Accumulating evidence shows that granulosa cells within both mammalian and avian ovaries have the ability to synthesize fatty acids through de novo lipogenesis and to accumulate triglycerides essential for oocyte and ovarian development. However, very little is known about the exact roles of key genes involved in the lipid metabolic pathway in granulosa cells. The goal of this study was to investigate the differential actions of diacylglycerol acyltransferase (DGAT) 1 and 2, which are recognized as the rate-limiting enzymes catalyzing the last step of triglyceride biosynthesis, in regulating lipid metabolism and steroidogenesis in granulosa cells of goose follicles at different developmental stages. It was observed that the mRNAs encoding DGAT1 and DGAT2 were ubiquitous in all examined granulosa cell layers but exhibited distinct expression profiles during follicle development. Notably, the mRNA levels of DGAT1, DGAT2, FSHR, LHR, STAR, CYP11A1, and 3βHSD remained almost constant in all except for 1–2 follicles within the 8−10 mm cohort, followed by an acute increase/decrease in the F5 follicles. At the cellular level, siRNA-mediated downregulation of DGAT1 or DGAT2 did not change the amount of lipids accumulated in both undifferentiated- and differentiated granulosa cells, while overexpression of DGAT2 promoted lipid accumulation and expression of lipogenic-related genes in these cells. Meanwhile, we found that interfering DGAT2 had no effect but interfering DGAT1 or overexpressing DGAT2 stimulated progesterone secretion in undifferentiated granulosa cells; in contrast, interference or overexpression of DGAT1/2 failed to change progesterone levels in differentiated granulosa cells but differently modulated expression of steroidogenic-related genes. Therefore, it could be concluded that DGAT1 is less efficient than DGAT2 in promoting lipid accumulation in both undifferentiated- and differentiated granulosa cells and that DGAT1 negatively while DGAT2 positively regulates progesterone production in undifferentiated granulosa cells.

越来越多的证据表明，哺乳动物和禽类卵巢中的颗粒细胞都具有通过从头脂肪生成合成脂肪酸并积累卵母细胞和卵巢发育必不可少的甘油三酸酯的能力。然而，关于颗粒细胞中脂质代谢途径中涉及的关键基因的确切作用的了解甚少。这项研究的目的是研究二酰基甘油酰基转移酶（DGAT）1和2的差异作用，它们被认为是催化甘油三酸酯生物合成最后一步的速率限制酶，在调节鹅卵泡颗粒细胞的脂质代谢和类固醇生成中在不同的发展阶段。观察到编码DGAT1和DGAT2的mRNA在所有检查的颗粒细胞层中普遍存在，但在卵泡发育过程中表现出不同的表达特征。值得注意的是，除了8-10 mm队列中的1-2个卵泡之外，DGAT1，DGAT2，FSHR，LHR，STAR，CYP11A1和3βHSD的mRNA水平几乎保持恒定，随后F5卵泡急剧增加/减少。在细胞水平上，siRNA介导的DGAT1或DGAT2的下调不会改变未分化和分化的颗粒细胞中积累的脂质量，而DGAT2的过表达促进脂质积累和这些细胞中与脂肪相关的基因的表达。与此同时，我们发现，干扰DGAT2无效，但干扰DGAT1或过表达DGAT2会刺激未分化颗粒细胞中的孕激素分泌。相比之下，DGAT1 / 2的干扰或过表达未能改变分化的颗粒细胞中的孕酮水平，但调节了类固醇生成相关基因的表达。因此，可以得出结论，在未分化和分化的颗粒细胞中，DGAT1都比DGAT2促进脂质积累的效率低，而DGAT1负调控而DGAT2却在未分化的颗粒细胞中正调节着孕激素的产生。