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At least 19 recordsLinked to original sources
PubMed1978

Insulin resistance, insulin insensitivity, and insulin unresponsiveness: a necessary distinction.

Insulin resistance may be said to exist whenever normal concentrations of insulin produce a less than normal biologic response. Hormone resistant states may be divided into those due to decreased sensitivity to a hormone (i.e., a shift in the dose-response curve to the right), those due to a decrease in the maximal response to the hormone, and those that are combinations of decreased sensitivity and decreased responsiveness. This distinction is important, since the molecular mechanisms that produce these various forms of insulin resistance may be different. Disorders associated with alterations prior to the interaction of insulin with its receptor are more likely to produce states of decreased sensitivity, where disorders associated with alterations at the intracellular steps in insulin action are more likely to produce decreased responsiveness. Alterations in the insulin receptor itself may produce either, although most frequently changes in receptor affinity as well as in receptor number will be manifest as changes in sensitivity. This is a result of the large number of "spare" receptors for most insulin effects. In many studies, the differential diagnosis between states of altered sensitivity and altered responsiveness is difficult due to the complicated and interrelated nature of the metabolic pathways of insulin action. This is frequently further complicated by incomplete data (usually the result of studying response to only one hormone concentration rather than a full dose-response) and change in rates of basal metabolism in different diseases. The latter is a particularly difficult problem, but it is clear that use of "fold-" or "percent-" stimulation may further obscure the nature of the change when complete data are not provided. With more precise use of these terms and a more complete understanding of insulin action, it will be possible to begin to segregate the roles of the various prereceptor, receptor and postreceptor factors that are involved in producing the differing patterns of metabolism observed in disease.

Adipose Tissue↗
PubMed1977

[New data in the domain of insulin resistance].

Insulin resistance may occur to a variable degree in various disease conditions. Obesity is frequently accompanied by insulin resistance. The anti-insulin antibodies in patients treated with insulin are a classical cause, but in fact rare. Insulin resistance of variable degree may accompany certain metabolic disorders, e.g. diabetic ketosis and acidosis, and endocrine disorders, e.g. Cushing's syndrome, acromegaly. The measurement of insulin receptors brings a new dimension to the investigation of insulin resistance. Insulin receptors are reduced in number during obesity. The abnormality, partly responsible for insulin resistance, is reducible by reduction in calory intake. Circulating insulin anti-receptor antibodies appear to be responsible for insulin resistance which is particularly marked although exeptional, in nonobese diabetics with acanthosis nigrans and auto-immune symptoms.

Diabetes Mellitus↗
PubMed1979

Primary defect of insulin receptors in skin fibroblasts cultured from an infant with leprechaunism and insulin resistance.

Insulin binding to insulin receptors, on skin fibroblasts established in culture from an infant with insulin resistance and clinical features of leprechaunism was markedly decreased in comparison with cultures from an age-matched control. By contrast, the binding of epidermal growth factor, a polypeptide growth factor chemically unrelated to insulin, to patient's and control fibroblasts was indistinguishable. The selective defect in insulin binding to patient's fibroblasts was reflected in an impaired ability of insulin to stimulate 2-deoxyglucose uptake. These results most likely indicate a primary genetic defect of insulin receptors.

Biological Transport↗
PubMedDate not supplied

[Content of growth hormone in the blood in insulin-resistant and insulin-sensitive patients with diabetes mellitus during compensation].

The growth hormone and blood sugar level was determined during compensation in 38 insulin-resistant and in 48 insulin-sensitive patients with diabetes mellitus, on fasting stomach and after an intravenous injection of insulin. The insulin-resistant patients were given insulin in the amount of 100 and more Units per 24 hours at the period of achievement of compensation. In the insulin-sensitive patients with diabetes mellitus during the compensation the growth hormone level in the blood serum on fasting stomach displayed a significant reduction; no significant change occurred in the insulin-resistant patients. On the achievement of normoglycemia a high growth hormone level in the patients with insulin-resistant forms of diabetes mellitus was probably conditioned by disturbance of the adaptation processes, and possibly also by the preservation of decreased glucose metabolism at the cell level. Under these conditions the growth hormone apparently produced a diabetogenic action and prevented stable compensation creating conditions for the preservation of insulin resistance.

