Treatment of Insulin Dependent Diabetes Mellitus

"Juvenile onset" (type I) diabetes mellitus is caused by the destruction of insulin-producing B cells in the pancreas, necessitating replacement of insulin (daily dose approx. 40 U, equivalent to approx. 1.6 mg).

Therapeutic objectives are: (1) prevention of life-threatening hypergly-cemic (diabetic) coma; (2) prevention of diabetic sequelae (angiopathy with blindness, myocardial infarction, renal failure), with precise "titration" of the patient being essential to avoid even short-term spells of pathological hyperglycemia; (3) prevention of insulin overdosage leading to life-threatening hypoglycemic shock (CNS disturbance due to lack of glucose).

Therapeutic principles. In healthy subjects, the amount of insulin is "automatically" matched to carbohydrate intake, hence to blood glucose concentration. The critical secretory stimulus is the rise in plasma glucose level. Food intake and physical activity (increased glucose uptake into musculature, decreased insulin demand) are accompanied by corresponding changes in insulin secretion (A, left track).

In the diabetic, insulin could be administered as it is normally secreted; that is, injection of short-acting insulin before each main meal plus bedtime administration of a Lente preparation to avoid a nocturnal shortfall of insulin. This regimen requires a well-educated, cooperative, and competent patient. In other cases, a fixed-dosage schedule will be needed, e.g., morning and evening injections of a combination insulin in constant respective dosage (A). To avoid hypo- or hyperglycemias with this regimen, dietary carbohydrate (CH) intake must be synchronized with the time course of insulin absorption from the s.c. depot. Caloric intake is to be distributed (50% CH, 30% fat, 20% protein) in small meals over the day so as to achieve a steady CH supply—snacks, late night meal. Rapidly absorbable CH

(sweets, cakes) must be avoided (hyperglycemic—peaks) and replaced with slowly digestible ones.

Acarbose (an a-glucosidase inhibitor) delays intestinal formation of glucose from disaccharides.

Any change in eating and living habits can upset control of blood sugar: skipping a meal or unusual physical stress leads to hypoglycemia; increased CH intake provokes hyperglycemia.

Hypoglycemia is heralded by warning signs: tachycardia, unrest, tremor, pallor, profuse sweating. Some of these are due to the release of glucose-mobilizing epinephrine. Counter-measures: glucose administration, rapidly absorbed CH orally or 10-20 g glucose i.v. in case of unconsciousness; if necessary, injection of glucagon, the pancreatic hyperglycemic hormone.

Even with optimal control of blood sugar, s.c. administration of insulin cannot fully replicate the physiological situation. In healthy subjects, absorbed glucose and insulin released from the pancreas simultaneously reach the liver in high concentration, whereby effective presystemic elimination of both substances is achieved. In the diabetic, s.c. injected insulin is uniformly distributed in the body. Since insulin concentration in blood supplying the liver cannot rise, less glucose is extracted from portal blood. A significant amount of glucose enters extrahepatic tissues, where it has to be utilized.

Healthy subject B = Breakfast S = Snack L = Lunch D = Dinner N = Supper

Diabetic Lunch Meal
A. Control of blood sugar in healthy and diabetic subjects

Treatment of Maturity-Onset (Type II) Diabetes Mellitus

In overweight adults, a diabetic metabolic condition may develop (type II or non-insulin-dependent diabetes) when there is a relative insulin deficiency— enhanced demand cannot be met by a diminishing insulin secretion. The cause of increased insulin requirement is a loss of insulin receptors or an impairment of the signal cascade activated by the insulin receptor. Accordingly, insulin sensitivity of cells declines. This can be illustrated by comparing concentration-binding curves in cells from normal and obese individuals

(A). In the obese, the maximum binding possible (plateau of curve) is displaced downward, indicative of the reduction in receptor numbers. Also, at low insulin concentrations, there is less binding of insulin, compared with the control condition. For a given metabolic effect a certain number of receptors must be occupied. As shown by the binding curves (dashed lines), this can still be achieved with a reduced receptor number, although only at a higher concentration of insulin.

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