Camporez João-Paulo G, Petersen Max C, Abudukadier Abulizi, Moreira Gabriela V, Jurczak Michael J, Friedman Glenn, Haqq Christopher M, Petersen Kitt Falk, Shulman Gerald I
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520;
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520; Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520;
Proc Natl Acad Sci U S A. 2016 Feb 23;113(8):2212-7. doi: 10.1073/pnas.1525795113. Epub 2016 Feb 8.
Sarcopenia, or skeletal muscle atrophy, is a debilitating comorbidity of many physiological and pathophysiological processes, including normal aging. There are no approved therapies for sarcopenia, but the antihypertrophic myokine myostatin is a potential therapeutic target. Here, we show that treatment of young and old mice with an anti-myostatin antibody (ATA 842) for 4 wk increased muscle mass and muscle strength in both groups. Furthermore, ATA 842 treatment also increased insulin-stimulated whole body glucose metabolism in old mice, which could be attributed to increased insulin-stimulated skeletal muscle glucose uptake as measured by a hyperinsulinemic-euglycemic clamp. Taken together, these studies provide support for pharmacological inhibition of myostatin as a potential therapeutic approach for age-related sarcopenia and metabolic disease.
肌肉减少症，即骨骼肌萎缩，是包括正常衰老在内的许多生理和病理生理过程中一种使人衰弱的合并症。目前尚无获批用于治疗肌肉减少症的疗法，但具有抗肥大作用的肌动蛋白抑制素是一个潜在的治疗靶点。在此，我们表明，用抗肌动蛋白抑制素抗体（ATA 842）对年轻和老年小鼠进行4周治疗后，两组小鼠的肌肉质量和肌肉力量均有所增加。此外，ATA 842治疗还增强了老年小鼠胰岛素刺激的全身葡萄糖代谢，这可归因于通过高胰岛素-正常血糖钳夹法测得的胰岛素刺激的骨骼肌葡萄糖摄取增加。综上所述，这些研究为肌动蛋白抑制素的药理抑制作为治疗与年龄相关的肌肉减少症和代谢疾病的潜在治疗方法提供了支持。
