Adipose tissue beta-adrenergic and A1 adenosine receptors in suckling pigs.
During the first few weeks after birth, major changes occur in porcine adipocyte lipid metabolism. Two of the important receptors controlling lipid metabolism in adipocytes are the beta-adrenergic receptors (betaAR) and the A1 adenosine receptors (A1R). To gain insight into the role of these receptors in modulating neonatal adipocyte lipid metabolism, we measured receptor affinity and number in suckling pigs. Adipose tissue from crossbred (X-Bred) and genetically obese suckling pigs at 0, 3, 10, and 17 d of age was used to prepare crude membranes. The betaAR and A1R number and affinity were measured in membranes by equilibrium saturation binding with radioligands. Obese pigs were smaller than X-Bred pigs (average weight = 1.62 and 2.43 kg for obese and X-Bred, respectively; P < .01). Osmium-fixed adipocytes were larger in obese pigs than in X-Bred pigs (average cell diameter = 34.4 and 30.1 microm for obese and X-Bred, respectively; P < .01). In the obese and X-Bred pigs, the affinity of the betaAR for iodocyanopindolol was greater (lower Kd) at 17 d than at the younger ages (average Kd = 177 pM at 17 d compared with > 330 pM at younger ages; age effect P < .01). The pattern for the betaAR number was complex; the lowest receptor number was at 10 d of age in obese and X-Bred pigs (average number = 41 at 10 d compared with > 65 fmol/mg protein at older and younger ages; age effect P = .03). The higher betaAR Kd and the lower receptor number in younger animals suggest less regulation by physiologic concentrations of epinephrine and norepinephrine. This would allow greater anabolic lipid metabolism to proceed during the neonatal period, when adipocytes increase four- to sixfold in volume. There were no measurable A1R at any of these early ages; thus, adenosine control mechanisms to counteract the betaAR and provide negative controls to lipid accretion are not operable in suckling pigs.
Mersmann
H J
HJ
USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA. mersmann@bcm.tmc.edu
Carey
G B
GB
Smith
E O
EO
D017667:Adipocytes / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D000273:Adipose Tissue / Q000378:metabolism* / Q000503:physiopathology; D000375:Aging / Q000378:metabolism / Q000502:physiology; D000818:Animals; D000833:Animals, Suckling / Q000378:metabolism* / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D005260:Female; D020120:Iodocyanopindolol; D050356:Lipid Metabolism; D008297:Male; D008954:Models, Biological; D009765:Obesity / Q000235:genetics / Q000378:metabolism / Q000662:veterinary; D010869:Pindolol / Q000031:analogs & derivatives / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000032:analysis* / Q000378:metabolism / Q000502:physiology; D018047:Receptors, Purinergic P1 / Q000032:analysis* / Q000378:metabolism / Q000502:physiology; D013552:Swine / Q000378:metabolism* / Q000502:physiology; D013553:Swine Diseases / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology
D011943:Receptors, Adrenergic, beta; D018047:Receptors, Purinergic P1; D020120:Iodocyanopindolol; D010869:Pindolol