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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Eleven patients with type II diabetes mellitus were studied prior to, and after short- (10 days) and long-term (6 months) glibenclamide treatment. 2. A marked decrease in glucose level was observed after short- and long-term therapy using the oral glucose tolerance test (OGTT) and diet test (DT). 3. After short-term therapy, insulin level increased by 52.5% with the OGTT and by 37.6% with the DT; after long-term therapy, the increases were 78.6% and 69.5%, respectively. 4. Insulin binding to erythrocytes was unchanged by short- or long-term glibenclamide therapy. 5. These data suggest that the hypoglycemic effect of glibenclamide results from an increase in insulin secretion and that extrapancreatic actions at the receptor or post-receptor level are not necessarily involved.
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PMID:The effects of glibenclamide treatment on insulin secretion and on insulin binding to erythrocytes in type II diabetes mellitus. 314 Sep 92

Insulin binding to erythrocyte receptors was studied in 36 newly diagnosed male subjects with NIDDM, treated with diet alone (Group I; n = 10) or diet + glibenclamide (Group II; n = 12) or diet + glibenclamide + metformin (Group III; n = 14). Fourteen matched non-diabetic subjects were also studied as controls. Initially, mean (+/- SD) specific insulin binding was lower in NIDDM patients than in controls (p less than 0.001), due to decreased receptor number and affinity. Control of diabetes with short-term therapy (10 +/- 2 days) resulted in significantly increased specific insulin binding in Groups II and III (p less than 0.001). A marginal increase was observed in Group I (p less than 0.01). The improved insulin binding observed in Group II and III patients after short-term therapy was maintained even after long-term therapy (9 +/- 1 months). Analysis of the insulin binding data by Scatchard plots and average affinity profiles indicated increased receptor number and affinity after short-term therapy. However, changes in affinity were reversed with long-term therapy in Groups II and III and the predominant effect appeared to be an increase in the number of binding sites.
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PMID:Rapid improvement in insulin binding to erythrocyte insulin receptors in non-insulin-dependent diabetes mellitus during therapy. 314 5

Insulin resistance was assessed by Insulin Tolerance Test (ITT) in 12 patients with FCPD, 10 with NIDDM and 12 age and sex matched control subjects. The mean BMI of the FCPD was lower than the NIDDM and control groups (P less than 0.001). There was no significant difference between the mean fasting plasma glucose or HbA1 between the FCPD and NIDDM patients. The mean fasting C-peptide of the FCPD group was significantly lower than the NIDDM and control groups (P less than 0.001). The mean glucose disposal rate (KITT) was 5.57 +/- 2.28 in the control group, 2.15 +/- 2.00 in the FCPD and 1.77 +/- 0.91 in the NiDDM group (P less than 0.001, control vs FCPD and NIDDM). The difference in KITT between FCPD and NIDDM groups was not significant statistically. The data suggests that patients with FCPD have evidence of insulin resistance and this is similar to that seen in NIDDM patients.
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PMID:Insulin resistance in Fibrocalculous (tropical) pancreatic diabetes. 322 Apr 51

A study of non-infective skin associations of diabetes mellitus was conducted on 100 consecutive outpatient diabetics over a 3-month period. 10 were insulin-dependent diabetics (IDDM), 24 insulin-requiring and 66 non-insulin dependent diabetics (NIDDM). A total skin evaluation was done for each patient with skin biopsy whenever appropriate. Twenty-three patients had diabetic dermopathy; the frequency of retinopathy in this group (39.1%) is significantly higher than that without diabetic dermopathy (6.9%) (p less than 0.001). There were 20 instances of cutaneous complications of therapy; 10 had insulin lipodystrophy (29.4% of 34 insulin users). Twelve patients, 8 of whom were overweight, had acanthosis nigricans. There were 6 Indians among them and all the patients had NIDDM. Eight had xanthelasma. Vitiligo occurred in 3.3% of those with NIDDM. Classical scleredema diabeticorum and cheiroarthropathy occurred in 2% of patients. One patient had atypical granuloma annulare. There was a higher incidence of xanthelasma in our study compared with studies done previously. Insulin lipodystrophy and acanthosis nigricans in the absence of classically described syndromes of insulin resistance seem to be fairly common phenomena and merit further investigation locally.
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PMID:Non-infective skin associations of diabetes mellitus. 322 40

