Harris D M, Dunshea F R, Bauman D E, Boyd R D, Wang S Y, Johnson P A, Clarke S D
Department of Animal Science, Cornell University, Ithaca, NY 14853.
J Anim Sci. 1993 Dec;71(12):3293-300. doi: 10.2527/1993.71123293x.
The present study was undertaken to determine the effects of porcine somatotropin (pST) on glucose flux rates, lipogenic enzyme activities, and the abundance of fatty acid synthase mRNA in pig adipose tissue. Barrows were injected daily with 120 micrograms of pST/kg BW (n = 6) or excipient (n = 6). On d 11 of treatment, pigs were slaughtered (empty BW = 77 +/- 2 kg) and subcutaneous adipose tissue was collected. Basal incorporation of [14C]glucose into total lipid decreased by 86% with pST treatment, whereas glucose oxidation to CO2 decreased by 79%. Insulin (10 ng/mL) stimulated both glucose oxidation and incorporation into lipid by a small increment of similar magnitude for both treatment groups. Rates of lipogenesis determined in vitro were highly correlated with similar measurements made in vivo on the same set of animals (r = .76). The reduction in basal rates of lipogenesis corresponded to a 79% decrease in total (activated) acetyl-coenzyme A carboxylase activity and a 67% decrease in fatty acid synthase activity. Reduced nicotinamide adenine dinucleotide phosphate-generating enzymes were decreased to a lesser extent. Northern blot analysis of RNA from the same animals reveal a 90% decrease in mRNA for fatty acid synthase in the pST-treated group. The correlation between mRNA abundance and enzyme activity for fatty acid synthase was .90. These data indicate that the pST-induced reduction in adipose tissue lipid accretion in growing barrows is largely a result of diminished rates of lipogenesis that are manifestations of the decreased activities of the fatty acid-synthesizing enzymes. These changes seem to result from suppression of genes that encode for the lipogenic enzymes.
本研究旨在确定猪生长激素（pST）对猪脂肪组织中葡萄糖通量率、脂肪生成酶活性以及脂肪酸合酶mRNA丰度的影响。给阉公猪每日注射120微克pST/千克体重（n = 6）或赋形剂（n = 6）。在处理的第11天，宰杀猪（空腹体重 = 77 ± 2千克）并收集皮下脂肪组织。用pST处理后，[14C]葡萄糖向总脂质的基础掺入量降低了86%，而葡萄糖氧化为CO2的量降低了79%。胰岛素（10纳克/毫升）刺激两个处理组的葡萄糖氧化以及掺入脂质的量均有相似幅度的小幅增加。体外测定的脂肪生成率与对同一组动物体内进行的相似测量结果高度相关（r = 0.76）。脂肪生成基础率的降低对应着总（活化）乙酰辅酶A羧化酶活性降低79%以及脂肪酸合酶活性降低67%。还原型烟酰胺腺嘌呤二核苷酸磷酸生成酶的降低幅度较小。对同一批动物的RNA进行Northern印迹分析显示，pST处理组中脂肪酸合酶的mRNA降低了90%。脂肪酸合酶的mRNA丰度与酶活性之间的相关性为0.90。这些数据表明，pST诱导生长阉公猪脂肪组织脂质蓄积减少主要是脂肪生成率降低的结果，而脂肪生成率降低是脂肪酸合成酶活性降低的表现。这些变化似乎是由于编码脂肪生成酶的基因受到抑制所致。
