Hsu F.-L.Huang C.-F.Chen Y.-W.Yen Y.-P.Wu C.-T.Uang B.-J.RONG-SEN YANGLiu S.-H.2021-05-312021-05-3120130012-1797https://www.scopus.com/inward/record.uri?eid=2-s2.0-84873024799&doi=10.2337%2fdb12-0585&partnerID=40&md5=de8d157fcb98afac9081c72c6fc96859https://scholars.lib.ntu.edu.tw/handle/123456789/563698The therapeutic effect of pterosin A, a small-molecular-weight natural product, on diabetes was investigated. Pterosin A, administered orally for 4 weeks, effectively improved hyperglycemia and glucose intolerance in streptozotocin, high-fat dietfed, and db/db diabetic mice. There were no adverse effects in normal or diabetic mice treated with pterosin A for 4 weeks. Pterosin A significantly reversed the increased serum insulin and insulin resistance (IR) in dexamethasone-IR mice and in db/db mice. Pterosin A significantly reversed the reduced muscle GLUT-4 translocation and the increased liver phosphoenolpyruvate carboxyl kinase (PEPCK) expression in diabetic mice. Pterosin A also significantly reversed the decreased phosphorylations of AMP-activated protein kinase (AMPK) and Akt in muscles of diabetic mice. The decreased AMPK phosphorylation and increased p38 phosphorylation in livers of db/db mice were effectively reversed by pterosin A. Pterosin A enhanced glucose uptake and AMPK phosphorylation in cultured human muscle cells. In cultured liver cells, pterosin A inhibited inducerenhanced PEPCK expression, triggered the phosphorylations of AMPK, acetyl CoA carboxylase, and glycogen synthase kinase-3, decreased glycogen synthase phosphorylation, and increased the intracellular glycogen level. These findings indicate that pterosin A may be a potential therapeutic option for diabetes. ? 2013 by the American Diabetes Association.[SDGs]SDG3acetyl coenzyme A carboxylase; dexamethasone; glycogen synthase; glycogen synthase kinase 3; hydroxymethylglutaryl coenzyme A reductase kinase; insulin; metformin; natural product; phosphoenolpyruvate carboxykinase (ATP); protein kinase; pterosin a; streptozocin; unclassified drug; animal tissue; antidiabetic activity; article; cell culture; controlled study; diabetes mellitus; enzyme phosphorylation; glucogenesis; glucose tolerance; glucose transport; human; human cell; hyperglycemia; insulin resistance; lipid diet; liver cell; male; mouse; nonhuman; priority journal; protein phosphorylation; treatment duration; Animals; Biological Agents; Biological Transport; Cells, Cultured; Dexamethasone; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Disease Models, Animal; Glucose; Glucose Intolerance; Glucose Transporter Type 4; Humans; Hyperglycemia; Indans; Insulin; Insulin Resistance; Liver; Male; Mice; Muscle, Skeletal; Sesquiterpenesjournal article10.2337/db12-0585230696262-s2.0-84873024799