Assessment of serum with resistin concentrations and inflammatory markers in patients with Type 2 diabetes mellitus

Abstract

Diabetes mellitus (DM) is one of the most common endocrine disorders affecting almost 6% of the world's population. The prevalence of this chronic metabolic disease is on the increase (Townsend, 2000). This chronic metabolic disorder affects the metabolism of carbohydrates, protein, fat, water, and electrolytes, leading to structural changes in tissues of many organ systems in the body, especially those of the vascular system (Frank, 1957).

On the basis of its etiology, diabetes mellitus can be classified into two major types. Type 1 diabetes (formally referred to as insulin-dependent-diabetes mellitus, IDDM), caused by immunological destruction of pancreatic islets, is characterized by absolute insulin deficiency. Type 2 diabetes (formally referred to as non-insulin dependent diabetes mellitus, NIDDM) begins in the middle age or earlier and is characterized by deficient insulin secretion and or insulin resistance (The Expert Committee Report, 1997). Type 2 diabetes is, however, no longer a disease of the adult because it can occur in the young where it is referred to as maturity onset diabetes of the young (MODY) (Libman and Arslanian, 1999).

Major mechanisms proposed to lead to beta-cell death in Type 2 diabetes and discussed here include: increased circulating cell nutrients, endoplasmic reticulum (ER)­ stress, signalling factors from the adipocyte, and iatrogenic mechanisms (Verchere et al., 1996; Kahn et aL, 1999).

It has been shown that regular physical activity increases insulin sensitivity and glucose tolerance (Kriska et aL, 2001). Moreover, it has been shown that physical activity reduces the risk of type 2 diabetes (Helmriclt et aL, 1991).