Type 2 diabetes is featured by the conflation of insulin resistance and inappropriate insulin secretion. The levels of free fatty acids increase the plasma contribution to the insulin resistance which, in turn, decreases the transportation of glucose to the muscle cells and enhances the breakdown of the fat. The pathophysiology of the disease is debated on account of the role of insulin sensitivity and beta-cell functioning. Additionally, the specific roles played by these factors are still unclear. Nonetheless, there is considerable agreement that both these factors are crucial to explaining the disease's pathophysiology.
Diabetes Type II typically exists when both conditions(insulin resistance and improper secretion) coexist. The prolonged diabetic condition increases the occurrence of atrophy of pancreas. Research by Philleppe et al. confirmed the reduced pancreatic volume in people between 5 to 26 years.
Further studies have posited a crucial role of beta-cell dysfunction in diabetes type II. This dysfunction is characterized by the anomalies, usually the delay, in the first phase of insulin secretion. Glucose transport is also reduced thereby shifting the control point of secretion from glucokinase to glucose transport system. Gradually, desensitization of beta- cell may occur; this is a condition marked by the impairment in second phase release of newly synthesized insulin. Some other defects include decreased conversion of proinsulin to insulin and asymmetric release of insulin. Statistically speaking, a majority of patients( around 80 percent) either inherit or acquire the defects within beta cell. It is likely to cause the delay in insulin response.
Like insulin response and secretion, insulin resistance also plays a substantial role in the pathogenesis of the disease. Insulin resistance refers to the condition when different body cells as liver, muscles, and fat cells fail to respond to the insulin irrespective of its high levels. While liver cells fail are not able to build glycogen stores, muscle cells run short of energy sources. These situations, coupled together, trigger glucose levels in the blood. Reduction in glycogen stores decreases the availability of glucose when it is needed. Lack of physical activity is known to be the potential reason for insulin resistance.
Researchers have also acknowledged that increased adiposity co-morbid with the insulin resistance in most of the diabetic patients. As most of the patients are obese, central visceral adiposity is quite likely. There have been some recent developments in this area. Two emerging paradigms are ecoptic fat storage syndrome and adipose tissue as an endocrine organ hypothesis. Some scholarly articles have based the interplay between beta-cell dysfunction and insulin resistance on these two paradigms. More research studies in this direction will pave the way for better understanding of the disease.
References
Mahler, R. J., & Adler, M. L. (2009). Type 2 Diabetes Mellitus: Update on Diagnosis, Pathophysiology, and Treatment. The Journal of Clinical Endocrinology and Metabolism
Scheen, A. (2003). Pathophysiology of Type II Diabetes. Acta Clinica Belgica , 335-41.
Wondlfraw, H. (2015). Diabetes and Metabolism. J Diabetes Metab .