Non-insulin-dependent diabetes (NIDDM) is a major cause of premature morbidity and mortality among adults. Macrovascular disease of coronary and peripheral vessels is the primary cause of death in these patients. Numerous experimental and epidemiologic studies have suggested that hyperinsulinemia accelerates the development of atherosclerosis. In experimental models, insulin promotes diet-induced lesion development and overrides lesion regression and estrogen protection against atherosclerosis. Local hyperinsulinemia induced by selected arterial infusion accelerates atherosclerosis in the perfused artery. Insulin has been shown to stimulate subintimal smooth muscle and fibroblast cells in culture, and to increase the uptake and local synthesis of lipid by these cells. Insulin may also induce inhibition of fibrinolysis. Several prospective studies performed on nondiabetic patients show that either fasting or postprandial insulin levels are a sensitive predictor of the development of coronary disease independent of other risk factors. Two recent studies in NIDDM patients confirm this finding and suggest that glycemic control may not be a significant factor in the development of macrovascular disease. Diseases of carbohydrate tolerance, ie, NIDDM, impaired glucose tolerance, obesity, are frequently associated with elevated circulating insulin levels, either physiologically or secondary to treatment. Given the high prevalence of cardiovascular disease in these populations, modifying therapy to minimize hyperinsulinemia should be an important consideration in a treatment program. Use of oral agents such as glipizide or gliclazide, which induce less diurnal hyperinsulinemia, may be advantageous when compared to traditional oral agent or insulin therapy.
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PMID:Atherosclerosis in diabetes: the role of hyperinsulinemia. 327 13

Sera from 80 subjects with IDDM and NIDDM, together with sera from 20 patients with miscellaneous autoimmune conditions and 20 healthy adult subjects were tested for insulin receptor antibodies by (1) inhibition of 125I-insulin binding to EBV-transformed lymphoid cells, and by (2) immunoprecipitation of solubilized insulin receptors in the presence of an excess of mono-specific anti-human IgG or IgM; this test allowed the assessment of the class of antibody activity. Anti-insulin antibodies in the sera were also measured using a double antibody technique. Anti-insulin receptor antibodies were found in 13 of 33 subjects with IDDM and six of 47 with NIDDM. These were principally in the IgM class, and in both groups of diabetics there was a good correlation between % inhibition of insulin binding to intact cells, and % of antibody precipitated by IgM (P less than 0.001), but not by IgG (P greater than 0.1). There was also a good correlation between the % inhibition of insulin binding to intact cells and the daily dose of insulin used in treatment (P less than 0.001). Insulin antibodies were found in seven of 33 subjects with IDDM and six of 12 with NIDDM, all of whom were on insulin treatment. These six subjects were the only ones with NIDDM who also had anti-insulin receptor antibody activity, suggesting that such antibodies may represent auto-anti-idiotype activity. This study shows that autoimmunity in insulin dependent (Type I) diabetes is not limited to islet cells and that such patients also develop antibodies to the insulin receptor. While three out of five patients with relative insulin resistance (requirement greater than 90 u/day) also showed evidence of insulin receptor antibody activity, the clinical significance of these antibodies has yet to be determined.
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PMID:Insulin receptor antibodies in diabetes mellitus. 328 Jan 81

Diabetes mellitus is composed of a heterogeneous group of disorders characterized by high blood glucose levels. Four major types of diabetes have been defined by the National Diabetes Data Group. Insulin-dependent diabetes (IDDM), also called type I diabetes, is characterized by abrupt clinical onset, insulinopenia, proneness to ketosis even in the basal state, and dependence on exogenous insulin to sustain life. Non-insulin-dependent diabetes (NIDDM), also called type II diabetes, may remain relatively asymptomatic for years. Insulin levels may be normal, lower than normal, or elevated as a consequence of insulin resistance. Ketosis is not part of the general clinical picture except in times of metabolic stress, although the classic complications of diabetes can be expected to develop in long-duration diabetics. Gestational diabetes (GDM) refers to the recognition of abnormal glucose intolerance in pregnancy, although unrecognized abnormal tolerance may indeed have predated the pregnancy. Rates of macrosomia are higher than in non-GDM pregnancies, but fetal mortality and congenital anomalies appear to be no greater than in the general population. Other types of diabetes include a number of diverse conditions in which glucose intolerance is a feature and in which it may be etiologically related. Impaired glucose tolerance (IGT) is a class that encompasses persons whose glucose tolerance is intermediate between normal and diabetic. These individuals do not manifest the microvascular complications of diabetes, but they appear to have higher rates of macrovascular disease associated with the known cardiovascular risk factors. Two statistical risk categories have also been defined that replace the older terms prediabetes, potential diabetes, and latent diabetes. Diabetes can be diagnosed by the presence of classical signs and symptoms of diabetes and unequivocally elevated blood glucose levels; by a fasting plasma glucose greater than or equal to 140 mg/dl; or by an abnormal oral glucose tolerance test, with a venous plasma glucose value greater than or equal to 200 mg/dl at 2 hours after 75 grams oral glucose, being a hallmark criterion for diabetes. For the latter two criteria, the abnormality should be reconfirmed at a later occasion before a definitive diagnosis of diabetes is made. The oral glucose tolerance test has been standardized at a 75-gram glucose (or carbohydrate equivalent) load, given in the morning after an overnight fast. Glucose should be determined for two hours after administration of the challenge.
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PMID:Classification and diagnostic criteria for diabetes mellitus and other categories of glucose intolerance. 329 Sep 16

