{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T19:52:28Z","timestamp":1773777148952,"version":"3.50.1"},"reference-count":36,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2001,4,1]]},"abstract":"<jats:p>The present study investigated the role of amylin in lipid metabolism and its possible implications for insulin resistance. In 5- to 7-h-fasted conscious rats, infusion of rat amylin (5 nmol\/h for 4 h) elevated plasma glucose, lactate, and insulin ( P &lt;0.05 vs. control, repeated-measures ANOVA) with peak values occurring within 60 min. Despite the insulin rise, plasma nonesterified fatty acids (NEFA) and glycerol were also elevated ( P &lt; 0.001 vs. control), and these elevations (80% above basal) were sustained over the 4-h infusion period. Although unaltered in plasma, triglyceride content in liver was increased by 28% ( P &lt; 0.001) with a similar tendency in muscle (18%, P = 0.1). Infusion of the rat amylin antagonist amylin-(8\u201337) (125 nmol\/h) induced opposite basal plasma changes to amylin, i.e., lowered plasma NEFA, glycerol, glucose, and insulin levels (all P &lt; 0.05 vs. control); additionally, amylin-(8\u201337) blocked amylin-induced elevations of these parameters ( P &lt; 0.01). Treatment with acipimox (10 mg\/kg), an anti-lipolytic agent, before or after amylin infusion blocked amylin's effects on plasma NEFA, glycerol, and insulin but not on glucose and lactate. We conclude that amylin could exert a lipolytic-like action in vivo that is blocked by and is opposite to effects of its antagonist amylin-(8\u201337). Further studies are warranted to examine the physiological implications of lipid mobilization for amylin-induced insulin resistance.<\/jats:p>","DOI":"10.1152\/ajpendo.2001.280.4.e562","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:10:11Z","timestamp":1513966211000},"page":"E562-E569","source":"Crossref","is-referenced-by-count":16,"title":["Evidence that amylin stimulates lipolysis in vivo: a possible mediator of induced insulin resistance"],"prefix":"10.1152","volume":"280","author":[{"given":"Ji-Ming","family":"Ye","sequence":"first","affiliation":[{"name":"Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, New South Wales 2010, Australia; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Megan","family":"Lim-Fraser","sequence":"additional","affiliation":[{"name":"Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, New South Wales 2010, Australia; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gregory J.","family":"Cooney","sequence":"additional","affiliation":[{"name":"Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, New South Wales 2010, Australia; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Garth J. 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