Role of FNDC5 gene polymorphism in patients with diabetic nephropathy

Authors

1 Department of Medical Biochemistry, Faculty of Medicine, Sohag University

2 Department of Medical Biochemistry Department Faculty of Medicine Sohag University

3 Department of Medical Biochemistry Faculty of Medicine Sohag University

4 Internal medicine departement sohag university hospital.sohag.egypt

Abstract

A category of metabolic illnesses known as diabetes mellitus (DM) is characterized by levels

of hyperglycemia that persist for an extended length of time. The primary underlying cause of

Type 2 diabetes mellitus (DM) is insulin resistance, which may also be accompanied by

substantially decreased insulin production. The long-term presence of hyperglycemia causes

several problems, including diabetic nephropathy. White adipose tissue (WAT) and brown adipose

tissue (BAT) are the two separate compartments that make up adipose tissue. BAT has a

thermogenic activity and controls body temperature by dissipating energy through heat generation.

It is believed that the browning of adipose tissue will increase insulin sensitivity and lessen weight

gain. Muscle-adipose tissue cross-talk may be facilitated by irisin, a newly identified exercise-mediated myokine that controls energy metabolism by transforming white into brown fat. When

the precursor plasma membrane protein fibronectin type III domain-containing protein 5 (FNDC5)

is broken down, irisin is created and released into the bloodstream. In individuals with diabetic

nephropathy and chronic kidney disease (CKD), irisin was discovered to be related to renal

functioning. To identify variations in the incidence of diabetic nephropathy among diabetic

patients, the role of FDNC5 genetic polymorphism and irisin expression in T2DM nephropathy is

being studied

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