Insulin action at the target tissue level in non-insulin dependent diabetes mellitus was investigated using human adipose tissue. Specific adipocyte receptor binding of insulin and the effects of the hormone on glucose oxidation and lipolysis were determined in subcutaneous adipose tissue. The study included 25 patients with untreated non-insulin dependent diabetes mellitus and 38 healthy control subjects matched for age, sex and body weight. Insulin stimulated adipose tissue glucose oxidation in a dose-dependent way in the control subjects. On the other hand, a marked inhibition of this insulin effect was observed in the diabetics. A weak stimulation was observed only at high unphysiological hormone concentrations [greater than or equal to 0.7 nmol/l] and the maximal insulin response was 6 times lower than that in the control subjects. However, neither specific insulin receptor binding nor the antilipolytic effect of insulin were inhibited in diabetes. Similar results with insulin binding and the metabolic effects of insulin were obtained in non-obese normoinsulinemic diabetics as compared to moderately obese hyperinsulinemic diabetics. It is concluded that adipose tissue insulin resistance in non-insulin dependent diabetes mellitus only involves glucose metabolism and not antilipolysis. Furthermore, it may solely be due to postreceptor defects in insulin action and seems not to be influenced by obesity or oversecretion of insulin.
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PMID:Insulin receptor binding and metabolic effects of insulin in human subcutaneous adipose tissue in untreated non-insulin dependent diabetes mellitus. 329 83

Insulin resistance was assessed by euglycaemic clamp studies in matched groups of MODY, classical NIDDM patients and non-diabetic control subjects. The MODY patients metabolised less glucose (4.8 +/- 0.3 mg/Kg/min) than the classical NIDDM patients (7.0 +/- 0.5 mg/Kg/min) at an insulin infusion rate of 1.0 mU/Kg/min (p less than 0.05). At an insulin infusion rate 10 mU/Kg/min the differences between the MODY and the classical NIDDM patients were not significant. At both infusion rates the two diabetic groups metabolised less glucose than the control subjects. The results indicate that despite their younger age, the patients with MODY are more insulin resistant than the patients with classical NIDDM.
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PMID:Insulin resistance in maturity onset diabetes of the young. 330 43

To elucidate the mechanism of impaired insulin release in case of non-insulin-dependent diabetes (NIDDM), we investigated insulin release and 45Ca++ efflux from perifused islets obtained from neonatal streptozotocin diabetic model rats. The model rats were prepared by the intraperitoneal administration of 65 mg/kg streptozotocin (STZ) to neonatal males. Rats treated with STZ did not differ from controls in body weight from 1 week to 16 weeks. The model rats had significant hyperglycemia both in the fasting state and after intraperitoneal administration of 2 g/kg glucose. Although the diameter of the islets from the model rats was not significantly different from that of controls, immunoreactivity to anti-insulin was slightly diminished, and degranulation was slightly observed in B-cells. Insulin content was reduced to 45.6% of the control. Insulin release from the perifused islets of STZ-treated rats responded little to 16.7 mmol/L glucose, but normally to 20 mmol/L arginine in the presence of 5.5 mmol/L glucose. In experiments to test the 45Ca++ efflux from the perifused islets prelabeled with 45Ca++, a rise of 45Ca++ efflux concomitant with the second phase of insulin release from the islets of the model rats was inhibited although a sharp increase of 45Ca++ efflux concomitant with the first phase of insulin release was maintained. 45Ca++ uptake for 30 minutes was reduced in the islets from the model rats in the basal and stimulated state of insulin secretion although the incremental 45Ca++ uptake was similar. It is possible that the abnormal calcium handling in pancreatic B-cells may be one of the causes of defect in insulin release in our model rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal calcium handling by perifused pancreatic islets from neonatal streptozotocin diabetic model rats. 330 76


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