Zhou Yanbing, Ling Defeng, Wang Liyi, Xu Ziye, You Wenjing, Chen Wentao, Nong Qiuyun, Valencak Teresa G, Shan Tizhong
College of Animal Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Key Laboratory of Molecular Animal Nutrition (Zhejiang University), Ministry of Education, Hangzhou, Zhejiang 310058, China.
Research (Wash D C). 2024 Sep 26;7:0492. doi: 10.34133/research.0492. eCollection 2024.
Activation of mitochondrial function and heat production in adipose tissue by the modification of dietary fat is a promising strategy against obesity. However, as an important source of lipids for ketogenic and daily diets, the function of fats extracted from different adipose tissue sites was largely unknown. In this study, we illustrated the function of fats extracted from adipose tissues with different "beigeing" properties in the ketogenic diet and identified lipid profiles of fats that facilitate energy expenditure. We found that the anti-obesity effect of ketogenic diets was potentiated by using "beigeing" fat [porcine subcutaneous adipose tissue (SAT)] as a major energy-providing ingredient. Through lipidomic analyses, phosphatidylserine (PS) was identified as a functional lipid activating thermogenesis in adipose tissue. Moreover, in vivo studies showed that PS induces adipose tissue thermogenesis and alleviates diet-induced obesity in mice. In vitro studies showed that PS promotes UCP1 expression and lipolysis of adipocytes. Mechanistically, PS promoted mitochondrial function in adipocytes via the ADCY3-cAMP-PKA-PGC1α pathway. In addition, PS-PGC1a binding may affect the stability of the PGC1α protein, which further augments PS-induced thermogenesis. These results demonstrated the efficacy of dietary SAT fats in diminishing lipid accumulation and the underlying molecular mechanism of PS in enhancing UCP1 expression and mitochondrial function. Thus, our findings suggest that as dietary fat, "beigeing" fat provides more beneficial lipids that contribute to the improvement of mitochondrial function, including PS, which may become a novel, nonpharmacological therapy to increase energy expenditure and counteract obesity and its related diseases.
通过改变膳食脂肪来激活脂肪组织中的线粒体功能和产热是一种很有前景的抗肥胖策略。然而,作为生酮饮食和日常饮食中脂质的重要来源,从不同脂肪组织部位提取的脂肪的功能在很大程度上尚不清楚。在本研究中,我们阐述了在生酮饮食中从具有不同“米色化”特性的脂肪组织中提取的脂肪的功能,并确定了促进能量消耗的脂肪的脂质谱。我们发现,使用“米色化”脂肪[猪皮下脂肪组织(SAT)]作为主要能量供应成分可增强生酮饮食的抗肥胖作用。通过脂质组学分析,磷脂酰丝氨酸(PS)被确定为一种在脂肪组织中激活产热的功能性脂质。此外,体内研究表明,PS可诱导小鼠脂肪组织产热并减轻饮食诱导的肥胖。体外研究表明,PS可促进脂肪细胞中UCP1的表达和脂解。机制上,PS通过ADCY3-cAMP-PKA-PGC1α途径促进脂肪细胞中的线粒体功能。此外,PS与PGC1a的结合可能会影响PGC1α蛋白的稳定性,从而进一步增强PS诱导的产热。这些结果证明了膳食SAT脂肪在减少脂质积累方面的功效以及PS增强UCP1表达和线粒体功能的潜在分子机制。因此,我们的研究结果表明,作为膳食脂肪,“米色化”脂肪提供了更多有益的脂质,有助于改善线粒体功能,包括PS,这可能成为一种新的非药物疗法,以增加能量消耗并对抗肥胖及其相关疾病。