| | Type of study model | Experimental method [subject (age/weight), treatment dosage, duration of treatment] | Major activity | Mechanism of action | Reference |
| | In vitro study | C2C12 cells, DSW 100, 500, 1000, 1500, and 2000 hardness, indicated time of 0, 1, 2, and 3 days | Increased mitochondrial biogenesis and function.
| Enhanced gene expression of peroxisome proliferator-activated receptor gamma coactivator 1 α (PGC-1a), nuclear respiratory factor-1 (NRF-1), and mitochondrial transcription factor A (TFAM); mitofusin-1/2 (MFN1/2) and dynamin-related protein 1 (DRP1) for mitochondrial fusion; optic atrophy 1 (OPA1) for mitochondrial fission; translocase of outer mitochondrial membrane 40 (TOMM40) and translocase of inner mitochondrial membrane 44 (TIMM44) for mitochondrial protein import; carnitine palmitoyltransferase 1α (CPT1α) and medium-chain acyl-CoA dehydrogenase (MCAD) for fatty acid oxidation; and cytochrome c (CytC) for oxidative phosphorylation.
Increased mitochondria staining, citrate synthase (CS) activity, CytC oxidase activity, NAD+ to NADH ratio, and the phosphorylation of signalling molecules such as AMPK and sirtuin 1 (SIRT1). | [26] |
| | In vitro study | 3T3-L1 cells, DSW 100, 500, and 1000 hardness, 3 days | Decreased lipid accumulation. | Reduced expression mRNA levels of PPARγ and C/EBPα and protein levels of fatty acid binding protein and adiponectin. | [13] |
| | In vivo study | HFD C57BL/6J mice (6 weeks), DSW 500, 1000, and 2000 hardness, ad libitum, 20 weeks | Enhanced mitochondrial biogenesis in muscles. | Improved mitochondrial DNA (mtDNA) content in the muscles of HFD-induced obese mice.
Enhanced expression of PGC-1α, NRF1, and mtTFA.
Enhanced estrogen-related receptor α (ERRα), PPARα, and PPARδ. | [26] |
| | In vivo study | HFD C57BL/6J mice (6–26 weeks), DSW 500, 1000, and 2000 hardness, ad libitum, 20 weeks | Suppressed body weight gain.
Inhibited increase in adipocyte size.
Suppressed the expression of adipogenic, lipogenic, lipolytic, and proinflammatory cytokine genes.
Increased the expression of adipokines and b-oxidation genes in fat.
| Suppressed mRNA expression of key adipogenic genes such as PPARγ, C/EBPα, and aP2.
Increased the expression of GLUT4, adiponectin, and leptin.
Decreased the expressions of IL-6 and TNF-a.
Decreased the expressions of sterol regulatory element-binding protein 1c (SREBP1c) and fatty acid synthase (Fas), which are involved in lipogenesis; adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), which are involved in lipolysis.
Increased the expression of MCAD and CPT1α, which are involved in b-oxidation.
Increased phosphorylation of IRS-1, LKB1, AMPK, and mTOR in fat. | [27] |
| | In vivo study | Male C57BL/6J ob/ob mice, DSW 1000 hardness, ad libitum, 84 days | Decreased body weight gain by 7%.
Reduced plasma glucose levels by 35.4%.
| Increased glucose disposal.
Increased plasma protein levels of adiponectin.
Decreased plasma protein levels of resistin, RBP4, and fatty acid binding protein.
Increased GLUT4 and AMP-activated protein kinase levels in skeletal muscle tissue.
Decreased PPARγ and adiponectin in adipose tissue. | [1] |
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