Effects of pancreas transplantation on postprandial glucose metabolism

Article Abstract:

Patients with insulin-dependent diabetes mellitus, also called juvenile or type I diabetes, require injections of insulin to assist in the metabolism of blood sugar. However, these injections cannot adjust glucose metabolism to changing conditions with the same sensitivity as a functioning pancreas. Attempts have been made to treat diabetes with transplantation of the pancreas. However, the transplantation procedure transplants a pancreas with a kidney, and the pancreas empties its insulin product into the systemic blood stream. This contrasts with the normal pancreas, which releases insulin into veins travelling directly to the liver. Under normal circumstances, the liver removes half of this insulin. The liver's response to insulin is a critical part of glucose metabolism, since the liver removes excess glucose from the blood and stores it in the form of glucagon. Therefore, the transplanted pancreas may not return the glucose metabolism of a diabetic patient to normal. The ability of the body to properly metabolize glucose after a meal was examined in seven diabetic patients who had received pancreas-kidney transplants. The results were compared with seven nondiabetic patients who had received kidney transplants. This control group accounted for any influences that the transplantation procedure and the immunosuppressive drugs might have had. It was found that the diabetic patients had higher insulin levels both before and after a meal. This was apparently due to a decrease in the clearance of insulin rather than increased production. The production of insulin results in a protein fragment, C-peptide, as a by product. The amount of C-peptide was the same in both groups. Despite the higher blood insulin, the uptake and metabolism of glucose was similar in both groups, which suggests that the tissues of the diabetic patients were more resistant to the effects of insulin. The results indicate that even without supplying insulin directly to the liver, a transplanted pancreas can maintain sugar metabolism similar to that of control subjects. It is not known, however, what the long-term effects of greater amounts of insulin in the blood might be for these patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

Care and treatment, Diabetes, Diabetes mellitus, Type 1 diabetes, Glucose metabolism, Pancreas, Pancreas transplantation

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Insulin resistance - mechanisms, syndromes, and implications

Article Abstract:

This article reviews the mechanisms and implications of insulin resistance as well as the clinical conditions associated with it. Insulin resistance is defined as an abnormally low response by the body's tissues to insulin. Although the effects of this hormone are diverse, the term insulin resistance is usually used to refer to insulin's role in maintaining normal glucose (sugar) balance. This role is most apparent in liver, muscle, and fat, where insulin binds to a receptor protein (the gene for which has been identified) before exerting its effects. The receptor protein is described and diagrammed. Different physiological processes (such as fat production in fatty tissue) are stimulated in different organs by insulin because each organ contains a different complement of enzymes. Insulin resistance can be the result of defects in the insulin receptor (primary resistance); these defects may be due to genetic mutations. It may also be the result of other factors such as physiologic states or substances circulating in the blood (secondary resistance). The physiology of both kinds of resistance is reviewed. Insulin resistance produces clinical symptoms as a result of either insufficient or excessive insulin action. Genetic syndromes associated with severe insulin resistance include the Type A syndrome (defects in receptor expression or signalling capacity), leprechaunism, lipodystrophy, and Type B syndrome (in which autoantibodies to the insulin receptor are manufactured). Non-insulin-dependent diabetes (NIDDM) is the result of insulin resistance and a defect in the secretion of insulin by the beta cells in the pancreas. Insulin resistance is very common in obese people. The physiologic abnormalities associated with NIDDM are outlined. Other disorders in which insulin resistance is present include polycystic ovary syndrome and certain cases of high blood pressure. It is likely that the mild levels of insulin resistance seen in hypertension and cardiovascular disease will be a research focus in coming years. (Consumer Summary produced by Reliance Medical Information, Inc.)

Complications and side effects, Insulin resistance, Insulin receptors

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