在糖尿病的症狀中，常會伴隨肌少症的發生，且根據一些研究統計顯示，若年長者又同時患有糖尿病時，其罹患肌少症之機率將較於同年齡者高。而造成此現象之原因可能為糖尿病有關的胰島素阻抗。也就是說，對於胰島素阻抗的患者來說，可能加重了患者的代謝紊亂並也影響了在治療上的反應。在本實驗室先前於小鼠動物模型研究之微陣列 (Microarray) 實驗中顯示，相較於控制組，糖尿病小鼠模型之Grn表現有下調的情況，且在本研究顯示，相較於控制組，在肌少症之動物模型中，其GRN之表現量有下調的現象，並在臨床上的肌少症病患中，也發現了相同的現象。因此我們首先以觀察葡萄糖代謝以及蛋白質代謝路徑來確認GRN對於肌肉細胞之影響。而結果表明，GRN不僅能促進骨骼肌細胞的葡萄糖攝取，亦能增強細胞中的蛋白質合成，此外，GRN更有抑制細胞自噬的功能。故根據此結果推斷，GRN能透過促進細胞中之葡萄糖攝取，而有調控血糖之潛力，且因GRN能促進骨骼肌細胞中蛋白質合成，故有以增加肌肉細胞之質量之潛力，更因GRN有抑制骨骼肌細胞自噬之功能，由此結果我們認為，GRN在治療糖尿病肌少症上具有很大的潛力，值得未來的進一步開發。

Sarcopenia is a risk factor for other subsequent physical symptoms, such as disability, deterioration of mobility and even death. In fact, sarcopenia caused by type 2 diabetes imposes a considerable burden on the Taiwan’s medical care system. At the beginning of this study, we found that GRN may be able to regulate cell glucose uptake. Moreover, GRN is related to the metabolism of skeletal muscle. For example, GRN stimulates phosphorylation of the protein kinase Akt in cells. If the phosphorylation of Akt was reduced, it would inhibit the downward transmission of metabolism signal. Therefore, we wanted to learn more about the effects of GRN’s function on metabolic pathways of skeletal muscle cells. Then, based on the results in this study, we found that the GRN enhanced the protein synthesis in skeletal muscle cells. Furthermore, according to other results in this study, we inferred that GRN could also increase the concentration of calcium in cells through the signaling receptor EphA2, which in turn enhances the phosphorylation of Akt, and thereby inducing the translocation of GLUT4 to increase glucose uptake in cells.

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