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Diabetes mellitus is a chronic disorder of carbohydrate, fat & protein metabolism.   Visit: Pancreatic Pathology Online

It causes long-term complications in blood vessels, kidneys, eyes and nerves leading to morbidity & mortality.

   Visit: Pathological changes in the eye in diabetes melllitus

Two types:

Type-I (Juvenile diabetes)-10 to 20%

Type-II (Adult onset)- 80 to 90%

Physiology of Insulin:

Insulin is synthesized & stored in the beta-cells of pancreatic islets. Rise of blood glucose stimulates beta-cells for immediate release of insulin and also initiate synthesis of insulin.

Insulin is a major anabolic hormone, necessary for:

i) Trans-membrane transport of glucose & amino acids.

ii) Glycogen formation in the liver & skeletal muscles.

iii) Conversion of glucose to triglycerides.

iv) Nucleic acid synthesis & protein synthesis.

Main metabolic function of insulin is to increase the rate of glucose transport into the striated muscles, myocardial cells, fibroblasts & fat cells. These tissues constitute two-thirds of the entire body weight.

Action of insulin is regulated by the “receptors of insulin” (Tyrosine kinase), which is present in the tissue cells.

 Initially “Glucose transport units” is translocated from Golgi apparatus to plasma membrane and facilitate cellular uptake of glucose.

Only feature of diabetes mellitus is the impaired glucose tolerance.

Glucose tolerance test:

In a normal person, ingestion of 75 Gms. of glucose after overnight fasting will raise the blood glucose, returning to normal within one hour. (maximum 140mg.%).

In a diabetic/potential diabetic, rise of blood glucose will be very high (more than 200 mg.%), and remain at that high level for several hours (2 hrs. or more).

This is due to the lack of insulin secretion by beta cells or lack of utilization of receptors in the target cells or both.

Pathogenesis:

Type-I :

This is due to severe or absolute lack of insulin caused by the reduction of beta-cell mass.

It develops in childhood and becomes severe at puberty.

Patient survives on the supply of insulin. Without insulin supply they develop keto-acidosis & coma.

Genetic factor, autoimmunity & immune mediated injury are implicated as the cause of beta-cell loss.

Type-II :

Two basic metabolic defects:

i) Primary factor is the impaired insulin release by beta-cells

ii) Debatable factor is the inability of the peripheral tissues to respond to insulin.

In addition to genetic factor following points are also considered in the pathogenesis of Type-II diabetes.

I. Obesity- 80 % of Type II diabetes are obese.  Weight loss and physical exercise reverse impaired glucose tolerence.

II. The protein “Amylon” is co-secreted with insulin by the beta-cells, in response to ingestion of food. Amylon accumulates in the pancreatic sinusoids around beta-cells in close contact with cell membrane, and ultimately forms amyloid. Amyloid may contributes to beta-cell-non- responsive to glucose.

Long-term complications of diabetes mellitus (mostly after 10 to 15 years):

1. Arteries:  Atherosclerosis - i) Myocardial infarct   ii) Gangrene foot.

2. Basement membrane of small vessels:  Microangiopathy - cerebral infarct & hemorrhage.

3. Kidney: Diabetic nephropathy.

4. Retina: Retinopathy ; Cataract ; Glaucoma.

5. Nerves:  Diabetic neuropathy - peripheral symmetric neuropathy of hands & feet. Autonomic neuropathy - disturbance of bladder & bowel functions.    

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