本研究以發炎因子tumor necrosis factor-alpha (TNF-α) 處理小鼠肝臟細胞株(FL83B)，使其產生胰島素抗性，並評估紅麴二次代謝物減緩胰島素抗性及改善糖尿病之能力。Monacolin K為紅麴主要活性成分，本研究探討monacolin K與TNF-α共同處理細胞24小時後，對肝細胞吞噬葡萄糖能力之影響。結果發現，monacolin K處理可提升FL83B肝細胞對螢光葡萄糖 (2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-d-glucose; 2-NBDG) 之攝入量。本研究也發現monacolin K減緩胰島素抗性是透過增加insulin receptor substrate-2 (IRS-2) 磷酸化所達成，進而增加Akt [或稱PKB/Akt，是一種serine/threonine kinase] 磷酸化，使得glucose transporter 2 (GLUT 2) 表現量增加，此外monacolin K也可增加胞內NADPH/NADP+ 之比率，顯示monacolin K應具有抗氧化效應，而保持NADPH不被氧化。綜合試驗結果得知，紅麴之二次代謝物monacolin K除具血脂調節功能外，更可改善肝細胞之胰島素抗性，具開發成治療糖尿病藥物之潛力。

In the present study we used tumor necrosis factor-alpha (TNF-α) to induce insulin resistance in mouse liver cell lines (FL83B). We examined the improvement effects of Monascus-fermented product, monacolin
K, on insulin resistance and diabetes. Monacolin K is the main active component in Monascus-fermented products. In this study, we co-treated the mouse hepatocytes with monacolin K and TNF-α for 24 hours. First,
we observed that monacolin K could increase the fluorescent glucose (2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-d-glucose; 2-NBDG) uptake in FL83B cell. We also observed that monacolin K improved
insulin resistance through increasing phosphorylation of insulin receptor substrate-2 (IRS-2), which results in increasing phosphorylation of Akt. At last, it raised the expression of glucose transporter 2 (GLUT 2). In
addition, monacolin K could increase the ratio of NADPH and NADP+. This indicated that monacolin K has an antioxidative effect, which could keep NADPH in a reduced form. Based on these data, we suggested that
Monascus-fermented product, monacolin K, not only possesses the function of modulating blood lipids, but also improves insulin resistance in liver cells. It truly had the potential to develop into a diabetes drug.