Pathogenesis of NIDDM
(NIDDM) is caused by an imbalance between insulin sensitivity and insulin secretion. Both longitudinal and cross-sectional studies have shown that early abnormalities that can be detected in NIDDM are impaired in the body’s ability to respond to insulin. Because the pancreas is able to increase insulin secretion appropriately to offset insulin resistance, glucose tolerance remains normal. However, over time, a beta cell fails to maintain high insulin secretion rate, and relative insulin deficiency (ie, insulin resistance) leads to impaired glucose tolerance and eventually diabetes progression.
The cause of pancreatic “exhaustion”
pancreatic “exhaustion” is still unknown but may be linked to the effect of glucose toxicity in a genetically engineered beta-cell. Information on loss of insulin secretion in phase I, change in insulin release pulses and insulin-enhancing. insulin secretion was discussed as it related to the function of beta cells modified in NIDDM.
Insulin resistance in NIDDM
Insulin resistance in NIDDM includes both hepatic and peripheral tissues. In the case of the postabsorptive state, the production of hepatic glucose is normal or increased, despite the presence of fasting hyperinsulinemia, while the glucose absorption efficiency is lower in tissues. In response to insulin that is secreted internally or administered externally, hepatic glucose production fails naturally and glucose absorption in the muscles is reduced. The accelerated rate of total hepatic glucose production is due to increased blood sugar. In muscle, many cellular abnormalities were described in insulin work including the impaired activity of insulin receptors tyrosine to insulin receptors, decreased glucose transmission, decreased glycogen synthetase enzyme and hydrogenase peroxides. Anomalies account for disorders in the two major intracellular pathways to dispose of glucose, glycogen synthesis, and glucose oxidation.
Early stages of NIDDM
In the early stages of NIDDM, the main defect is the inability of insulin to promote glucose uptake and storage such as glycogen. Other doable mechanisms to clarify insulin resistance include increased fat oxidization, altered muscle capillary density/ fiber type/ blood flow, impaired intravenous insulin transport, increased amylene, calcitonin gene-related peptide levels, and glucose toxicity.