Natural product-derived therapy for glucose homeostasis and TIIDM: Sulforaphane, isolated from Broccoli, 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, 25/June/2017, 11.42 pm

Natural product-based therapy for Metabolic diseases: Sulforaphane, isolated from Broccoli, increases the expression of Caveolin-1, stabilizes insulin receptor, promotes insulin sensitivity, incrases vasorelaxation, and decreases the risk of hyperglycemia and TIIDM via up regulation of its target gene.., 25/June/2017, 10.43 pm
June 25, 2017
Natural product therapy for pulmonary arterial hypertension: 5,7-Dihydroxy-6-geranyl flavanone (DGF), isolated from Amorpha Fructicosa, inhibits the development of pulmonary arterial hypertension via down regulation of Notch3 and its target gene Hes-5, 26/June/2017, 10.36 pm
June 26, 2017
Show all

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: Natural product-derived therapy for glucose homeostasis and TIIDM: Sulforaphane, isolated from Broccoli, 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


Significance of the study:

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 Natural product-based therapy for TIIDM and obesity-associated metabolic deficits. Sulforaphane, by increasing the expression of its target gene, it may increase the expression of Barr2.

Figure 1 Mechanistic insights into how Sulforaphane functions as an antidiabetic agent. Sulforaphane, by increasing the expression of Barr2 and the activity of CamKII, it 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, pharmacological formulations encompassing Sulforaphane or its analogues either alone or in combination with other drugs” may be used to treat TIIDM and Obesity-associated metabolic deficits/abnormalities.

price-quote[easy_payment currency=”USD”]


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 Sulforaphane increase the expression of Barr2 to promote insulin secretion?

Amount: $500#

# Research cooperation

For purchase and payment details, you may reach us at info@genomediscovery.org

* Research cooperation


References:

Web: http://genomediscovery.org or http://newbioideas.com/

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Citation: Boominathan, L., Natural product-derived therapy for glucose homeostasis and TIIDM: Sulforaphane, isolated from Broccoli, 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, 25/June/2017, 11.41 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

Comments are closed.