Introduction: What they say
A study from Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; Departments of Medicine and Pharmacology, University of California, San Diego School of Medicine, La Jolla, CA 92093, USA; Division of Metabolism, Endocrinology, and Diabetes, Department of Medicine, and Brehm Center for Diabetes, University of Michigan Medical School, Ann Arbor, MI 48105, USA; and Gene Expression Laboratory, Salk Institute for Biological Sciences, La Jolla, CA 92037, USA shows that “Inhibition of IKKε and TBK1 Improves Glucose Control in a Subset of Patients with Type 2 Diabetes”. This research paper was published, in the 5 July 2017 issue of the journal “Cell Metabolism” [One of the best research journals in Metabolism with an I.F of 17.303], by Prof. Saltie Alan R, Evans RM, and Oral EA and others.
Earlier, Prof. Saltie Alan R, Reilly SM and others had shown that “An inhibitor of the protein kinases TBK1 and IKK-ε improves obesity-related metabolic dysfunctions in mice”. This research paper was published in the 10 February’13 issue of the journal “Nature Medicine” [One of the best research journals in Metabolism with an I.F of 29.886].
What we say:
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Natural product-based Combinatorial therapy for TIIDM and Metabolic disease: A therapeutic mix encompassing Cholecalciferol, Oleanolic acid and Magnolol decreases blood glucose levels, stifles Hemoglobin A1c and fructosamine levels, brings down the levels of inflammatory mediators, augments insulin sensitivity, increases energy expenditure, promotes weight loss and alleviates TIIDM, metabolic disease and hepatic steatosis 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) diabetic disease results in a number of health complications, including diabetic cardiomyopathy (DCM), diabetic nephropathy, diabetic retinopathy, and diabetic neuropathy; (3) one third of people with diabetes suffer from diabetic kidney disease (DKD); and one third of them will develop kidney failure; (4) Obesity plays a central role in the development of TIIDM; (5) Diabetes is going to be one of the top 10 causes of death by 2030; (6) the life-long painful injection/drug treatment is required to treat DM; (7) 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?
It is known for years that inflammation plays a central role in the development of obesity and type 2 diabetes. Evidently, inflammatory kinases, such as IKKε and TBK1, have recently been shown to be upregulated in Obesity; and ablation of them in obese mice decreases body weight, increases insulin sensitivity, inhibits fatty liver formation and attenuates inflammation.
Prof. Saltie AR’s research team has recently shown that treating obese patients with type 2 diabetes and nonalcoholic fatty liver disease with amlexanox, an inhibitor of IKKε and TBK1; and an approved drug in the treatment of aphthous ulcers and asthma: (1) decreases Hemoglobin A1c and fructosamine levels; (2) increases insulin sensitivity; (3) inhibits the development of hepatic steatosis; (4) decreases inflammatory mediators, such as Mcp1 or Rantes, TNF-α, IL-1α & Mip-1α, gene expression; (5) increases Slc2a4 ; Pparγ; UCP-1 expression; and (6) increases energy expenditure, suggesting that combined inhibition of IKKε and TBK1 may improve glucose control and inhibit the development of metabolic disease, including Type 2 Diabetes, and hepatic steatosis.
From Research findings to Therapeutic opportunity:
This study suggests a combinatorial therapy for Obesity-induced T2D and hepatic steatosis patients. A therapeutic mix encompassing Cholecalciferol, Oleanolic acid and Magnolol, by increasing the expression of its target genes, it may decrease the expression of IKK-ε and TBK1. Thereby, it may: (1) decrease blood glucose levels; (2) stifle Hemoglobin A1c levels; (3) lower fructosamine levels: (4) increase insulin sensitivity; (4) inhibit the expression of inflammatory mediators; (5) increase thermogenesis and energy expenditure; (6) augment lipolysis and weight loss; (5) protect against diet-induced obesity and weight gain; and (6) inhibit the development of hepatic steatosis, TIIDM and metabolic disease (Fig.1).
Thus, pharmacological formulations encompassing “Cholecalciferol, Oleanolic acid and Magnolol or their analogues, either alone or in combination with other drugs” may be used to treat patients with hepatic steatosis, Obesity, TIIDM and metabolic disease.
Given the non-toxic nature of the natural product-derived and the Vitamin-based therapeutic mix compared to reported compound amlexanox, it may be an ideal therapeutic agent of choice in the treatment of obesity-related metabolic dysfunctions and in T2D.
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 a therapeutic mix encompassing Cholecalciferol, Oleanolic acid and Magnolol decrease the expression of IKK-ε and TBK1 to promote insulin sensitivity and weight loss?
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Citation: Boominathan, L., Natural product-based Combinatorial therapy for TIIDM and Metabolic disease: A therapeutic mix encompassing Cholecalciferol, Oleanolic acid and Magnolol decreases blood glucose levels, stifles Hemoglobin A1c and fructosamine levels, brings down the levels of inflammatory mediators, augments insulin sensitivity, increases energy expenditure, promotes weight loss and alleviates TIIDM, metabolic disease and hepatic steatosis via up regulation of its target gene, 17/July/2017, 11.59 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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