Derivatives | Model | Experimental outcome | Reference |
---|---|---|---|
Cinnamic acid | TNF-α-treated insulin-resistant mouse FL83B hepatocytes. | - Increased expression of glycogen synthase, whereas the expression of glycogen synthase kinase and phosphorylation of glycogen synthase at Ser641 in insulin-resistant mouse hepatocytes was decreased. | [111] |
 | STZ-induced diabetic Wistar Albino rats | - Improved glucose tolerance and carbohydrate metabolizing enzymes, | [13] |
Ferulic acid | STZ-induced diabetic mice (0.01 and 0.1Â % FA of diet) | - Decreased elevated blood glucose level | [14] |
 | KK-Ay mice (0.05 % FA of Diet) | - Suppress blood glucose level | [14] |
 | C57BL/KsJ db/db mice | - Decreased blood glucose level by increasing glycogen synthesis. Increased glucokinase activity. | [112] |
 | Streptozotocin induced diabetes rats | - Prevents lipid peroxidation and improved the antioxidant enzymes such as glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) | [114] |
 | Otsuka Long-Evans Tokushima Fatty (OLETF) diabetic rats (0.2 % FA in diet) | - Improved |  |
 | Male C57BL/6 N mice (0.5 % FA of diet) | - Lower blood glucose level and glucose-6-phosphatase (G6pase) and phosphoenolpyruvate carboxykinase (PEPCK) activities. | [113] |
 | Stroke-prone spontaneously hypertensive rats (SHRsp) (0 · 01 g/kg FA of diet) | - Improved hypertension as well as glucose tolerance, plasma nitric oxide (NOx). Also increased several mRNA expressions of metabolic parameters involved in glucose and lipid metabolisms | [129] |
 | - high-fat and fructose-induced type 2 diabetic adult male rats | - FA treatment to diabetic animals restored blood glucose, serum insulin, glucose tolerance, and insulin tolerance to normal range. - Hepatic glycogen concentration, activity of glycogen synthase, and glucokinase were significantly increased, whereas activity of glycogen phosphorylase and enzymes of gluconeogenesis (phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase)) were decreased in diabetic animals due to FA treatment | [130] |
- FA (50 mg/(kg body weight · day)(−1), orally) for 30 days | |||
 | - high-fat and fructose-induced type 2 diabetic adult male rats | - Authors suggested that FA treatment reduced the GLUT2 expression in diabetic animals by impairing the interaction between these transcription factors (SREBP1c, HNF1α and HNF3β) and GLUT2 gene promoter. | [131] |
- FA (50 mg/(kg body weight · day)(−1), orally) for 30 days | |||
Caffeic acid | C57BL/KsJ-db/db mice | - Reduction of the blood glucose and glycosylated hemoglobin levels. Caffeic acid also markedly increased glucokinase activity and its mRNA expression and glycogen content and simultaneously lowered glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities and their respective mRNA expressions, accompanied by a reduction in the glucose transporter 2 expression in the liver | [115] |
 | Streptozotocin induced diabetes rats | - Improved lipid peroxidation and antioxidant enzyme status in liver of rats | [132] |
 | Mouse liver FL83B cells | - Tumor necrosis factor-α was used to induce insulin resistance. may promote insulin receptor tyrosyl phosphorylation, up-regulate the expression of insulin signal associated proteins, including insulin receptor, phosphatidylinositol-3 kinase, glycogen synthase, and glucose transporter-2, increase the uptake of glucose, and alleviate insulin resistance | [118] |
 | TNF-α-treated insulin-resistant mouse FL83B hepatocytes. | - Increased expression of glycogen synthase, whereas the expression of glycogen synthase kinase and phosphorylation of glycogen synthase at Ser641 in insulin-resistant mouse hepatocytes was decreased. - Also suppressed the expression of hepatic nuclear factor-4 and activity of phosphoenolpyruvate carboxykinase | [111] |
 | High fat diet in male BLTW: CD1(ICR) mice | - Improved the glucose intolearance and normalized plasma insulin, adiponectin. - also suppress TNF-alpha, PEPCK and increased GLUT4 | [119] |
 | L6-GLUT4myc cells | - Increased glucose uptake and GLUT4 translocation to the cell membrane of L6-GLUT4myc cells. - Increased phosphorylation of AMPK and increased GLUT4 content | [120] |
 | Streptozotocin (STZ)-induced diabetic rats | - Phoshoenolpyruvate carboxykinase mRNA expression was decreased. - Decreased the fasting blood levels of glucose, alanine aminotransferase, cholesterol, and triglyceride induced by diabetes. - increased expressions of glucokinase and pyruvate kinase mRNAs and increased the liver glycogen level. | [116] |
 | Swiss mice fed high fat diet | - Improved glucose intolerance in high fat diet fed mice. - Improvement in insulin-stimulated phosphorylation of the insulin receptor substrate-2, followed by an increase in Akt phosphorylation. - Reduced the induction of the inflammatory pathway, c-jun-N- terminal kinase, the nuclear factor kappa B, and cyclooxygenase-2 expression. | [117] |
 | Male Sprague–Dawley rats | - Increased the phosphorylation of AMPKα Thr172 in skeletal muscle. - AMPKα2 activity increased significantly, whereas AMPKα1 activity did not change. | [133] |
 | Male Balb/cA mice (2.5 % CFA of Diet) | - Increased plasma insulin and decreased blood glucose and plasma HbA1c levels. - Lowered renal levels of IL-6, IL-1b, tumor necrosis factor (TNF)-a and monocyte chemoattractant protein 1 (MCP-1) and decreased TNF alpha and MCP-1 mRNA expression. | [11] |
Chlorogenic acid | db/db mice | - Improved the fasting blood glucose level. - Stimulates glucose transport in skeletal muscle via the GLUT 4 translocation and phosphorylation of AMPK and Akt. | [121] |
 | Male Sprague–Dawley rats (CGA (120 mg · kg–1) | - Improved glucose metabolism as seen in decreased AUC. | [134] |