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中年减肥为何格外艰难?《Science》揭示:年龄增长使脂肪细胞激增5倍,代谢失衡、慢性疾病接连袭来!
GLP1减重宝典· 2026-01-11 03:02
以下文章来源于肥胖世界ObesityWorld ,作者肥胖世界 肥胖世界ObesityWorld . 《肥胖世界》Obesity World - 同步传真肥胖及代谢国际新学术进展,为医学减重临床、教研人员搭建一座与国际接轨的桥梁,「每医健」旗下内容平台。 你是否有这样的困惑:步入30或40岁后,腹部赘肉变得异常难缠?明明饮食比年轻时更加节制,运动也更为积极,腰围却依然不断扩张…… 别急着自责缺乏毅力!《Science》杂志最新研究揭示了中年发福、腹部脂肪难以消除的真相:我们内脏脂肪中存在一种特殊细胞,它们会随 着衰老过程变得异常活跃,大量促进脂肪生成。所以,中年腹部减肥困难,或许真不完全是你的错! 中年发福的真相:不只是脂肪细胞变大那么简单 先抛出一个灵魂拷问:你的身材是如何逐渐"圆润"起来的?虽然炸鸡啤酒确实"功不可没",但从生物学角度看,体重增加主要通过两种机制实 现: 脂肪细胞数量增加 单个脂肪细胞体积膨胀 传统观点认为,成年后脂肪细胞数量基本固定,体重上升主要是因为现有脂肪细胞"长胖"了。然而,这次小鼠实验却揭示了脂肪堆积的新秘 密:主要原因竟是新脂肪细胞大量生成! 为深入探究,科学家对小鼠的成熟脂肪 ...
震惊!中年减肥为何如此艰难?《Science》揭秘:年龄增长导致脂肪细胞暴增5倍,代谢崩溃、慢性疾病接踵而至!
GLP1减重宝典· 2025-08-29 03:02
Core Viewpoint - The article discusses the biological mechanisms behind weight gain in middle age, particularly focusing on the role of a specific type of fat precursor cell (CP-A) that becomes more active with aging, leading to increased visceral fat accumulation [7][12][24]. Summary by Sections Mechanisms of Weight Gain - Traditional views suggest that fat cell numbers remain constant after adulthood, with weight gain primarily due to the enlargement of existing fat cells. However, recent studies indicate that new fat cells are generated in significant numbers, especially in middle-aged individuals [9][10]. Discovery of CP-A Cells - Researchers identified a specific type of fat precursor cell, CP-A, which becomes predominant in visceral fat as individuals age. In middle-aged mice, CP-A cells constituted 34.23% of the visceral white fat tissue, indicating a shift in the cellular composition of fat tissue [12][15]. Implications of Increased Visceral Fat - The accumulation of visceral fat, coupled with a decrease in muscle mass, can lead to sarcopenic obesity, where individuals may appear to have a normal BMI but suffer from metabolic disorders due to fat distribution [13][24]. CP-A Cell Characteristics - CP-A cells exhibit enhanced proliferation and differentiation capabilities compared to younger fat precursor cells. They are 2.5 times more proliferative and produce significantly more mature fat cells [17][19]. Targeting LIFR for Intervention - The LIFR (leukemia inhibitory factor receptor) pathway was identified as a potential target for controlling the proliferation of CP-A cells. Inhibition of LIFR significantly reduced fat generation in CP-A cells while having minimal effect on younger cells [20][22][23]. Conclusion on Middle-Aged Fat Gain - The increase in visceral fat in middle age is attributed to the emergence of new fat cells, particularly CP-A cells, which are regulated by the LIFR-JAK-STAT3 signaling pathway. Targeting this pathway may offer new strategies for managing stubborn fat in middle-aged individuals [24][25].
中年减肥为何如此艰难?《Science》揭秘:年龄增长导致脂肪细胞暴增5倍,代谢崩溃、慢性疾病接踵而至!
GLP1减重宝典· 2025-08-19 10:01
Core Viewpoint - The article discusses the biological mechanisms behind weight gain in middle age, particularly focusing on the role of a specific type of fat precursor cell (CP-A) that becomes more active with aging, leading to increased visceral fat accumulation [7][24]. Group 1: Mechanisms of Weight Gain - Traditional views suggest that fat cell numbers remain constant after adulthood, with weight gain primarily due to existing fat cells enlarging. However, recent studies indicate that new fat cells are generated in significant numbers during middle age [9][10]. - A specific type of fat precursor cell, known as CP-A, becomes predominant in visceral fat tissue as individuals age, contributing to increased fat generation [12][15]. Group 2: Characteristics of CP-A Cells - CP-A cells exhibit enhanced proliferation and differentiation capabilities compared to younger fat precursor cells, leading to a higher rate of fat cell production [17][19]. - In middle-aged mice, CP-A cells account for approximately 34.23% of the visceral white fat tissue, indicating a significant shift in fat cell composition with aging [15]. Group 3: Potential Interventions - The LIFR signaling pathway has been identified as a potential target for controlling the proliferation and fat-generating activity of CP-A cells. Inhibition of LIFR significantly reduces fat generation in CP-A cells while having minimal effect on younger fat precursor cells [20][22]. - Targeting LIFR could provide a new strategy to combat stubborn fat accumulation in middle-aged individuals, offering a scientific solution to a common issue [25].