| | Type of study model | Experimental method [subject (age/weight), treatment dosage, duration of treatment] | Major activity | Mechanism of action | Reference |
| | In vitro study | Differentiated C2C12 cells, DSW 100, 500, 1000, 1500, and 2000 hardness, 1 hr | Increased glucose uptake. | Stimulated the phosphorylation of IRS-1, LKB1, AMPK, and mTOR and improved impaired phosphorylation of these molecules. | [28] |
| | In vitro study | Matured 3T3-L1 cells, DSW 500, 1000, and 2000 hardness, 1 hr | Increased glucose uptake. | Increased AMPK phosphorylation in 3T3-L1 pre- and mature adipocytes.
Stimulated phosphoinositol-3-kinase and AMPK pathway-mediated glucose uptake. | [29] |
| | In vivo study | Streptozotocin- (STZ-) induced diabetic male ICR mice (4–9 weeks), DSW 1000, 2000, and 4000 hardness, ad libitum, 4 weeks | Improved impaired glucose tolerance.
Regulated blood glucose levels by inhibited glucose production and enhanced glucose uptake via regulation of gene expression. | Increased adiponectin and leptin levels and reduced the levels of the proinflammatory cytokines IL-6 and TNF-α.
Improved architecture of pancreatic islets of Langerhans and enhanced insulin secretion from β-cells.
Stimulated the phosphorylation of IRS-1, LKB1, AMPK, and mTOR and improved impaired phosphorylation of these molecules in muscle.
Downregulated the expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose 6-phosphatase (G6Pase), both of which are required for gluconeogenesis; glucokinase (GK) and citrate synthase (CS), both of which are required for glucose oxidation; and liver glycogen phosphorylase (LGP), which is required for glycogenolysis.
Upregulated glycogen synthase (GS) expression.
Upregulated the expression of GLUT1 and GLUT4 in skeletal muscle, which are required for glucose transport; glucokinase and citrate synthase, which are required for glucose oxidation; and acyl-CoA oxidase (ACO), CPT1α, and MCAD, which are required for β-oxidation. | [28] |
| | In vivo study | HFD-induced diabetic male C57BL/6J mice (6–25 weeks), DSW 500, 1000, and 2000 hardness, ad libitum, 20 weeks | Improved impaired glucose tolerance.
Suppressed the expression of hepatic genes involved in glucogenesis, glycogenolysis, and glucose oxidation.
Increased glucose uptake, β-oxidation, and glucose oxidation in muscle.
Improved impaired AMPK phosphorylation in the muscles and livers. | Recovered size of the pancreatic islets of Langerhans and increased the secretion of insulin and glucagon.
Increased adiponectin levels.
Decreased IL-6 and TNF-α levels.
Downregulated the expression of PEPCK and G6Pase for gluconeogenesis; GK and CS for glucose oxidation; and LGP for glycogenolysis.
Upregulated the expression of GS for glycogenesis.
Upregulated the GLUT1 and GLUT4 for glucose transport, GK and CS for glucose ACO, CPT1α, and MCAD for β-oxidation in skeletal muscle.
Increased the expression of SIRT family proteins such as SIRT1, SIRT4, and SIRT6. | [29] |
| | In vivo study | Male C57BL/6J ob/ob mice, DSW 1000 hardness, ad libitum, 84 days | Reduced glucose levels in plasma by 35.4%.
| Increased glucose disposal.
Increased adiponectin levels in plasma.
Decreased plasma protein levels of resistin, RBP4, and fatty acid binding protein.
Increased GLUT4 and AMP-activated protein kinase levels in skeletal muscle tissue. | [1] |
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