A master’s thesis in Karbala Medicine discusses the levels of nesfatin 1, nucleobandin 2 genetic variants and their roles in inducing type 2 diabetes mellitus in obese Iraqi women.

The master’s thesis discussed at the University of Karbala, College of Medicine, for the (medical) biochemistry branch, by the student Esraa Khalil Ibrahim, and tagged with the title: (Nesfatin 1 levels, nucleobindin 2 genetic variants with their roles in the occurrence of type 2 diabetes in obese Iraqi women), as type 2 diabetes is considered It is a metabolic disorder and is caused by a combination of two underlying factors: inadequate secretion of insulin by the cells of the pancreas or failure of insulin-sensitive tissues to respond adequately to insulin.

Nesfatin 1 is secreted by nuclei of the hypothalamus and is responsible for appetite control and influences several functions such as regulatory effects on energy metabolism through suppression of food intake. In addition, it regulates heart function, reduces blood glucose levels, acts as a neuroendocrine regulator, and causes weight loss along with reducing energy expenditure. Nisfatin-1, which originated from its precursor protein named (NUCB2, a nucleobindin that plays an important role in glucose metabolism and diabetes). This study explored the relationship between genetic variants.

NUCB2 and type II diabetes (T2DM) target was

The study aimed to evaluate the diagnostic accuracy of serum nesfatin-1 in type 2 diabetes mellitus and its relationship to C-peptide level in obese and non-obese type 2 diabetic women from the Iraqi population.

A significant relationship was found between circulating levels of Nesfatin-1 and type 2 diabetes. It appears that Nesfatin-1 is able to contribute to the treatment of obesity and diabetes due to its anorexic and anti-hyperglycemic effects. In addition, C-peptide is a well-known biomarker of insulin resistance and beta cell function. Highly specific and sensitive analysis results were obtained by ROC analysis for both markers

in type 2 diabetes as a result of genotype.