{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T05:02:57Z","timestamp":1790398977771,"version":"4.1.0"},"reference-count":41,"publisher":"American Physiological Society","issue":"4","funder":[{"name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","award":["2 T32 HL007854-19"],"award-info":[{"award-number":["2 T32 HL007854-19"]}]},{"name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","award":["5 U24 DK076169-09"],"award-info":[{"award-number":["5 U24 DK076169-09"]}]},{"DOI":"10.13039\/100000901","name":"Juvenile Diabetes Research Foundation International (JDRF)","doi-asserted-by":"crossref","award":["17-2012-429"],"award-info":[{"award-number":["17-2012-429"]}],"id":[{"id":"10.13039\/100000901","id-type":"DOI","asserted-by":"crossref"}]},{"name":"NIH\/NIDDK","award":["UC4DK104207"],"award-info":[{"award-number":["UC4DK104207"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2016,10,1]]},"abstract":"<jats:p> Short-term high-fat consumption stimulates mouse islet \u03b2-cell replication through unknown mechanisms. Resident macrophages (M\u03a6s) are capable of secreting various factors involved in islet development and tissue remodeling. We hypothesized that a short-term high-fat diet (HFD) promotes M\u03a6 infiltration in pancreatic islets and that M\u03a6s serve as a regulator of \u03b2-cell replication. To test these hypotheses and dissect mechanisms involved in HFD-induced \u03b2-cell replication, adult C57BL\/6J mice were fed a HFD for 7 days with or without administration of clodronate-containing liposomes, an M\u03a6-depleting agent. Mouse body and epididymal fat pad weights, and nonfasting blood glucose and fasting serum insulin levels were measured, and pancreatic islet \u03b2-cell replication, oxidative stress, and M\u03a6 infiltration were examined. Short-term HFD promoted an increase in body and epididymal fat pad weight and blood glucose levels, along with an increased fasting serum insulin concentration. \u03b2-Cell replication, islet M\u03a6 infiltration, and the percentage of inducible NO synthase positive M\u03a6s in the islets increased significantly in mice fed the HFD. Immunofluorescence staining for 8-oxo-2\u2032-deoxyguanosine or activated caspase-3 revealed no significant induction of DNA damage or apoptosis, respectively. In addition, no change in stromal-derived factor 1-expressing cells was found induced by HFD. Despite continuous elevation of nonfasting blood glucose and fasting serum insulin levels, depletion of M\u03a6s through treatments of clodronate abrogated HFD-induced \u03b2-cell replication. These findings demonstrated that HFD-induced M\u03a6 infiltration is responsible for \u03b2-cell replication. This study suggests the existence of M\u03a6-mediated mechanisms in \u03b2-cell replication that are independent of insulin resistance. <\/jats:p>","DOI":"10.1152\/ajpendo.00092.2016","type":"journal-article","created":{"date-parts":[[2016,8,30]],"date-time":"2016-08-30T22:44:28Z","timestamp":1472597068000},"page":"E763-E771","source":"Crossref","is-referenced-by-count":19,"title":["Short-term high-fat feeding induces islet macrophage infiltration and \u03b2-cell replication independently of insulin resistance in mice"],"prefix":"10.1152","volume":"311","author":[{"given":"David C.","family":"Woodland","sequence":"first","affiliation":[{"name":"Columbia Center for Translational Immunology, Columbia University Medical Center, New York, New York;"},{"name":"Department of Surgery, Columbia University Medical Center, New York, New York;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Liu","sequence":"additional","affiliation":[{"name":"Columbia Center for 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