title: Pinealectomy causes glucose intolerance and decreases adipose cell responsiveness to insulin in rats.
abstract: Although the pineal gland influences several physiological systems, only a few studies have investigated its role in the intermediary metabolism. In the present study, male Wistar rats, pinealectomized or sham-operated 6 wk before the experiment, were submitted to both intravenous glucose tolerance tests (IVGTT) and insulin binding as well as glucose transport assays in isolated adipocytes. The insulin receptor tyrosine kinase activity was assessed in liver and muscle. The insulin secretory response during the IVGTT was impaired, particularly in the afternoon, and the glucose transport responsiveness was 33% lower in pinealectomized rats. However, no difference was observed in the insulin receptor number of adipocytes between groups as well as in insulin-stimulated tyrosine kinase activity, indicating that the initial steps in the insulin signaling were well conserved. Conversely, a 40% reduction in adipose tissue GLUT-4 content was detected. In conclusion, pinealectomy is responsible for both impaired insulin secretion and action, emphasizing the influence of the pineal gland on glucose metabolism.
authors.affiliation: Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, 05508-900 Sao Paulo, Brazil.
authors.forename: F B
authors.initials: FB
authors.lastname: Lima
authors.forename: U F
authors.initials: UF
authors.lastname: Machado
authors.forename: I
authors.initials: I
authors.lastname: Bartol
authors.forename: P M
authors.initials: PM
authors.lastname: Seraphim
authors.forename: D H
authors.initials: DH
authors.lastname: Sumida
authors.forename: S M
authors.initials: SM
authors.lastname: Moraes
authors.forename: N S
authors.initials: NS
authors.lastname: Hell
authors.forename: M M
authors.initials: MM
authors.lastname: Okamoto
authors.forename: M J
authors.initials: MJ
authors.lastname: Saad
authors.forename: C R
authors.initials: CR
authors.lastname: Carvalho
authors.forename: J
authors.initials: J
authors.lastname: Cipolla-Neto
mesh_terms: D000273:Adipose Tissue / Q000166:cytology / Q000187:drug effects; D000818:Animals; D001692:Biological Transport / Q000502:physiology; D003847:Deoxyglucose / Q000493:pharmacokinetics; D005947:Glucose / Q000378:metabolism; D018149:Glucose Intolerance / Q000209:etiology*; D005951:Glucose Tolerance Test; D051275:Glucose Transporter Type 4; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism / Q000494:pharmacology*; D008099:Liver / Q000201:enzymology; D008297:Male; D009004:Monosaccharide Transport Proteins / Q000378:metabolism; D009124:Muscle Proteins; D018482:Muscle, Skeletal / Q000201:enzymology; D010870:Pineal Gland / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism
chemical_list: D051275:Glucose Transporter Type 4; D007004:Hypoglycemic Agents; D007328:Insulin; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; C495694:Slc2a4 protein, rat; D003847:Deoxyglucose; D020794:Receptor Protein-Tyrosine Kinases; D011972:Receptor, Insulin; D005947:Glucose