Adolescent↗
PubMedDate not supplied

[Dynamics of levels of growth hormone and free fatty acids in the blood, and catecholamines in the urine of insulin-resistant and insulin-sensitive diabetes mellitus patients during insulin hypoglycemia].

The changes in the content of STH and FFA in the blood and of catecholamines in the urine under the effect of insulin hypoglycemia were studied in 28 insulin-sensitive and 40 insulin-resistant patients suffering from diabetes mellitus. Patients with diabetes mellitus who needed 100 or more insulin units per 24 hours for compensation of the affection were referred to the insulin-resistant ones. In these cases a less pronounced elevation of the blood STH level and of urinary catecholamines was noted in response to insulin hypoglycemia. This was accompanied by a considerable reduction of lipolysis in the insulin-resistant patients. It is suggested that in the insulin-resistant patients, due to reduction of the STH and catecholamine stimuli, FFA is incapable of providing the necessary energy balance at the cellular level in insulin insufficiency. This accounts for an increased requirement in exogenous insulin in the insulin-resistant patients with diabetes mellitus. Reduction of the FFA and catecholamine reserves in the insulin-resistant patients suffering from diabetes mellitus is postulated to be one of the main factors in the resistance pathogenesis.

Adolescent↗
PubMedDate not supplied

Insulin-resistant diabetes with insulin receptor autoantibodies in a male patient without acanghosis nigricans.

A 51-yr-old, nonobese, male patient presented with hyperglycemia and a recent 40-pound weight loss. Severe insulin resistance was documented in studies in which high amounts of insulin were infused using the Biostator GCIIS. Diabetic control was finally achieved with subcutaneous injections of 470 U of insulin per day. Positive laboratory findings included a mild pancytopenia, elevated erythrocyte sedimentation rate, decreased C3 and properdin, and increased IgA. Antinuclear or other autoantibodies were not present. Insulin antibody levels were within the range usually present in insulin-treated diabetic patients. Acanthosis nigricans was not present. Incubation of the patient's serum with IM-9 lymphoblastoid cells revealed that an insulin receptor antibody was present in a serum dilution of 1:80. Insulin-resistant diabetes mediated by insulin receptor antibodies may present in patients with immunologic findings but without overt dermatologic stigmata.

Acanthosis Nigricans↗
PubMed1978

Insulin resistance due to a defect distal to the insulin receptor: demonstration in a patient with leprechaunism.

We have studied a 2-year-old girl with acanthosis nigricans, glucose intolerance, marked hyperinsulinemia, and somatic features characteristic of the leprechaunism syndrome. Circulating plasma insulin levels were increased up to 50-fold and the patient showed a blunted hypoglycemic response to an injection of exogenous insulin (0.2 units/kg), indicating the presence of severe insulin resistance. Insulin purified from the patient's plasma was normal on the basis of chromatographic, electrophoretic, and immunologic criteria. Furthermore, the purified insulin competed effectively with (125)I-labeled insulin for binding to insulin receptors on cultured IM-9 lymphocytes and rat fat cells and also exhibited normal biological potency when tested on rat fat cells. Anti-insulin receptor and anti-insulin antibodies were not detected in the patient's plasma, and plasma levels of glucagon, growth hormone, and cortisol were normal. Insulin binding to the patient's circulating monuclear leukocytes was only slightly depressed into the low normal range and could not account for the severe insulin resistance. Studies on the patient's fibroblasts revealed normal levels of insulin receptors but a total absence of insulin's ability to accelerate glucose transport. Because rates of glucose transport and metabolism were normal in the basal state in the absence of insulin, we conclude that this patient's insulin resistance is due to an inherited cellular defect in the coupling mechanism between occupied insulin receptors and the plasma membrane glucose transport system.

Autoantibodies↗
PubMed1978

Insulin resistance, acanthosis nigricans, and normal insulin receptors in a young woman: evidence for a postreceptor defect.

