Adipogenesis is inhibited by brief, daily exposure to high-frequency, extremely low-magnitude mechanical signals
Adipogenesis is inhibited by brief, daily exposure to high-frequency, extremely low-magnitude mechanical signals
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DOI：
10.1073/pnas.0708467104
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发表时间：
2007-11-06
影响因子：
11.1
通讯作者：
Judex, S.
中科院分区：
文献类型：
--
作者：
Rubin, C. T.;Capilla, E.;Judex, S.
肥胖是一种全球性的流行病，它使数百万人身体虚弱，并给社会带来数百亿美元的医疗保健费用负担。虽然人们认为，越是剧烈的身体挑战，它将是更有效的抑制肥胖，这里显示，15周的短暂，每天暴露于高频机械信号，诱导的幅度远低于这将出现在步行过程中，抑制脂肪形成的27%，在C57 BL/6 J小鼠。机械信号还降低了11型糖尿病发病的关键风险因素，肝脏中的非酯化游离脂肪酸和脂肪含量分别降低了43%和39%。在9周内，这些相同的信号抑制了C3H.B6- 6 T同类小鼠品系中22%的脂肪产生，该品系表现出与年龄相关的身体组成加速变化。为了理解脂肪产生被抑制的方式，接受来自杂合GFP（+）小鼠的骨髓移植的辐射小鼠显示，6周的这些低强度机械信号使间充质干细胞分化为脂肪细胞的承诺减少了19%，表明这些模型中脂肪组织的形成受到干细胞脂肪生成显著减少的阻碍。翻译到人类，这可能是通过发育而不是代谢途径实现的肥胖及其后遗症的非药物预防的基础。
Obesity, a global pandemic that debilitates millions of people and burdens society with tens of billions of dollars in health care costs, is deterred by exercise. Although it is presumed that the more strenuous a physical challenge the more effective it will be in the suppression of adiposity, here it is shown that 15 weeks of brief, daily exposure to high-frequency mechanical signals, induced at a magnitude well below that which would arise during walking, inhibited adipogenesis by 27% in C57BL/6J mice. The mechanical signal also reduced key risk factors in the onset of type 11 diabetes, nonesterified free fatty acid and triglycericle content in the liver, by 43% and 39%, respectively. Over 9 weeks, these same signals suppressed fat production by 22% in the C3H.B6-6T congenic mouse strain that exhibits accelerated age-related changes in body composition. In an effort to understand the means by which fat production was inhibited, irradiated mice receiving bone marrow transplants from heterozygous GFP(+) mice revealed that 6 weeks of these low-magnitude mechanical signals reduced the commitment of mesenchymal stem cell differentiation into adipocytes by 19%, indicating that formation of adipose tissue in these models was deterred by a marked reduction in stem cell adipogenesis. Translated to the human, this may represent the basis for the nonpharmacologic prevention of obesity and its sequelae, achieved through developmental, rather than metabolic, pathways.