Table 1.
Highlights of a summary of in vitro and in vivo studies showing effective doses of IP6 targeted toward various disorders.
| Reference | Concentration/Doses | Observed Effects | Benefits | Disease Prevention | |
|---|---|---|---|---|---|
| 1 | Dilworth et al., 2005 [8] Omoruyi et al., 2013 [50] |
1, 4% PA, normal, diabetic rats for 4 weeks. | Decreased random blood glucose, triglyceride, and increased HDL. | Management of glucose and levels in diabetes. | Diabetic and cardiovascular disease. |
| 2 | Foster et al., 2016 [30] Foster et al., 2017 [51] Foster et al., 2019 [35] |
650 mg/kg body weight/day of PA + inositol type 2 diabetic rats for 4 weeks. | Decreased blood glucose, insulin resistance, triglycerides, cholesterol, and food intake. Increased concentration of hepatic reduced glutathione and up-regulation of hepatic superoxide dismutase and catalase. | Effective in type 2 diabetes management, improvement of renal and pancreatic function. Improved anti-oxidant status and preservation of liver cell integrity. | Metabolic disorders via the regulation of some aspects of lipid and carbohydrate metabolism. Prevention of type II diabetic complications. |
| 3 | Vucenik and Sham-Suddin, 2006 [37] | 1.0–2.0 g/day prophylactic and 8–12 g/day dose of PA + inositol in cancer patients. Values were extrapolated from animal data. | Enhanced anti-cancer effects of conventional chemotherapy control of cancer metastases. | Improved quality of life and safe long-term survival of cancer patients. | Potentially enhanced cancer therapy by synergistic action with conventional chemotherapy. |
| 4 | Sanchis et al., 2018 [48] | 380 mg of Ca-Mg IP6 three a day, type 2 diabetic patients for 12 weeks. IP6 concentrations (0 to 2 µM) in vitro AGE formation and observed for 7 days. |
Decreased AGEs and HbA1c levels and decreased AGE formation. | Effective in reducing the development of diabetes-related diseases. | Prevention of AGE-related disorders and complications. |
| 5 | Kumar et al., 2004 [52] | 150 mg PA/Kg b.w. Single treatment. | Significant protection from ulcers, decrease in gastric tissue malondialdehyde levels in ethanol-treated rats, and reductions in necrosis, erosions, congestion, and hemorrhage. | Gastro-protective effects and cytoprotection of the gastric mucosa. | Inflammation and ulcers. |
| 6 | Kim et al., 2014 [53] | 3T3-L1 cells treated with IP6 or myoinositol −0, 50, or 200 μmol/L for 4 or 24 h. | Increased lipid accumulation in a dose-dependent manner. Increased insulin-stimulated glucose uptake. | Increased insulin sensitivity, inhibition of lipolysis, and improved glucose uptake. | Diabetes and its complications. |
| 7 | Wee et al., 2021 [54] | Bone marrow-derived macrophage cells were treated with 200 μM PA for 24 h. | Reduced pro-inflammatory responses and up-regulation of anti-inflammatory genes. | Shaping the function of macrophages without cytotoxicity. Resolution of inflammation. | Prevention of diseases associated with uncontrolled inflammation. |
| 8 | Lee et al., 2005 [55] | Inositol (2% w/v), IP6 (2% w/v), or a combination of both were added to the drinking water of rats for 8 weeks. | Enhanced GST activity, reduced TBARS concentration, and catalase activity. | Potential prevention of chemically induced hepatocarcinogenesis by inositol and/or IP6 supplementation. | Induction of carcinogen detoxifying enzyme (GST) and scavenging of reactive oxygen species. |
| 9 | Shan et al., 2022 [56] | 1 μM, 3 μM, and 5 μM PA- in vitro cancer cells for 24, 48, and 72 h. 300 mg PA/kg b.w. Swiss albino mice for 13 days. |
Induced cytotoxicity in vitro, apoptosis, and cell cycle arrest. Reduced angiogenesis and a revival of the anti-oxidant defense system. | Anti-oxidant, anti-angiogenic, and anti-tumor activities. | In vitro cytotoxic effects and in vivo angiogenic and anti-tumor effect. |
| 10 | Norazalina et al., 2010 [57] | 0.2% (w/v) and 0.5% (w/v) PA in drinking water fed to rats for 8 weeks. | Reduced formation of aberrant crypt foci and reduction in the incidence and multiplicity of total tumors. | Anti-tumor and reduced pre-neoplastic legion formation. | Reduction of colon cancer risk. |
| 11 | Schröterová et al., 2010 [58] | IP6 and inositol at three concentrations: 0.2, 1, and 5 mM for 24, 48, and 72 h on cancer cell lines. | Decreased proliferation and metabolic activities of all cell lines and increased apoptosis. | Anti-proliferative and increased apoptotic. | Reduction of proliferation and up-regulation of apoptosis. |
| 12 | Vucenik et al., 1998 [59] | In vitro: 0.1–10 mM IP6 on a cancer cell line for 72 h. In vivo: 40 mg IP6/Kg in 0.1 mL PBS in mice for 2 weeks. |
Suppressed tumor cell line growth and reduction in tumor size. | Rhabdomyosarcoma therapy. | Suppression of tumor. |
| 13 | Wawszczyk et al., 2012 [60] | 1 and 2.5 mM IP6 for 3, 6, and 12 h on cancer cell line. | Modulation of the expression of p50 and IκBα genes in Caco-2 human colon adenocarcinoma cells. Decreases in the expression of IL-6 and IL-8. | Immuno-regulatory effects on intestinal epithelium. | Anti-inflammatory. |
| 14 | Vucenik et al., 2005 [61] | 2 mM IP6 for 24 h on MCF-7 human breast cancer cells. | 3.1-fold increase in the expression of anti-proliferative PKCdelta. | IP6-induced apoptosis in MCF-7 human breast cancer cells. | Possible anti-proliferative and anti-cancer activity. |
| 15 | Zhang et al., 2005 [62] | 2% IP6 in the drinking water of rats for 21 weeks. | Increased blood NK cell activity. Reduced tumor size and number. | Inhibits tumor growth. | Inhibition of tumor growth and metastasis. |
| 16 | Karmakar et al., 2007 [63] | 0.25, 0.5, and 1 mM IP6 for 24 h on human cancer cell line. | Decreased T98G cell viability with morphological and biochemical features of apoptosis. | IP6 promotes apoptosis in human malignant glioblastoma T98G cells. | Up-regulation of apoptosis in T98G cells. |
| 17 | Sanchis et al.,2021 [64] | Diet-rich IP6 consumption greater than 307 mg/day. | Inhibits hydroxy-apatite dissolution | Maintains normal bone mineral density. | Reduces incidences of bone degenerative diseases. |
INS—inositol, GST—glutathione S-transferase, b.w.—body weight, AGE—advance glycation end-product. In the provided table (Table 1), IP6 supplementation demonstrates a diverse range of effects that cannot be universally applied. The reported therapeutic levels of IP6 differ across various disease models, which may also contribute to varying adverse effects. Therefore, it is crucial to conduct a comprehensive assessment of the optimal levels of IP6 usage in human subjects to ensure favorable outcomes in the management of different diseases.