title: Basal plasma levels of insulin, leptin, ghrelin, and amylin do not signal adiposity in rats recovering from forced overweight.
abstract: This study examined how adiposity signals are related to adiposity during recovery from forced overweight (OW). Rats were rendered OW by chronic intragastric overfeeding (OW). Overfeeding was stopped when OW rats reached 126-129% of saline-infused normal-weight (NW) rats. Adipose tissue (AT) mass was estimated by computed tomography, and blood was drawn from chronic atrial cannulas throughout. Basal levels (i.e. after 2-3 h fasts late in the diurnal phase) of the hypothesized adiposity signals insulin, leptin, ghrelin, and amylin were assayed. OW rats gained approximately 130 g more body weight (BW) and approximately 100 g more AT mass during overfeeding. Plasma levels of insulin and leptin increased, whereas those of ghrelin decreased, linearly with AT mass; amylin did not change reliably. During recovery, OW rats' BW and AT mass decreased but were still elevated vs. NW rats after 39 d. OW rats' insulin returned to NW levels on d 1 of recovery and decreased below NW levels thereafter. Leptin was no longer elevated after d 8 of recovery. Ghrelin and amylin did not change reliably during recovery. Although AT mass decreased in OW rats during each intermeasurement interval between d 0 and d 23 of recovery, insulin and leptin did so during only the first interval (d 0-5). Insulin and leptin levels were exponentially related to AT mass during recovery. These data indicate that basal insulin, leptin, ghrelin, and amylin do not encode AT mass in rats dynamically regulating BW and adiposity during recovery from OW.
authors.affiliation: Physiology and Behavior Laboratory, Institute of Food, Nutrition, and Health, ETH Zurich, Schorenstrasse 16, 8603 Schwerzenbach, Switzerland.
authors.forename: Viktoria L
authors.initials: VL
authors.lastname: Gloy
authors.forename: Thomas A
authors.initials: TA
authors.lastname: Lutz
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Langhans
authors.forename: Nori
authors.initials: N
authors.lastname: Geary
authors.forename: Jacquelien J
authors.initials: JJ
authors.lastname: Hillebrand
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D050154:Adiposity / Q000502:physiology*; D000682:Amyloid / Q000097:blood*; D000818:Animals; D001835:Body Weight / Q000502:physiology; D004435:Eating / Q000502:physiology; D054439:Ghrelin / Q000097:blood*; D007118:Immunoassay / Q000379:methods; D007328:Insulin / Q000097:blood*; D058228:Islet Amyloid Polypeptide; D020738:Leptin / Q000097:blood*; D008297:Male; D050177:Overweight / Q000503:physiopathology*; D051381:Rats; D020318:Rats, Long-Evans; D015398:Signal Transduction / Q000502:physiology; D013997:Time Factors
chemical_list: D000682:Amyloid; D054439:Ghrelin; D007328:Insulin; D058228:Islet Amyloid Polypeptide; D020738:Leptin