The Pathophysiology of Type 2 Diabetes Mellitus (NIDDM)

The patient with non-insulin dependent diabetes mellitus (NIDDM) has detectable levels of circulating insulin, unlike patients with insulin dependent diabetes mellitus (IDDM). The pathophysiology of type 2 diabetes mellitus is illustrated in the figure below.

figure : diabetes mellitus type 2 pathophysiology

The important elements of NIDDM can be divided into four different groups based on oral glucose tolerance testing:

1. Those with normal glucose tolerance.
2. Chemical diabetes mellitus (also called impaired glucose tolerance).
3. Diabetes mellitus with minimal fasting hyperglycemia (fasting plasma glucose less than 140 mg/ dl).
4. Diabetes mellitus in association with over fasting hyperglycemia (fasting plasma glucose greater than 140 mg/ dl).

A person with impaired glucose tolerance has hyperglycemia in spite of having highest levels of plasma insulin, indicating that their body are resistant to the action of insulin. In the progression from impaired glucose tolerance to diabetes mellitus disease, the level of insulin declines indicating that patients with NIDDM have decreased insulin production.

Insulin deficiency and insulin resistance are common in the average patients with NIDDM. Insulin resistance is the major cause of NIDDM. However, some researcher opines that insulin deficiency is the main reason because a moderate degree of insulin resistance is not good enough to cause NIDDM disease. Most patients with the common form of NIDDM have both defects.

Recent proof has demonstrated a role for a member of the nuclear hormone receptor super family of proteins in the etiology of type 2 diabetes mellitus (Read more : epidemiology and etiology of type 2 diabetes mellitus). Relatively new classes of medications used to raise the sensitivity of the body to insulin are the thiazolidinedione drugs. These compounds bind to and change the utility of the peroxisome proliferators-activated receptor g (PPARg).

PPARg is also a transcription factor and when activated, binds to another transcription factor known as the retinoid x receptor (RXR). When these two proteins are complexed a characteristic set of genes becomes activated. PPARg is a key regulator of adipocyte differentiation; it can induce the differentiation of fibroblasts or other undifferentiated cells into mature fat cells. PPARg is also involved in the synthesis of biologically active compounds from vascular endothelial cells and immune cells.

source:

The pathogenesis and pathophysiology of type 1 and type 2 diabetes mellitus by Ozougwu, J. C., Obimba, K. C., Belonwu, C. D., and Unakalamba, C. B.

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