Laboratory of Molecular Biology, Nutrition and Biotechnology, Universitat de les Illes Balears, and CIBER de Fisiopatología de la Obesidad y Nutrición, Palma de Mallorca, Spain.
J Nutr Biochem. 2012 Sep;23(9):1041-50. doi: 10.1016/j.jnutbio.2011.05.008. Epub 2011 Sep 22.
Adipose triglyceride lipase (ATGL) hydrolyzes triacylglycerols to diacylglycerols in the first step of lipolysis, providing substrates for hormone-sensitive lipase (HSL). Here we studied whether ATGL messenger RNA (mRNA) and protein levels were affected by 24-h cold exposure in different white adipose tissue depots and in interscapular brown adipose tissue of lean and obese Zucker rats submitted to feeding and 14-h fasting conditions. HSL mRNA expression was also studied in selected depots. In both lean and obese rats, as a general trend, cold exposure increased ATGL mRNA and protein levels in the different adipose depots, except in the brown adipose tissue of lean animals, where a decrease was observed. In lean rats, cold exposure strongly improved fasting up-regulation of ATGL expression in all the adipose depots. Moreover, in response to fasting, in cold-exposed lean rats, there was a stronger positive correlation between circulating nonesterified fatty acids (NEFA) and ATGL mRNA levels in the adipose depots and a higher percentage increase of circulating NEFA in comparison with control animals not exposed to cold. In obese rats, fasting-induced up-regulation of ATGL was impaired and was not improved by cold. The effects of obesity and cold exposure on HSL mRNA expression were similar to those observed for ATGL, suggesting common regulatory mechanisms for both proteins. Thus, cold exposure increases ATGL expression and improves its fasting-up-regulation in adipose tissue of lean rats. In obese rats, cold exposure also increases ATGL expression but fails to improve its regulation by fasting, which could contribute to the increased difficulty for mobilizing lipids in these animals.
脂肪甘油三酯脂肪酶 (ATGL) 在脂肪分解的第一步中将甘油三酯水解为二酰基甘油，为激素敏感脂肪酶 (HSL) 提供底物。在这里，我们研究了在不同的白色脂肪组织和瘦素和肥胖 Zucker 大鼠的肩胛间棕色脂肪组织中，24 小时冷暴露是否会影响 ATGL 信使 RNA (mRNA) 和蛋白质水平，并分别在进食和 14 小时禁食条件下。还研究了选定部位的 HSL mRNA 表达。在瘦鼠和肥胖鼠中，作为一般趋势，冷暴露增加了不同脂肪组织中 ATGL mRNA 和蛋白质水平，除了在瘦鼠的棕色脂肪组织中观察到下降。在瘦鼠中，冷暴露强烈改善了禁食对所有脂肪组织中 ATGL 表达的上调。此外，在禁食时，冷暴露的瘦鼠中，脂肪组织中循环非酯化脂肪酸 (NEFA) 和 ATGL mRNA 水平之间存在更强的正相关，并且与未暴露于冷的对照动物相比，循环 NEFA 的百分比增加更高。在肥胖鼠中，禁食诱导的 ATGL 上调受损，冷暴露不能改善这种上调。肥胖和冷暴露对 HSL mRNA 表达的影响与对 ATGL 的观察结果相似，这表明这两种蛋白质具有共同的调节机制。因此，冷暴露增加了瘦鼠脂肪组织中 ATGL 的表达并改善了其对禁食的上调。在肥胖鼠中，冷暴露也增加了 ATGL 的表达，但不能改善其对禁食的调节，这可能导致这些动物动员脂肪的难度增加。
