Type 2 Diabetes Mellitus [Non Insulin Dependent DM]

Type 2 Diabetes  mellitus: pathophysiology and prevention of T2DM

Type 2 diabetes  mellitus is very common disease in the world . These type of diabetes high rate thab other type of Diabetes and common in obese and inactive population.

Type 2 diabetes mellitus

Type 2 diabetes  mellitus  occurs due to insulin resistance, and or abnormal insulin secretion, some study show insulin secretion begins inadequate.

Type 2 diabetes mellitus is described by three pathophysiological abnormality.

  1.  impaired insulin secretion
  2.  peripheral insulin resistance
  3.  excessive hepatic glucose production 

Type 2 diabetes mellitus  is very common in obese person due to adipocytes secrets some chemical substance such as: Leptin, Tumor necrosis factor alpha, FFA or Free Fatty Acids, Resistin and adeponectin etc. That modulates too much insul8n secretion and may also contribute to the insulin resistance.

In fast stage of T2DM or Type 2 Diabetes mellitus glucose tolerance normal in spite of insulin resistance due to the beta cell of pancreas compensate by raising insulin output.  As compensatory hyperinsulinaemia and insulin resistance gradually progress, the pancreatic islet in individuals are not able to sustain.

Metabolic abnormalities in Non-insulin dependent diabetes mellitus  or  type 2 diabetes mellitus :

Insulin resistance : 

Insulin resistance occurs on insulin is decreased on peripheral target tissue ( specially liver and muscle tissue). This is prominent  feature of T2DM or type 2 diabetes mellitus.

Insulin resistance is relative in T2DM or NIDDM (Non insulin dependent diabetes mellitus) normal concentration of seurm insulin normlise the plasma glucose. The curves of insulin-dose response, exhibit a rightward shift which are indicating decreased sensitivity, and reduce highest response,that is decrease maximum glucose utilization 30 t0 60 % lower than normal glucose level, impair glucose utilization by insulin sensitive tissue and increase glucose output in liver which is account for increased FPG levels, where as decrease peripheral glucose usage result in postprandial hyperglycaemia.

The pathogenesis of insulin resistance is focused on a PI-3 kinase signalling error, that decreases translocation of GLUT4(glucose transporter) to the plasma membrane among other defect/abnormality. Another emerging theory proposes which increased level of Free fatty acids or FFA a classic feature of obesity, that responsible to the pathogenesis of Type 2 Diabetes mellitus , FFA can impair sugar utilization in muscle(skeletal muscle),increase glucose production by the hepatocyte, an impair pancreatic beta cell physiology.

Impaired insulin secretion:

insulin secretion firstly increases as a result of insulin resistance to maintain normal glucose tolerance.  Chronic hyperglycaemia (increase glucose level in blood than normal level) paradoxically hampers islet cell function due to to glucose toxicity in pancreatic beta cell an leads to worsening hyperglycemia.

In addition, elevation of FFA level in blood and dietary fat may contribute to impair islet cell function.

Increased hepatic glucose production 

1. Suppress gluconeogenesis

2. Decrease glycogen storage.

Prevention of type 2 diabetes mellitus :

Type 2 diabetes mellitus is prevented or delayed by some ways such as-


2.exercise for 30 minutes / day  five times / week.

3. Some study sgow Ramipril and provastating reduced the number of new diabetes case.

Risk factors of type 2 DM :

  • Obesity
  • Positive family history
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