**2. Diabetes mellitus type 2 and fem1b gene**

### **2.1 Diabetes mellitus type 2 occurrence and its diagnosis**

Diabetes mellitus type 2 is a metabolic disorder that is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency [3]. The pathophysiology of Type 2 diabetes mellitus involves impaired insulin secretion, and impaired insulin action in regulating glucose and fatty acid metabolism in the liver, skeletal muscle, and adipose tissue. Many individuals with Type 2 diabetes mellitus have hypertension and perturbations of lipoprotein metabolism, as well as other manifestations of the insulin resistant syndrome. In addition to the risk for development of diabetes - specific complications of retinopathy, Type 2 diabetes mellitus is recognized as a substantial risk factor for cardiovascular disease [4].

It is recommended by the National Diabetes Data Group that diagnosis of diabetes mellitus be based on [5]


Fasting plasma glucose was selected as the primary diagnostic test because it predicts adverse outcomes (e.g., retinopathy) and is easy to perform in a clinical setting.

A mammalian Fem1 gene family, encoding homologs of fem-1, has been characterized and consists of at least three members in the mouse, designated Fem1a, Fem1b, and Fem1c; these have highly conserved homologs in humans, designated FEM1A, FEM1B, and FEM1C, respectively. Mammalian homologs of two other nematode sex determination genes, tra-2 and tra-3, have recently been implicated in glucose homeostasis and type 2 diabetes mellitus. In producing susceptibility to type 2 diabetes mellitus, NIDDM1 is known to interact with a gene, whose identity is unknown, on human chromosome 15 near the CYP19 locus at 15q21.3 [6]. This is near 15q22, where FEM1B, the human homolog of mouse Fem1b, localizes [7].
