Introduction: What they say
A study from the Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA shows that “ß-arrestin-2 is an essential regulator of pancreatic ß-cell function under physiological and pathophysiological conditions.” This research paper was published in the 1 February 2017 issue of the journal “Nature communications” [One of the best research journals in General Science with an I.F of 11.329] by Prof. Wess J Dor and Zhu L and others.
What we say:
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Laminar shear stress-based therapy for glucose homeostasis and TIIDM: Laminar shear stress increases Barr2 expression, augments the functional activity of CAMKII, increases insulin secretion, promotes glucose homeostasis, prevents progression to TIIDM and ameliorates obesity-associated metabolic deficits via down 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. Wess’s research team has recently shown that deletion of Barr2 (ß-arrestin-2 gene) in adult mice results in (1) impaired insulin release (in response to calorie-rich diet); (2) exacerbated glucose intolerance; (3) impairment of glucose-induced insulin secretion; and (4) impairment of CAMKI (Multi-functional Ser/Thr protein kinase) function. On the other hand, overexpression of Barr2: (1) improves metabolic deficits in mice consuming HFD; and (2) promotes ß-cell function and insulin secretion, suggesting that increasing the expression of Barr-2 may alleviate metabolic deficits in diabetic patients.
From Research findings to Therapeutic opportunity:
This study suggests a Laminar shear stress therapy for TIIDM and obesity-associated metabolic deficits. Laminar shear stress, by increasing the expression of its target gene, it may increase the expression of Barr2.
Figure 1 Mechanistic insights into how Laminar shear stress functions as an antidiabetic agent. Laminar shear stress, by increasing the expression of Barr2 and the activity of CamKII, may promote insulin secretion.
Thereby, it may: (1) promote glucose-induced insulin secretion; (2) promote proper functioning of L-type Ca2+ channels; (3) promote proper functioning of voltage-dependent Ca2+ channels; (4) promote Ca2+ entry into ß-cells; (5) increase the activity of CAMKII; (6) promote CAMKII-dependent phosphorylation of a number of signalling proteins involved in insulin exocytosis, including Synapsin I; (7) promote CAMKII-dependent insulin secretion; (8) ameliorate HFD-induced metabolic deficits; and (9) promote glucose homeostasis (Fig.1).
Thus, physicians/diabetologists may consider encouraging their diabetic patients to undergo Laminar shear stress therapy. Taken together, Laminar shear stress therapy may be used to treat TIIDM and Obesity-associated metabolic deficits/abnormalities..
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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 Laminar shear stress increase the expression of Barr2 to promote insulin secretion?
Amount: $500
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References:
Web: http://genomediscovery.org or http://newbioideas.com/
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Citation: Boominathan, L., Laminar shear stress-based therapy for glucose homeostasis and TIIDM: Laminar shear stress increases Barr2 expression, augments the functional activity of CAMKII, increases insulin secretion, promotes glucose homeostasis, prevents progression to TIIDM and ameliorates obesity-associated metabolic deficits via down regulation of its target gene, 24/May/2017, 7.30 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org