Site is Being Upgraded

Treating blood sugar disease with low-calorie sweeteners: D-Allulose-based therapy for diabetes (TIIDM): D-Allulose/D-Psicose, a low-calorie sweetener isolated from natural products, 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, 9/June/2018, 10.32 pm

Interleukin-based therapy for body weight control, energy homeostasis and TIIDM: Interleukin-2(IL-2) decreases CADM1 and its downstream target genes that inhibit 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, 7/June/2018, 6.38 am
June 7, 2018
CD24-based therapy for cardiomyocyte proliferation and heart regeneration: Cluster of Differentiation(CD-24) decreases tumor suppressor MiR-128 and cyclin-dependent kinase inhibitor p27 expression, increases SUZ12 expression, increases Cyclin E and CDK2 expression, promotes proliferation/re-entry of postnatal/adult cardiomyocytes, attenuates fibrosis, ameliorates cardiac dysfunction, and promotes heart repair in response to myocardial infarction, via up regulation of its target gene, 9/June/2018, 10.41 pm,
June 9, 2018
Show all

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 low-calorie sweeteners: D-Allulose-based therapy for diabetes (TIIDM): D-Allulose/D-Psicose, a low-calorie sweetener isolated from natural products, 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 D-Allulose, 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 “D-Allulose or its analogues, either alone or in combination with other drugs,” may be used to treat TIIDM (Figure 2).

Figure 1. Mechanistic insights into how D-Allulose functions as an antidiabetic agent. D-Allulose, by up regulating its target genes, it may: a) increase cAMP levels; b) increase insulin sensitivity; c) increase increase secretion; and d) attenuate hyperglycemia.

Figure 2. D-Allulose  functions as an anti-diabetic agent. D-Allulose increases CAV1 and GLP-IR through up regulation of its target gene


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 D-Allulose increase the expression of GLP1R and CAV-1?

Amount: $500#

# Research cooperation

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

* Research cooperation[easy_payment currency=”USD”]


References:

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

Citation: Boominathan, L., Treating blood sugar disease with low-calorie sweeteners: D-Allulose-based therapy for diabetes (TIIDM): D-Allulose/D-Psicose, a low-calorie sweetener isolated from natural products, 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, 9/June/2018, 10.31 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

Courtesy: When you cite, drop us a line at info@genomediscovery.org

 

 

Comments are closed.