Introduction: What they say
A study from Nutritional Sciences and Toxicology Department, University of California, Berkeley, Berkeley, United States shows that “Dnmt3a is an epigenetic mediator of adipose insulin resistance.” This research paper was published, in the 1 Nov 2017 issue of the journal “Elife”, by Prof.Kang S, You D and others.
What we say:
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for body weight control, energy homeostasis and TIIDM: AP-1 (Activator protein-1) inhibits DNA methyltransferase 3a (Dnmt3a) expression, increases FGF21 expression, augments insulin sensitivity, increases glucose tolerance, 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 387 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; (3) 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.Kang’s research team has recently shown that:(1) DNA methyltransferase 3a (Dnmt3a) promotes insulin resistance; (2) DNMT3a null mice are resistant to diet-induced insulin resistance and glucose intolerance; (3) FGF21 is a negative target of DNMT3a gene and its promoter region is heavily methylated in patients with diabetes; and (4) FGF21 induction attenuates Dnmt3a-mediated insulin resistance, suggesting that decreasing the expression of DNMT3a may result in (a) induction of FGF21; (b) increased insulin sensitivity and glucose tolerance; and (3) attenuation of Obesity-associated TIIDM.
AP-1 (Activator protein-1), by increasing the expression of its target gene, it may decrease the expression of DNMT3a. Thereby, it may: (1) decrease methylation at the FGF21 promoter region; (2) increase FGF21 expression; (3) augment insulin sensitivity; (4) increase glucose tolerance; and (5) inhibit diet-induced insulin resistance (Fig.1). Thus, pharmacological formulations encompassing “compounds that activate AP-1 protein, either alone or in combination with other drugs,” may be used to treat Obesity-associated TIIDM (Fig.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 mechanistic information: How does AP-1 decrease the expression of DNMT3a to promote insulin sensitivity?
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Citation: Boominathan, L., Molecular therapy for body weight control, energy homeostasis and TIIDM: AP-1 (Activator protein-1) inhibits DNA methyltransferase 3a (Dnmt3a) expression, increases FGF21 expression, augments insulin sensitivity, increases glucose tolerance, and protects from diet-induced obesity and TIIDM, via up-regulation of its target gene, 20/December/2018, 10.59pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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