Abstract
In vitro measurements of metabolism were made in subcutaneous and perirenal adipose tissue (AT) and liver from prenatally androgenized ewe lambs (TE), control ewe lambs (CE), and control wether lambs (CW). In adipose tissue slices, release of glycerol or fatty acids into the medium was not different among treatments, but glycerol release was greater (P < .01) from subcutaneous AT than from perirenal AT. Basal fatty acid release and the free fatty acid pool were greater (P < .05) for perirenal AT than for subcutaneous AT; fatty acid release and the fatty acid response (increased NEFA in media and tissue) were increased more by lipolytic stimuli in subcutaneous AT than in perirenal AT. Adipose tissue from CW had the greatest (P < .05) fatty acid response under conditions of near-maximal stimulation; rates from TE were intermediate to those from CW and CE. Incorporation of glucose into fatty acids and glycerol in subcutaneous AT was lowest (P < .05) for TE. Oxidation of glucose and acetate to CO2 and incorporation of acetate into fatty acids or glycerol in subcutaneous AT, glucose and acetate metabolism in perirenal AT, and cellularity measurements for both AT did not differ among treatments. In liver slices, oxidation of [1-14C]propionate to CO2 was greater (P < .05) for CE than for TE or CW, and gluconeogenic capacity from [1-14C]propionate tended to be greater (P < .10) for CE than for TE. Glucose and CO2 production from [2-14C]propionate, [U-14C]alanine, or [U-14C]glycerol and total and peroxisomal first cycle of beta-oxidation of [1-14C]palmitate were not altered by prenatal androgenization or sex. There were no effects (P > .1) of prenatal exposure to testosterone on mitochondrial protein content of liver, rates of mitochondrial state 3 or state 4 respiration, the ratio of ADP:oxygen in the presence of respiratory substrates, or hepatic contents of lipid, triglyceride, or glycogen. Protein content of liver was greater (P < .05) for CW than for CE; TE were intermediate. Collectively, there were minimal modifications of in vitro metabolism in AT or liver attributable to prenatal androgenization or sex that would directly influence ADG and carcass composition.
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