In this article we will discuss about the Diabetes Mellitus:- 1. Types of Diabetes Mellitus 2. Treatment of Diabetes Mellitus 3. Complications 4. Changes.
Types of Diabetes Mellitus:
1. Primary Idiopathic or Essential Diabetes:
Diabetes mellitus means the hyperglycemia due to lack of insulin. This also takes place due to the over-production of other hormones, e.g., glucagon, hormones of the anterior pituitary, adrenal and thyroid which are antagonists to insulin or due to increased production of insulinase which inactivates insulin. In India, males are more prone to diabetes mellitus than females.
Classification:
Primary diabetes is classified into the following subgroups, depending on the degree of severity of the disease:
(a) Potential diabetic (pre-diabetic):
The individual with normal glucose tolerance test but with a family history of the disease.
(b) Latent diabetic (suspected diabetic):
The individual with a normal glucose tolerance test but has a diabetic type of glucose tolerance curve after cortisone administration, pregnancy or severe infection.
(c) Asymptomatic diabetic (chemical diabetic):
The individual with a diabetic glucose tolerance curve but without signs of diabetes.
(d) Clinical diabetic (overt diabetic):
(i) Juvenile-onset type,
(ii) Adult or maturity onset type.
Juvenile-onset type:
(i) This condition develops during the first 40 years of life in normal or less than normal body weight.
(ii) The symptoms become severe and if insulin treatment is delayed, ketoacidosis and diabetic coma develop.
(iii) Insulin secretion is very low.
(iv) The P-cells of pancreas are exhausted and the cells become atrophied, resulting in diabetes mellitus.
Adult or Maturity-onset type:
(i) This condition appears after 40 years of age who are obese.
(ii) This is a mild type of diabetes which can be controlled by diet and oral hypoglycemic drugs.
(iii) Insulin levels are lower than normal because the P-cells secrete less amount of insulin.
2. Secondary Diabetes:
Damage to pancreas:
In chronic pancreatitis and pancreatic carcinoma, the pancreatic destruction results in absolute insulin deficiency.
Presence of insulin antagonists:
Excess growth hormone secretion (Acromegaly) or excess glucocorticoid secretion (Cushing’s syndrome) act as antagonists to insulin.
Inhibition of insulin secretion:
The secretion of insulin by P-cells is inhibited by the excess secretion of epinephrine and thyroxine resulting in the breakdown of liver glycogen. A diabetes-like condition can be produced in experimental animals by injecting alloxan which is a pyrimidine derivative containing 400xO groups.
Alloxan destroys the β-cells of pancreas for which insulin production is inhibited. But the α-cells remain unaffected and the glucagon production remains intact. Dehydroascorbic acid, if injected in large doses, also destroys P-cells of pancreas and produces alloxan-type diabetes.
If growth hormone is repeatedly injected into experimental animals, the β-cells of the pancreas are stimulated to secrete insulin. The cells become hypertrophied and insulin secretion finally stops resulting in permanent diabetes mellitus in the animals.
Diabetic coma:
1. In case of diabetes, if the insulin is not taken and the diet is not controlled, diabetes becomes severe leading to diabetic coma.
2. In diabetic coma, there is ketonerriia and ketonuria.
3. The patient becomes semi-conscious or fully unconscious with dehydration.
4. The patient should be treated with soluble insulin (50 units) immediately followed by normal saline containing 10 per cent glucose intravenously.
5. The treatment should be controlled by frequent estimation of glucose in blood and urine every 30 minutes to make sure that blood glucose does not fall below normal level.
Treatment of Diabetes Mellitus:
1. Administration of oral anti-diabetic drugs like diabenese-which are not polypeptides-in moderate diabetes and insulin in severe diabetes.
2. High protein and low carbohydrate and fat diet are advisable. High protein meal serves as a prolonged source of carbohydrate without rapid hyperglycemic effect and it has protective effect on liver.
3. Exercise lowers the blood sugar level stimulating the P-cells of pancreas to liberate more insulin to act on blood sugar for glycogenesis and glycolysis.
4. The patient suffering from diabetes mellitus should have normal psychological affairs. The psychological stress and strain stimulate the alpha cells of pancreas and adrenal medulla causing the liberation of glucagon and epinephrine, respectively, which have glycogenolytic effect resulting in increased blood sugar (hyperglycemia).
5. A diabetic patient requiring more than 200 units/day of insulin is regarded as insulin resistant which is due to antigenic effect of insulin.
Complications of Diabetes Mellitus:
1. Preventable complications are due to infections, injury, neglect in treatment, unsuitable diet or alcohol.
2. Delayed complications occur in all diabetics after some years since the onset of the disease.
These are due to:
(a) Hyperglycemia leading to cataract of the lens of the eyes.
(b) Atherosclerosis involves coronary and peripheral arteries.
(c) Hypertension, particularly systolic hypertension, is more.
(d) Development of ulcers in the foot becomes a very difficult problem.
(e) Severity of nephropathy results in Proteinuria.
Changes in Diabetes Mellitus:
Carbohydrate Metabolism:
1. Diminished entry and oxidation of glucose in muscle and other tissues.
2. Decreased glycogen formation in liver and muscle.
3. Decreased synthesis of fat and increased breakdown of glycogen in liver.
Fat Metabolism:
1. Fats are mobilized from adipose tissue and fatty acids are oxidized producing large amounts of acetyl-CoA. Due to lack of carbohydrate metabolism, acetyl-CoA is not oxidized via TCA cycle. Hence, two molecules of acetyl-CoA condense to form ketone bodies.
2. The ketone bodies in large amounts in blood produce ketosis which leads to coma in severe diabetes mellitus.
3. Administration of insulin corrects the condition.
Protein Metabolism:
1. Since the energy is not available by oxidation of carbohydrate and fat, the breakdown of tissue protein occurs leading to negative energy balance. The synthesis of tissue protein from dietary proteins requires insulin. Due to lack of insulin, tissue protein is not formed from dietary protein.
The concentration of amino acids in blood and liver increases. The amino acids are deaminated in liver and glucose is produced from keto-acids by gluconeogenesis. The urea excreted more in urine. The body will be in negative nitrogen balance.
2. Administration of insulin corrects the condition. Insulin promotes oxidation of glucose to meet the energy needs and also the synthesis of tissue protein from dietary protein. Insulin also suppresses gluconeogenesis.