Table 1.
Included studies.
| Study | Year | Evaluated INS | Study Characteristics | Main Results |
|---|---|---|---|---|
| Animal Studies—Deficiency | ||||
| Hayashi [36] | 1974 | MI | Rats fed with an MI-deficient diet or the same diet with the addition of 0.5% MI for up to five weeks. | Increased levels of liver TG, CE, and non-esterified fatty acids and concomitant increase in serum non-esterified fatty acids in the MI-deficient group. |
| Hayashi [37] | 1974 | MI | Rats fed with an MI-deficient diet or the same diet with the addition of 0.5% MI for one or two weeks. | Liver TG levels were increased in MI-deficient rats, especially in palmitic, palmitoleic, and oleic acids. |
| Thakur [38] | 2011 | PI | Zebrafish mutants incapable of PI synthesis. | Mutants exhibited hepatomegaly with microscopic NAFLD features with upregulated endoplasmic reticulum stress markers. |
| Animal Studies—Supplementation | ||||
| Katayama [39] | 1994 | MI | Rats fed with either corn starch or a high-sucrose diet, with or without MI, for 16–17 days. | Reduction in the increase of liver weight, total lipids, TG, and CE by MI in high-sucrose fed rats; reduction in serum TG increase in the same group. |
| Katayama [40] | 1997 | MI, sodium phytate | Rats fed with either corn starch or a high-sucrose diet, with or without the addition of MI or sodium phytate for 12–13 days. | MI and sodium phytate reduced liver enlargement and suppressed to normal levels liver TG and total lipids levels; reduced liver G6PD, ME, and FASN. |
| Geethan [41] | 2008 | Pinitol | Streptozotocin-induced diabetic rats treated with or without 100 mg/kg Pinitol for 30 days. | Pinitol reduced blood glucose and serum TG, free fatty acids, and CE; decreased TG and CE liver concentration; decreased the concentration of liver phospholipids and free fatty acids; increased HDL and reduced LDL. |
| Zhou [42] | 2008 | Pinitol | Rats fed with a high-fat diet for 8 weeks, with or without 0.1%, 1.0%, or 2.0% Pinitol, and induced hepatic injury by a single administration of GalN. | After GalN administration, Pinitol suppressed the increase in ALT and AST; attenuated liver CE increase; reduced TNFα levels; reduced lipid peroxidation; increased glutathione levels; increased liver catalase; Mn–SOD; GR activities. |
| Choi [43] | 2009 | Pinitol | Hamsters fed with a high-fat, high-cholesterol diet with or without 0.05% or 0.1% Pinitol for 10 weeks. | Pinitol reduced epididymal and perirenal white adipose tissue; reduced plasma total CE, non-HDL CE, glucose, and total-CE/HDL ratio; reduced liver TG and CE; lowered HMGR and ACAT activities; suppression of liver lipid accumulation and reduction in adipocyte size. |
| Sivakumar [44] | 2010 | Pinitol | Streptozotocin-induced diabetic rats treated with Pinitol, gliclazide, or neither for 30 days. | Both Pinitol and gliclazide reversed increase in blood glucose and glycosylated Hgb; reduced blood TNF-α, IL-6, and IL-1β; reduced liver peroxides and hydroperoxides; contrasted the diabetes-induced microscopic liver alterations normalizing the tissue architecture. |
| Shimada [45] | 2019 | MI | Rats fed with either a high-glucose or high-fructose diet, with or without MI 0.05% or 0.25% supplementation for 15 days. | MI dose-dependent reduction of liver TG content and expression levels of G6PD, ME1, FASN, ACCα, and S14 in fatty liver high-fructose induced rats; reduction in hepatic ChREBPβ expression; reduction in ChREBP binding to the ChoRE ChREBPβ and FASN genes. |
| Human Studies—Supplementation | ||||
| Lee [46] | 2019 | Pinitol | Double-blind RCT on 90 NAFLD patients taking Pinitol 600 mg, 1000 mg or PBO for 12 weeks | No significant between groups differences in liver fat content at 12 weeks; significant reduction in liver fat content in the 600 mg arm compared to its baseline. Pinitol significantly reduced AST levels at 12 weeks; reduced lipid peroxidation in terms of urinary MDA stability compared to PBO increased GPx. Pinitol reduced blood TG increase after postprandial high-fat formula compared to PBO. |
INS = inositol; MI = myoinositol; PI = phosphatidylinositol; TG = triglycerides; GalN = D-galactosamine; ALT = alanine aminotransferase; AST = aspartate aminotransferase; TNFα = tumor necrosis factor alpha; Mn–SOD = MN-superoxide dismutase; GR = glutathione reductase; CE = cholesterol; HMGR = HMG-CoA-Reductase; ACAT = acyl-CoA cholesterol acetyltransferase; Hgb = hemoglobin; G6PD = glucose-6-phosphate-dehydrogenase; ME1 = malic enzyme 1; FASN = fatty acid synthase; ACCα = acetyl-CoA-carboxylase alpha; S14 = modulator of fatty acid synthesis; ChREBP = carbohydrate-responsive element-binding protein; RCT = randomized controlled trial; PBO = placebo; MDA = malondialdehyde; GPx = glutathione peroxidase; non-alcoholic fatty liver disease = NAFLD.