研究油菜籽二酰基甘油(RDG)对C57BL/6J小鼠脂质积累和代谢的影响。肥胖小鼠接受高脂肪饮食,其中45%的总能量来自RDG(RDGM组)或菜籽三酰甘油油(RTGM组).该饮食干预在肥胖小鼠模型建立后进行12周。实验结束时,RTGM和RDGM组小鼠的血清葡萄糖水平分别为13.0±1.3mmol/L和9.7±1.5mmol/L,分别。同时,RDGM组的血清甘油三酯水平比RTGM组低26.3%。RDGM组的减肥效果伴随着白色脂肪组织(WAT)指数的显着降低。RDG干预在体内没有显著改变菜籽油的抗氧化和抗炎特性。RDG饮食改善了高脂饮食引起的肝脏脂质代谢异常,导致降低肝损伤指数值(AST和ALT)。此外,与RTGM组相比,成脂基因PPAR-γ和DGAT在肝脏和肠道中的表达分别下降了21.7%和16.7%和38.7%和47.2%,分别,在RDGM组。Further,RDG干预后,BAT中大多数脂解基因均无明显变化。这意味着RDG通过改变肝脏中脂肪生成基因的表达来调节脂质代谢,肠,和脂肪组织,从而减少WAT的积累。此外,RDG饮食增强肠道菌群多样性,增加小鼠肠道中未分类的Muribaculaceae的相对水平,并降低Dubosiella和Faecalibaculum的水平,可能加速脂质代谢。因此,对肥胖小鼠进行为期三个月的RDG饮食干预在调节体型方面表现出益处,血清肥胖相关指标,肠道菌群结构,脂肪组织中的脂质代谢,肝脏,和肠。
To investigate the effects of rapeseed diacylglycerol oil (RDG) intake on lipid accumulation and metabolism in C57BL/6J mice, obese mice were fed a high-fat diet in which 45% of the total energy content came from RDG (RDGM group) or rapeseed triacylglycerol oil (RTGM group). This diet intervention was conducted for 12 weeks following the establishment of the obese mouse model. By the end of the experiment, the serum glucose levels of the mice in the RTGM and RDGM groups were 13.0 ± 1.3 mmol/L and 9.7 ± 1.5 mmol/L, respectively. Meanwhile, the serum triglyceride level in the RDGM group was 26.3% lower than that in the RTGM group. The weight-loss effect in the RDGM group was accompanied by a significant decrease in the white adipose tissue (WAT) index. The RDG intervention did not significantly change the antioxidant and anti-inflammatory properties of the rapeseed oil in vivo. The RDG diet improved the liver lipid metabolism abnormalities induced by a high-fat diet, leading to decreased liver damage index values (AST and ALT). Additionally, compared to that in the RTGM group, the expression of the adipogenic genes PPAR-γ and DGAT decreased in both the liver and intestine by 21.7% and 16.7% and by 38.7% and 47.2%, respectively, in the RDGM group. Further, most lipolytic genes in BAT showed no significant change after the RDG intervention. This implies that RDG regulates lipid metabolism by altering the expression of adipogenic genes in the liver, intestine, and adipose tissue, thereby reducing the accumulation of WAT. Furthermore, the RDG diet enhanced gut flora diversity, increasing the relative levels of unclassified Muribaculaceae and decreasing the levels of Dubosiella and Faecalibaculum in the mouse gut, potentially accelerating lipid metabolism. Thus, a three-month RDG diet intervention in obese mice exhibited benefits in regulating the somatotype, serum obesity-related indices, gut flora structure, and lipid metabolism in the adipose tissue, liver, and intestine.