Study summary · research use only
Inositol and Non-Alcoholic Fatty Liver Disease: A Systematic Review on Deficiencies and Supplementation
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This systematic review examined preclinical animal-model and clinical evidence for inositol supplementation in non-alcoholic fatty liver disease, retrieving 10 studies in animal models assessing myo-inositol or pinitol deficiency or supplementation and one human randomized controlled trial. The abstract reports that inositol deficiency was associated with increased fatty liver in animals, while inositol supplementation in animal models reduced hepatic triglyceride and cholesterol accumulation and maintained normal liver histopathology; in the human RCT, pinitol supplementation was reported to produce similar results, reducing liver fat and post-prandial triglycerides, lowering AST levels, and reducing lipid peroxidation while increasing glutathione peroxidase activity. The authors describe the results as limited, indicating a need for further evaluation in larger clinical trials.
Abstract
Liver lipid accumulation is a hallmark of non-alcoholic fatty liver disease (NAFLD), broadly associated with insulin resistance. Inositols (INS) are ubiquitous polyols implied in many physiological functions. They are produced endogenously, are present in many foods and in dietary supplements. Alterations in INS metabolism seems to play a role in diseases involving insulin resistance such as diabetes and polycystic ovary syndrome. Given its role in other metabolic syndromes, the hypothesis of an INS role as a supplement in NAFLD is intriguing. We performed a systematic review of the literature to find preclinical and clinical evidence of INS supplementation efficacy in NAFLD patients. We retrieved 10 studies on animal models assessing Myoinosiol or Pinitol deficiency or supplementation and one human randomized controlled trial (RCT). Overall, INS deficiency was associated with increased fatty liver in animals. Conversely, INS supplementation in animal models of fatty liver reduced hepatic triglycerides and cholesterol accumulation and maintained a normal ultrastructural liver histopathology. In the one included RCT, Pinitol supplementation obtained similar results. Pinitol significantly reduced liver fat, post-prandial triglycerides, AST levels, lipid peroxidation increasing glutathione peroxidase activity. These results, despite being limited, indicate the need for further evaluation of INS in NAFLD in larger clinical trials.
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