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. Lansoprazole, 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 “Lansoprazole 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.
Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/
Undisclosed mechanistic information: How does Lansoprazole 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): Lansoprazole 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, 10/February/2017, 11.59 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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