Huether and McCance (2012) explained that "many genes have been identified that are associated with type 2 diabetes, including those that code for beta-cell mass, beta-cell function (ability to sense blood glucose levels, insulin synthesis, and insulin secretion), proinsulin and insulin molecular structures, insulin receptors, hepatic synthesis of glucose, glucagon synthesis, and cellular responsiveness to insulin stimulation
These genetic abnormalities combined with environment influences, such as obesity; result in the basic pathophysiologic mechanisms of type 2 diabetes: insulin resistance and decreased insulin secretion by beta cells (pg. 462). Huether and McCance, (2012) further went into explaining, insulin resistance is defined as suboptimal response of insulin sensitive tissues (especially liver, muscle, and adipose tissue) to insulin is associated with obesity (pg. 462). Diabetes type 2 is a metabolic syndrome that the body can not sufficiently respond to insulin and has an impaired pancreatic production of insulin. .
Obesity is a huge contribution to diabetes and the development of insulin resistance through different mechanisms, Adipokines are changes associated with inflammation and decreased insulin sensitivity. Elevated levels of serum free fatty acids, such as triglycerides and cholesterol are also found in obese individuals, which contribute to a process known as lipotoxicity, Inflammatory cytokines and interleukin-6 are released from intra-abdominal adipocytes or adipocyte-associated mononuclear cells, that are cytotoxic to beta cells, obesity is correlated with hyperinsulinemia and decreased insulin receptor density (Huether & McCance, 2012, pg. 463). B-cell dysfunction is a major defect affecting patients with diabetes type 2. Reducing ability of B-cells to secrete insulin in response to hyperglycemia. Beta cell dysfunction is one of the core defects in diabetes type 2.