| | Type of study model | Experimental method [subject (age/weight), treatment dosage, duration of treatment] | Major activity | Mechanism of action | Reference |
| | In vitro study | HepG2 cells, DSW 200, 400, 600, 800, and 1000 hardness, 24 hr | Decreased lipids accumulation.
| Inhibited the activity of HMGCR by 30.2%.
Increased the phosphorylation level of AMPK by 15.2%.
Reduced p68 of SREBP-1 levels by 55%.
DSW of hardness 600, 800, and 1,000 increased p68 levels of SREBP-2 by 12, 42, and 80%, respectively.
DSW of hardness 600, 800, and 1,000 increased level of CYP7A1 by 41, 115, and 162%, respectively.
DSW of hardness 1,000 increased Apo AI content by 20.3%. | [19] |
| | In vivo study | HFD male Wistar rats (200–220 g), DSW 1,000 hardness, ad libitum, 4 weeks | Decreased levels of TC and TG in liver.
Improved liver function. | Decreased serum levels of AST and ALT.
| [19] |
| | In vivo study | HFD C57BL/6J mice (6–26 weeks), DSW 500, 1000, and 2000 hardness, ad libitum, 20 weeks | Suppressed the expression of genes involved in lipogenesis and cholesterol synthesis; and increased the expression of genes related to b-oxidation in liver.
Improved severe liver steatosis.
Regulated mitochondrial biogenesis and function in liver. | Decreased the expression of Fas and acetyl-CoA carboxylase 1 (ACC1), which are involved in lipogenesis, and liver X receptor a (LXR a), and 5-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoAR), which are involved in cholesterol metabolism.
Increased the expression of MCAD and CPT1α, which are involved in b-oxidation.
Increased the phosphorylation of IRS-1, LKB1, AMPK, and mTOR in liver.
Increased expression of PGC1a, NRF1, Tfam, and mtDNA content in liver. | [27] |
| | In vivo study | HFD male Golden Syrian hamsters (5 weeks), DSW 300, 900, and 1500 hardness, ad libitum, 6 weeks | Decreased lipids accumulation in liver.
Regulated hepatic fatty acid homeostasis.
Improved hepatic antioxidative levels.
Attenuated hepatic damage. | Increased daily faecal lipid and bile acid outputs.
Upregulated genes of hepatic PPARα, retinoid X receptor-alpha, and uncoupling protein-2 (UCP-2) gene expression.
Maintained higher liver glutathione and TEAC levels.
Reduced lipid peroxidation status (MDA content) in liver. | [33] |
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