Significance of the study:
Given that: (1) 15-30% of Western populations suffer from Non-alcoholic fatty liver disease (NAFLD), while 6-25% of Asian populations suffer from it; (2) 75 to 100 million people in the US succumb to this disease; (3) obesity and type 2 diabetes are risk factor for the development of NAFLD; and (4) the global economic cost spent for NAFLD is enormous, there is an urgent need to find: (i) a way to decrease cholesterol deposition in liver; (ii) a cheaper alternative to the existing expensive drugs; (iii) a side-effect-free natural product-based drug; and (iv) a way to cure, not just treat, NAFLD.
From Research findings to Therapeutic opportunity:
This study suggests a small molecule-based therapy for NAFLD. Omeprazole, by increasing the expression of its target gene, it may suppress the expression of HMGCR (Fig.1). Thereby, it may: (1) decrease Triglycerides, free cholesterol and total cholesterol levels; (2) attenuate lipid deposition in liver; and (3) inhibit progression to NAFLD (Fig. 1). Thus, pharmacological formulations encompassing ” Omeprazole or its analogues, either alone or in combination with other drugs” may be used to treat NAFLD.
Details of the research findings:
Idea Proposed/Formulated (with experimental evidence) by:
Dr L Boominathan Ph.D.
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Undisclosed mechanistic information: How does Omeprazole decrease the expression of HMGCR to prevent progression of NAFLD?
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Citation: Boominathan, L., Molecular therapy for Non-alcoholic fatty liver disease (NAFLD): Omeprazole promotes degradation of HMGCR, decreases the levels of triglycerides, free cholesterol, and total cholesterol and prevents the progression of Non-alcoholic fatty liver disease (NAFLD via down regulation of its target gene, 19/February/2017, 11.59 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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