Insulin hormone is a chemical messenger secreted by the beta cells of pancreas, which allows the body to utilize glucose from carbohydrates and convert the extra glucose into energy for future use. Insulin maintains the sugar balance in the body by keeping blood sugar level from getting too high (hyperglycemia) or too low (hypoglycemia). Glucose obtained from the food does not directly convert into energy. When we eat food, the blood sugar levels rise and beta cells of the pancreas are then signaled to release insulin into the blood stream. Then the released insulin absorbs the sugar by binding to insulin receptors and converts excess of the sugar in glycogen (energy), which get stored in the liver. It has dual mode of action i.e. an excitatory one and an inhibitory one:
- It stimulates glucose uptake and lipid synthesis.
- It inhibits the breakdown of lipids, proteins and glycogen, and inhibits the glucose pathway (gluconeogenesis) and production of ketone bodies (ketogenesis).
Sometimes glucose metabolism gets impaired, characterized by hyperglycemia which may be due to either pancreas does not secrete insulin or insulin receptors do not respond to the insulin properly. This condition is also known as diabetes mellitus. So it becomes essential to take the insulin externally.
Endogenous insulin (that which is found naturally in the body) acts on the principle of feedback. If glucose levels rise when eating something sweet, insulin secretion is increasing, too.
Exogenous insulin Patients suffering from Type I Diabetes are treated by doses of insulin produced by sources external to the body of the patient and administered in addition to the endogenous insulin. This type of insulin produced by sources other than human body is called exogenous insulin.
RISKS OF INSULIN INTAKE
When the insulin metabolism in the body gets impaired, then sometimes it becomes necessary to provide it externally. But there are certain side effects of insulin therapy. These are:
when blood sugar levels fall below the normal limits. If the insulin dose is high, then the blood glucose levels may decrease abruptly and if remain untreated may lead to seizure, death or coma. Hypoglycemia is associated with increased plasma dopamine, epinephrine and plasma renin activity. Signs and symptoms of low blood sugar are feeling weak, drowsy, or dizzy, experiencing shakiness, confusion, anxiety, nausea, or headache, blurred vision and loss of consciousness.
Weight gain during insulin therapy is the common problem that may be presented as edema. Weight gain may be associated with abrupt restoration of glucose control in a patient whose control was poor previously. It may be due to more efficient use of calories during insulin therapy, suggesting additional benefits of dietary and exercise modifications. Insulin therapy leads to increase in body fat as a result of the elimination of glycosuria and reduction in 24-hour energy expenditure which results in an insulin-associated decrease in triglyceride or free fatty acid cycling, glucose and protein metabolism and hence weight gain.
Insulin therapy may also cause renal complications such as decreased renal plasma flow, glomerular filtration rate and significantly increased urinary albumin excretion rate. However, these changes are reversible upon resolution of hypoglycemia. Therefore changes in kidney function during insulin-induced hypoglycemia may result from direct stimulation of the efferent sympathetic nerves to the kidney and hormonal counter regulatory mechanisms.
Patients on insulin therapy may experience allergic reactions in response to insulin. Sometimes these reactions may be minor like hives or itchiness, but sometimes may be life threatening such as swollen tongue, tightness in chest, difficulty breathing, dizziness or fainting and may need hospitalization. These reactions may be localized (such as rashes at the injection site) or systemic (itching, redness, muscle cramps.).
Hypophosphatemia is one of the major metabolic complications of insulin therapy, particularly in the patients who are on treatment of diabetic ketoacidosis (DKA) as insulin increases intracellular phosphate transport. Sometimes hypokalemia and hypomagnesaemia may also occur during insulin therapy.
Skin related complications
Other adverse effects of insulin include loss or overgrowth of fat tissue at injection sites. Repeated use of the same injection site increases the risk of lipoatrophy — with time, patients learn that these areas are relatively pain free and continue to use them. However, the absorption of insulin from lipoatrophic areas is erratic leading to frequent difficulties in achieving ideal blood glucose control.
Lipohypertrophy is the most common cutaneous complication of insulin therapy.
Exogenous insulin interactions include alpha and beta-blockers and other high blood pressure drugs, steroids, hormone-based contraceptive pills, asthma and cold medications, aspirin, thyroid medications, and even other diabetes drugs.
Administration of exogenous insulin provides a different insulin gradient than that occurring after endogenous insulin secretion. Endogenous insulin secretion acts initially on the liver where a major portion of it is taken up and <50% reaches the peripheral tissues. Exogenously administered insulin must circulate through the peripheral tissues before it can reach the liver; therefore, peripheral hyperinsulinemia is necessary to attain adequate insulin to regulate the liver. Another downside of insulin therapy is the need to increase the dose and the regimen complexity with time, the increase in severe hypoglycemia, and the potential increase in mortality as well as the potential increased risk for specific cancers.
It becomes all the more important for medical practitioner, patients and other stake holders to USE EXOGENOUS INSULIN INTELLIGENTLY, CAUTIOUSLY & JUDICIOULY.