Introduction: What they say
A study from the Max Delbrück Center for Molecular Medicine, Berlin, Germany shows that “Regulation of body weight and energy homeostasis by neuronal cell adhesion molecule1.” This research paper was published, in the June 2017 issue of the journal “Nature Neuroscience” [One of the best research journals in Neuroscience with an I.F of 17.398], by Prof. Matthew N Poy and Thomas Rathjen 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: Atorvastatin, a lipid-lowering agent, decreases CADM1 and its downstream target genes that promote 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 half a billion adults are obese worldwide ; (2) obesity is more prevalent in western countries than in asian countries; (3) obesity results in deregulated blood pressure, cholesterol, triglycerides and insulin sensitivity; and the risks of coronary heart disease, ischemic stroke and TII diabetes mellitus(TIIDM) increase ; (4) more than 422 million people worldwide are affected by Diabetes mellitus (DM); (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; and (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, obesity-associated diseases, including diabetes.
What is known?
Prof. Matthew N Poy’s research team has recently shown that:(1) Cell adhesion molecule 1 (CADM1) and cell adhesion molecule 2 (CADM2) are over expressed in Obese mice;(2) induction of CADM1 in excitatory neurons promotes weight gain and reduces energy expenditure; and (3) loss of CADM1 protects mice from diet-induced and genetically induced Obesity. Furthermore, decreasing CADM1 levels in mice results in weight loss; and increased energy expenditure, suggesting that decreasing the expression of CADM1 may promote weight loss, augment insulin sensitivity, and alleviate Obesity-associated TIIDM
From research findings to Therapeutic opportunity:
This study provides insights into how the lipid-lowering medication Atorvastatin may promote Weight loss and attenuate Obesity-associated TIIDM. Atorvastatin, by increasing the expression of its target gene, it may decrease the expression of CADM1. 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 “Atorvastatin or its analogues, either alone or in combination with other drugs,“ may be used as a weight-loss medication; and to treat Obesity-associated TIIDM.
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 atorvastatin decrease the expression of CADM1 to promote Weight loss?
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Citation: Boominathan, L., Molecular therapy for body weight control, energy homeostasis and TIIDM: Atorvastatin, a lipid-lowering agent, decreases CADM1 and its downstream target genes that promote 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, 14/November/2017, 6.41 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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