as observed in the PLA\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>+\/+<\/jats:sup>\n                    mice. To investigate the mechanism by which PLA\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice exhibit decreased weight gain while on a high-fat diet, fat absorption studies were performed. The PLA\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice displayed 50 and 35% decreased plasma [\n                    <jats:sup>3<\/jats:sup>\n                    H]triglyceride concentrations 4 and 6 h, respectively, after feeding on a lipid-rich meal containing [\n                    <jats:sup>3<\/jats:sup>\n                    H]triolein. The PLA\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice also displayed increased lipid content in the stool, thus indicating decreased fat absorption in these animals. These results suggest a novel role for PLA\n                    <jats:sub>2<\/jats:sub>\n                    in the protection against diet-induced obesity and obesity-related insulin resistance, thereby offering a new target for treatment of obesity and diabetes.\n                  <\/jats:p>","DOI":"10.1152\/ajpendo.00110.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T14:50:01Z","timestamp":1425394201000},"page":"E994-E1001","source":"Crossref","is-referenced-by-count":88,"title":["Protection against diet-induced obesity and obesity- related insulin resistance in Group 1B PLA\n                    <sub>2<\/sub>\n                    -deficient mice"],"prefix":"10.1152","volume":"283","author":[{"given":"Kevin W.","family":"Huggins","sequence":"first","affiliation":[{"name":"Center for Lipid and Arteriosclerosis Studies, Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 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