Introduction: What they say
A study from the Comprehensive Diabetes Center and Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Alabama at Birmingham, Birmingham, AL shows that “miR-204 Controls Glucagon-Like Peptide 1 Receptor Expression and Agonist Function.” This research paper was published, in the 3 November 2017 issue of the journal “Diabetes” [One of the best research journals in diabetic research with an I.F of 10 plus], by Prof. Shalev A, Jo S and others.
What we say:
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Treating blood sugar disease with antidepressants: Duloxetine-based therapy for diabetes (TIIDM): Duloxetine (Brand name: Cymbalta), used in the treatment of major depressive disorder, generalized anxiety disorder, fibromyalgia, neuropathic pain and others, increases GLP1R and Caveolin-1 (CAV-1) expression, promotes glucose-induced insulin secretion, improves insulin sensitivity, increases energy utilization, promotes weight loss and protects from diet-induced obesity and TIIDM, via up regulation of its target gene
From significance of the study to public health relevance:
Given that: (1) more than 422 million people worldwide are affected by Diabetes mellitus (DM); (2) Diabetes is going to be one of the top 10 causes of death by 2030; (3) the life-long painful injection/drug treatment is required to treat DM; (4) the global economic cost spent for diabetes treatment in 2014 was little more than 600 billion US dollars, there is an urgent need to find: (i) a way to induce regeneration of adult ß-cells that were lost in DM; (ii) a cheaper alternative to the existing expensive weight-loss drugs; (iii) a side-effect-free natural product-based drug; and (iv) a way to cure, not just treat, diabetes.
What is known?
Prof. Shalev A’s research team has recently shown that:(1) MiRNA-204, the highly expressed miRNA in ß-cells, inhibits GLP1R expression; (2) deletion of miR-204: (a) increases cAMP production; (b) increases insulin secretion; (c) augments response to GLP1R activators or agonists; and (d) protects against diabetes; (3) deletion of thioredoxin-interacting protein, the upstream regulator of miR-204, (a) increases GLP1R expression; (b) ameliorates glucose intolerance; (c) improves cAMP production; (d) increases insulin secretion; and (e) protects against diabetes, suggesting that decreasing the expression of MiR-204 or its upstream regulator thioredoxin-interacting protein may promote insulin sensitivity, and alleviate TIIDM.
From Research findings to Therapeutic opportunity:
This study suggests, for the first time, that Duloxetine, by increasing the expression of its target gene, it may increase the expression of GLP1R and Caveolin-1 (CAV-1). Thereby, it may: (1) increase pancreatic beta-cell proliferation; (2) increase expression of genes that promote insulin sensitivity and insulin secretion; (3) promote weight loss; (4) augment energy expenditure; (5) decrease metabolic stress; and (6) promote energy homeostasis (Fig.1). Thus, pharmacological formulations encompassing “Duloxetine or its analogues, either alone or in combination with other drugs,” may be used to treat TIIDM (Figure 2).
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 information: How does Duloxetine increase the expression of GLP1R and CAV-1?
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Citation: Boominathan, L., Treating blood sugar disease with antidepressants: Duloxetine-based therapy for diabetes (TIIDM): Duloxetine (Brand name: Cymbalta), used in the treatment of major depressive disorder, generalized anxiety disorder, fibromyalgia, neuropathic pain and others, increases GLP1R and Caveolin-1 (CAV-1) expression, promotes glucose-induced insulin secretion, improves insulin sensitivity, increases energy utilization, promotes weight loss and protects from diet-induced obesity and TIIDM, via up regulation of its target gene, 18/April/2018, 9.49 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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