title: Beta-adrenergic receptors in porcine adipocyte membranes: modification by animal age, depot site, and dietary protein deficiency.
abstract: Adipocyte lipid metabolism is primarily regulated by insulin and the catecholamines norepinephrine and epinephrine. Stimulation of the beta-adrenergic receptors (beta-AR) by catecholamines causes an increase in the rates of adipocyte lipid degradation and a decrease in the rates of lipid synthesis. These catabolic effects are in opposition to insulin, which causes net anabolic effects. Because most of the postnatal development of adipose tissue mass in pigs results from hypertrophy of adipocytes (rapid in first few weeks of life) caused by increased net synthesis of triacylglycerol, there is interest in the modulation of beta-AR in adipocytes of growing pigs. The beta-AR are characterized by measuring ligand binding to the receptor to ascertain the affinity of the ligand for the receptor and the receptor number. We found the affinity of the receptor did not vary with animal age (10, 28, and 75 d), with adipose tissue depot site, or in adipocytes of protein-deficient pigs. The beta-AR in obese pigs tended to have greater affinity than those in crossbred pigs of the same age and weight. The beta-AR number was not different when expressed per milligram of adipocyte membrane protein in pigs of different age, in obesity, in different adipose tissue depots, or during protein deficiency. The number expressed per cell or per unit adipocyte surface area did not differ between depots or during protein deficiency. The number per cell tended to be greater in the larger cells from 75-d-old pigs than in the smaller cells from 10- and 28-d pigs. It was greatest in obese pigs with the largest adipocytes. Under the various experimental conditions (age, obesity, depot, protein deficiency), the membrane fatty acid composition was greatly different, but in most cases there was no modulation of beta-AR affinity.
authors.affiliation: USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston TX 77030-2600, USA.
authors.forename: K A
authors.initials: KA
authors.lastname: Akanbi
authors.forename: H J
authors.initials: HJ
authors.lastname: Mersmann
mesh_terms: D017667:Adipocytes / Q000737:chemistry* / Q000502:physiology / Q000648:ultrastructure; D000375:Aging / Q000502:physiology*; D000818:Animals; D002462:Cell Membrane / Q000737:chemistry / Q000502:physiology / Q000648:ultrastructure; D018753:Diet, Protein-Restricted / Q000009:adverse effects / Q000662:veterinary; D005227:Fatty Acids / Q000032:analysis; D005260:Female; D050356:Lipid Metabolism; D008055:Lipids / Q000032:analysis; D008066:Lipolysis / Q000502:physiology; D008297:Male; D009765:Obesity / Q000503:physiopathology / Q000662:veterinary; D011488:Protein Deficiency / Q000503:physiopathology / Q000662:veterinary*; D011943:Receptors, Adrenergic, beta / Q000032:analysis* / Q000187:drug effects / Q000502:physiology; D013552:Swine / Q000378:metabolism / Q000502:physiology*; D013553:Swine Diseases / Q000503:physiopathology*; D014280:Triglycerides / Q000032:analysis
chemical_list: D005227:Fatty Acids; D008055:Lipids; D011943:Receptors, Adrenergic, beta; D014280:Triglycerides