难怪减肥总难见效！《自然》子刊揭示：肥胖会损害线粒体，脂肪堆积速度加快

Core Insights - The article discusses the rising prevalence of obesity and diabetes in modern society, highlighting that the number of obese individuals globally has quadrupled since 1975 [6] - It emphasizes the metabolic dysfunction of adipose tissue as a key reason for the difficulty in reversing obesity, particularly focusing on mitochondrial impairment [7][8] Group 1: Obesity and Metabolic Dysfunction - Obesity is not merely an accumulation of fat but involves complex metabolic changes, including inflammation and hormonal resistance, which contribute to insulin resistance and increased diabetes risk [8] - Recent research indicates that mitochondrial dysfunction in fat cells is a significant factor in obesity, where excessive energy intake leads to mitochondrial impairment and reduced energy expenditure [7][8] Group 2: Role of RalA Gene - The study identifies the RalA gene as a critical player in the fragmentation of mitochondria in obese individuals, which exacerbates fat accumulation [10][12] - In normal conditions, RalA is activated by insulin to promote glucose absorption and assist in the degradation of damaged mitochondria, maintaining metabolic health [10] - In obesity, RalA becomes overactive, leading to excessive mitochondrial fragmentation and loss of function, further promoting weight gain [10][12] Group 3: Potential Therapeutic Target - The research suggests that targeting the RalA gene could be a promising approach for obesity intervention, as knocking out this gene in mice resulted in lower fat content and improved glucose tolerance [12] - Enhancing mitochondrial energy metabolism through RalA modulation may lead to new obesity therapies aimed at increasing energy expenditure and reducing fat accumulation [12]