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: Mirtazapine-based therapy for diabetes (TIIDM): Mirtazapine/Remeron, used in the treatment of depression,anxiety disorders, insomnia, nausea and vomiting, 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 an antidepressnat-based therapy for Weight loss and TIIDM.
This study suggests, for the first time, that Mirtazapine/Remeron, 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 “Mirtazapine/Remeron 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 Mirtazapine/Remeron increase the expression of GLP1R and CAV-1?
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Citation: Boominathan, L., Treating blood sugar disease with antidepressants: Mirtazapine-based therapy for diabetes (TIIDM): Mirtazapine/Remeron, used in the treatment of depression,anxiety disorders, insomnia, nausea and vomiting, 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, 28/March/2018, 1.02 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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