We have previously described a group of young females with virilization, acanthosis nigricans, insulin resistance, and markedly decreased binding of insulin to its receptor (syndrome of insulin resistance and acanthosis nigricans type A). The present report concerns a 15-yr-old female with clinical features indistinguishable from the type A patients, including virilization, acanthosis nigricans, and extreme resistance to endogenous and exogenous insulin. Insulin levels were 400-650 microU/ml while fasting and were over 2200 microU/ml when stimulated. Proinsulin was less than 10% of the total immunoassayable insulin. In distinct contrast to the type A patients, insulin receptors on cells from this patient were entirely normal on the basis of specificity, negative cooperativity, affinity, concentration, and interaction with antiinsulin receptor antibodies. These findings suggest the presence of an intracellular defect as the cause of the observed insulin resistance.

Acanthosis Nigricans↗
PubMed1977

Insulin resistance and new insulins.

Insulin therapy is required in the treatment of diabetic patients manifesting persistent ketosis. Although most patients in this category are young, many elderly diabetics fall into this group. In patients without ketosis, the indications for insulin therapy are less easy to define. In general, insulin is required if blood glucose levels cannot be maintained below 200mg/100ml following adequate diet, attainment of ideal body weight, and oral hypoglycaemic therapy.

Diabetes Mellitus↗
PubMedDate not supplied

Accelerated insulin degradation: an alternate mechanism for insulin resistance.

We have examined insulin and glucagon degrading activities of muscle and fat tissues in 11 subjects (4 lean controls, 3 insulin-resistant obese subjects, 2 non-insulin-dependent diabetic subjects, and 2 insulin-treated diabetic subjects) and correlated degrading activity with (1) basal insulin level and (2) state of insulin resistance. We found hyperinsulinemia and insulin resistance to be significantly correlated with accelerated insulin and glucagon degrading activity. Weight reduction in an insulin-resistant obese patients results in parallel reduction in both basal insulin level and insulin-glucagon degrading activity. These data are consistent with the hypothesis that an alternative mechanism for insulin resistance may be an accelerated insulin degradation at the level of target tissues.

Adipose Tissue↗
PubMed1979

A case of insulin resistant diabetes with possible antibodies to insulin receptors.

A case of a 19-year-old, non-obese female with insulin resistant diabetes mellitus and polycystic ovary syndrome was reported. The maximal insulin requirement attained 360 units per day, but a satisfactory control of diabetes did not follow. The patient's serum contained not only anti-insulin antibodies, but also possible anti-insulin receptor antibodies which were demonstrated by the 125I-insulin binding test using insulin receptors derived from human placental plasma membrane. The insulin resistance in this case was assumed to be caused primarily by possible blocking antibodies to insulin receptors and partly by anti-insulin antibodies because of the following observations. First, high serum free insulin (165 microunits/ml) without hypoglycemia indicates the presence of insulin resistance due to other factors than antiinsulin antibodies. Second, the titer of 125I-insulin binding capacity of serum was not unusually higher than those seen in chronically insulin-treated diabetics. Third, immunologically heterospecies insulin (fish insulin) was also ineffective. The clinical features such as absence of ketoacidosis and association with polycystic ovary syndrome resemble those of an unique diabetic syndrome reported previously though acanthosis nigricans and endogenous hyperinsulinemia were not found in this case. Her insulin resistance remitted spontaneously and over the next 18 months' observation, her diabetes remained regulated without insulin therapy.

Adult↗
PubMed1977

Development of insulin resistance in normal dogs following alloxan-induced insulin deficiency.

Insulin resistance was measured in 16 normal dogs by a method involving the continuous intravenous infusion of epinephrine, propranolol, glucose and insulin. With this approach, endogenous insulin secretin is inhibited, similar steady state levels of exogenous insulin are achieved in all doags, and the resultant steady state plasma glucose level provides a direct estimate of the ability of insulin to dispose of the infused glucose load. Thus, the higher the steady state plasma glucose level, the more the insulin resistance. Different amounts of alloxan were then administered to these dogs in order to produce insulin deficiency of varying degrees. Insulin resistance was then measured again in each dog. The results indicated that insulin resistance did not develop in dogs with only a moderate degree of insulin deficiency (fasting plasma glucose levels less than 150 mg/100 ml). On the other hand, a significant degree of insulin resistance developed in dogs with severe insulin deficiency (fasting plasma glucose greater than 150 mg/100 ml). Furthermore, the insulin resistance that developed in dogs with severe insulin deficiency could be returned to normal with insulin replacement for one week. These results indicate that insulin resistance can occur as a secondary manifestation of insulin deficiency.

Animals↗