Core Viewpoint - The article discusses a groundbreaking study published in "Nature Metabolism" that reveals a significant mechanism behind obesity, focusing on the role of a specific protein released by gut microbiota, which may explain the challenges faced by individuals trying to lose weight [7][10]. Group 1: Research Findings - A special protein called flagellin, released by gut microbiota, is identified as a key signaling molecule that regulates appetite [7]. - The study introduces the concept of "neurobiotic sense," establishing a high-speed communication channel between the gut and the brain [9]. - Analysis of 56 human adipose tissue samples shows that mitochondrial fragmentation creates a metabolic vicious cycle, making it harder for long-term obese individuals to lose weight [10]. Group 2: Practical Solutions - Following food intake, the activity of gut microbiota increases, leading to a significant rise in flagellin release, which is detected by specialized PYY neuroendocrine cells in the colon [11]. - The TLR5 receptor on these cells acts as a "microbial radar," triggering the secretion of PYY hormone, which sends a "stop eating" signal to the brain via the NPY2R receptor on the vagus nerve [11]. - Recommendations include optimizing fat intake by avoiding long-term high-fat diets, replacing saturated fats with monounsaturated fats, and controlling daily fat intake to 25-30% of total calories [12]. Group 3: Exercise Recommendations - High-Intensity Interval Training (HIIT) is suggested, with a regimen of three sessions per week, each lasting only 20 minutes [12]. - A specific exercise pattern of 30 seconds of all-out sprinting followed by 90 seconds of gentle recovery is recommended [19]. Group 4: Nutritional Strategies - Implementing targeted nutrient supplementation and managing meal timing by compressing the daily eating window to 8-10 hours, with at least 14 hours of fasting after dinner [19].

Core Insights - The article discusses a groundbreaking study published in *Nature Metabolism* that reveals a significant mechanism behind obesity, specifically the malfunction of "micro power plants" in fat cells, which may explain the challenges faced in weight loss efforts [7][10]. Group 1: Research Findings - A specific protein released by gut microbiota, known as flagellin, is identified as a key signaling molecule that regulates appetite [7]. - The study introduces the concept of "neurobiotic sense," establishing a high-speed communication channel between the gut and the brain [9]. - Analysis of 56 human fat tissue samples shows that mitochondrial fragmentation creates a metabolic vicious cycle, making it harder for long-term obese individuals to lose weight [10]. Group 2: Practical Solutions - Following food intake, the activity of gut microbiota increases, leading to a significant rise in flagellin release, which is detected by specialized PYY neuroendocrine cells in the colon [11]. - The TLR5 receptor on these cells acts as a "microbial radar," triggering the secretion of PYY hormone, which sends a "stop eating" signal to the brain via the NPY2R receptor on the vagus nerve [11]. - Recommendations include optimizing fat intake by avoiding long-term high-fat diets, replacing saturated fats with monounsaturated fats, and controlling daily fat intake to 25-30% of total calories [12]. Group 3: Exercise Recommendations - High-Intensity Interval Training (HIIT) is suggested, with a regimen of three sessions per week, each lasting only 20 minutes [12]. - A specific exercise pattern of 30 seconds of all-out sprinting followed by 90 seconds of gentle recovery is recommended [19]. Group 4: Nutritional Strategies - A targeted nutrient supplementation plan and scientific meal timing management are advised, including compressing the daily eating window to 8-10 hours and maintaining at least a 14-hour fasting period after dinner [19].

Core Viewpoint - The research highlights the mitochondrial origins of sleep pressure, suggesting that sleep is not merely a resting state for the brain but a crucial maintenance process for the body's energy supply system [4][11]. Group 1: Research Findings - A study published in Nature reveals that sleep pressure arises from ATP surplus in specific brain cells, indicating a physical basis for sleep drive [4]. - The research team conducted a comparative analysis of the single-cell transcriptome characteristics of fruit flies under sufficient sleep and sleep deprivation, finding significant gene expression changes related to mitochondrial respiration and ATP synthesis in sleep-deprived flies [6][11]. - Mitochondrial fragmentation and increased mitochondrial-autophagy were observed in affected neurons, which could be reversed by restoring sleep [6][9]. Group 2: Mechanisms of Sleep Regulation - The study found that mitochondrial dynamics (fusion and fission) significantly influence the excitability of sleep-regulating neurons, thereby affecting sleep demand [9][11]. - During wakefulness, especially under sleep deprivation, the activity of these neurons is suppressed, leading to increased ATP concentration due to reduced consumption [9]. - Manipulating mitochondrial dynamics can either enhance or reduce sleep duration, indicating a direct link between mitochondrial function and sleep regulation [9][11]. Group 3: Implications and Future Directions - The findings provide insights into the relationship between metabolism, sleep, and lifespan, suggesting that sleep may be an unavoidable byproduct of aerobic metabolism, similar to aging [10][11]. - The research opens new avenues for understanding sleep disorders and their potential interventions by targeting mitochondrial function in specific neurons [11].

Core Insights - The article discusses a groundbreaking study published in *Nature Metabolism* that reveals a significant mechanism behind obesity, specifically the malfunction of "micro power plants" in fat cells, which may explain the challenges faced in weight loss efforts [7][10]. Group 1: Research Findings - A specific protein called flagellin, released by gut microbiota, is identified as a key signaling molecule that regulates appetite [7]. - The study introduces the concept of "neurobiotic sense," establishing a high-speed communication channel between the gut and the brain [9]. - Analysis of 56 human fat tissue samples shows that mitochondrial fragmentation creates a metabolic vicious cycle, making it harder for long-term obese individuals to lose weight [10]. Group 2: Practical Solutions - Following food intake, the activity of gut microbiota increases, leading to a significant rise in flagellin release, which is detected by specialized PYY neuroendocrine cells in the colon [11]. - The expression level of the DNM1L gene correlates positively with BMI, indicating its role in obesity and insulin resistance [12]. - Recommendations include optimizing fat intake by avoiding long-term high-fat diets, replacing saturated fats with monounsaturated fats, and controlling daily fat intake to 25-30% of total calories [12]. Group 3: Exercise and Nutrition Strategies - High-Intensity Interval Training (HIIT) is suggested, with a regimen of three sessions per week, each lasting only 20 minutes [12]. - A targeted nutrient supplementation plan and time-restricted eating, compressing the daily eating window to 8-10 hours, are proposed to enhance weight management [19].