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Study of cellular mechanisms of glucose intolerance and DM2 control after bariatric surgery: the role of CD38/SIRT1/NAD axis

Grant number: 11/22598-0
Support Opportunities:Scholarships abroad - Research
Effective date (Start): July 21, 2012
Effective date (End): January 26, 2013
Field of knowledge:Health Sciences - Medicine - Surgery
Principal Investigator:Wilson Salgado Junior
Grantee:Wilson Salgado Junior
Host Investigator: Eduardo Nunes Chini
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Research place: Mayo Clinic, Minnesota, United States  

Abstract

We are living a great global epidemic of obesity, and so, there is an increasing concern about the high incidence of co morbidities associated with this rise in obesity, amongst them the type 2 diabetes (DM2). Investigators are searching for the causes of such illnesses. Much more that this, efforts have been undertaken to identify possible common final pathways, at cellular level, that can be focused for more effective therapies to those illnesses. In this context, some proteins linked with the cellular signaling have been made responsible to cause or to protect against obesity and metabolic syndrome. It is about the Nicotinamide adenine dinucleotide (NAD) / Sirtuin (SIRT1) axis and also the action of protein CD38. Bariatric surgery is considered one of the alternatives to the treatment of the metabolic syndrome in the obese patients. As it has been showing more effective and lasting weight loss when compared to clinical treatment, there is a growth in its indication. The responsible mechanisms in which the surgery acts to control the weight and specially the glycemia, are subjects of intense research. This study aims to evaluate the effect of bariatric surgery in the control of the glycemia, in an animal model of rats with DM2 (Goto-Kakizaki), focusing in the above described mechanisms of cellular signaling. It is an original study and the results will probably have some applications in the development of new therapies (clinical and surgical) for the metabolic syndrome. (AU)

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