title: Chronically administered islet amyloid polypeptide in rats serves as an adiposity inhibitor and regulates energy homeostasis.
abstract: OBJECTIVE
  Islet amyloid polypeptide (IAPP) reduces food intake and body weight in laboratory animals. In addition, IAPP appears to regulate nutrient metabolism. In the present studies, we investigated the effect of chronic IAPP treatment on different aspects of energy homeostasis.
  
  
  METHODS
  IAPP was infused (25 pmol/kg/min) from subcutaneous osmotic pumps for 2-7 days. Rats in 2 saline-infused control groups were fed ad libitum (AF) or pair-fed (PF) against the IAPP-treated rats.
  
  
  RESULTS
  As expected, the IAPP infusion reduced food intake and body weight gain. In addition, the IAPP treatment decreased the epididymal fat pad (vs. PF rats, p < 0.05) and lowered circulating levels of triglycerides (vs. PF rats, p < 0.05), free fatty acids (vs. PF rats, p < 0.05), leptin (vs. both AF and PF rats, p < 0.05) and insulin (vs. AF rats, p < 0.05). In contrast, glucose and protein metabolism in the IAPP-treated rats was largely unchanged, as shown in results regarding serum glucose, glucose transport in skeletal muscle, blood urea nitrogen, and glycogen and protein content in the liver and in skeletal muscle.
  
  
  CONCLUSIONS
  In summary, chronic IAPP exposure led to a changed lipid metabolism, which was characterized by decreased adiposity, hypolipidemia and hypoleptinemia, and to unchanged glucose and protein homeostasis. These results were similar to those seen in rodents during chronic exposure to another satiety/adiposity regulator, leptin. In conclusion, chronically administered IAPP plays a role as a satiety and adiposity signal in rats, and helps regulate energy homeostasis.
authors.affiliation: Arvid Wretlind Laboratory for Metabolic and Nutritional Research, Department of Surgery, Karolinska Institutet at Huddinge University Hospital, SE-141 86 Stockholm, Sweden. bengt.isaksson@hs.se
authors.forename: B
authors.initials: B
authors.lastname: Isaksson
authors.forename: F
authors.initials: F
authors.lastname: Wang
authors.forename: J
authors.initials: J
authors.lastname: Permert
authors.forename: M
authors.initials: M
authors.lastname: Olsson
authors.forename: B
authors.initials: B
authors.lastname: Fruin
authors.forename: M K
authors.initials: MK
authors.lastname: Herrington
authors.forename: L
authors.initials: L
authors.lastname: Enochsson
authors.forename: C
authors.initials: C
authors.lastname: Erlanson-Albertsson
authors.forename: U
authors.initials: U
authors.lastname: Arnelo
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000254:growth & development*; D000682:Amyloid / Q000008:administration & dosage / Q000494:pharmacology / Q000502:physiology*; D000818:Animals; D005247:Feeding Behavior / Q000187:drug effects / Q000502:physiology*; D015870:Gene Expression / Q000187:drug effects; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D007328:Insulin / Q000097:blood; D007473:Ion Channels; D058228:Islet Amyloid Polypeptide; D020738:Leptin / Q000097:blood; D026901:Membrane Transport Proteins / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D000071246:Uncoupling Protein 2; D015430:Weight Gain / Q000187:drug effects / Q000502:physiology
chemical_list: D000682:Amyloid; D007328:Insulin; D007473:Ion Channels; D058228:Islet Amyloid Polypeptide; D020738:Leptin; D026901:Membrane Transport Proteins; D024101:Mitochondrial Proteins; D000071246:Uncoupling Protein 2