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

Since the recently reported relationship between serum fructosamine and IgA concentrations appears to throw doubt on the clinical utility of fructosamine as a measure of hyperglycemic status if IgA concentration is not taken into account, we studied serum immunoglobulin concentrations in 169 diabetics and their relationship with various clinical and analytical parameters. Over 41% of the patients studied had abnormal serum IgA concentrations. Serum IgA concentration was negatively correlated with serum albumin, and among IDDM patients was positively correlated with age (so that the prevalence of abnormal IgA was 57.7% among IDDM patients aged over 30 years). Among NIDDM patients, abnormal IgA concentrations were especially prevalent among those being treated with oral hypoglycemics. Abnormal IgA was also more frequently found in both IDDM and NIDDM patients, who had been under treatment for 10 years or more. Abnormal IgG concentrations were found in 11.8% of the diabetics, and the mean IgM concentration found in the patients was 41.6% lower than in the normoglycemic group. We conclude that abnormal serum IgA concentrations are very common in diabetic patients and that further research should be carried out to verify whether the determination of serum immunoglobulins, IgA in particular, is of clinical use for monitoring diabetes or evaluating its secondary effects.
Clin Chim Acta 1991 Dec 16
PMID:Abnormal serum immunoglobulin concentrations in patients with diabetes mellitus. 177 77

To investigate the effects of carnitine on insulin sensitivity in non-insulin-dependent diabetes, insulin-mediated glucose disposal was measured in nine diabetic patients (age 54 +/- 3 years, BMI 27 +/- 1 kg/mq) during a primed (3 mmol) constant (1.7 mumol/min) intravenous infusion of carnitine. In control experiments, the same patients received saline instead of carnitine. Plasma glucose concentration was maintained constant at the level of 100 mg/dl during both studies while plasma insulin was raised to a plateau of 60 microU/ml. Despite similar insulin levels, whole-body glucose utilization was higher with carnitine (4.05 +/- 0.37 mg/kg/min) than saline infusion (3.52 +/- 0.36). Blood lactate concentrations were similar in the basal state and decreased significantly during carnitine infusion (P less than 0.05-0.005), whereas it remained substantially unchanged during saline infusion. Plasma FFA decreased to a similar level (0.1 mmol/l) in both studies. We conclude that an acute carnitine administration is able to improve insulin sensitivity in NIDDM patients. The lactate data suggest that this effect may at least in part be mediated by carnitine activation of pyruvate dehydrogenase.
Diabetes Res Clin Pract 1991 Dec
PMID:Carnitine improves peripheral glucose disposal in non-insulin-dependent diabetic patients. 177 12

There are two approaches to identify diabetes-susceptibility genes. One approach is to isolate and characterize genes expressed in the beta-cell and in insulin target tissues whose mutation or altered expression may contribute to the development of diabetes mellitus. Another approach is to clone a diabetes-susceptibility gene by a reverse genetic strategy. The first step for this strategy is to identify a DNA polymorphism that is linked to the disease locus. Using the strategy of the first approach, several candidate genes were examined. Among these genes, the mutation of insulin genes and insulin receptor genes was found in the patient with diabetes. By cDNA cloning or PCR-direct sequencing methods, we identified several mutations in the insulin receptor genes of four insulin-resistant diabetic patients. At least two mutants of insulin receptor genes were expressed in Chinese hamster ovary cells and these mutated receptors showed impaired ability to transduce insulin action in these cultured cells. The expression of these mutant genes in animals such as transgenic mice will be indispensable to establish the relationship between the gene mutation and the abnormality found in the patient. Using the strategy of the second approach, Bell et al. recently reported that the gene responsible for MODY (maturity-onset diabetes of the young) is tightly linked to the adenosine deaminase gene on chromosome 20q. However, this strategy will not be applicable for identification of diabetes-susceptibility genes of NIDDM, since this disorder is likely to be genetically heterogenous, with mutations in several different genes able to cause hyperglycemia, and this heterogeneity could confound the linkage analysis.
Rinsho Byori 1991 Dec
PMID:[Diabetes mellitus and molecular biology]. 177 65

Diabetic nephropathy, clinically defined by overt albuminuria, hypertension and declining GFR, affects 25-35% of IDDM patients. The risk of nephropathy peaks during the second decade of IDDM and declines thereafter, suggesting that only a subset of IDDM patients is at risk for nephropathy. A role for hypertension in the progression of established renal damage in IDDM is now accepted; however the role of hypertension in the genesis of diabetic nephropathy is not yet clear. Mesangial expansion is a characteristic lesion of diabetic nephropathology and correlates with renal function. Functional studies are not indicative of underlying renal pathology except relatively late, when glomerular injury is advanced. Microalbuminuria in the 'predictive' range (greater than 30 micrograms/min) and associated with hypertension and/or declining GFR is a marker of established diabetic glomerulopathy. Only carefully designed longitudinal studies of renal morphology and function with accurate blood pressure monitoring beginning early in the course of IDDM will clarify the relationships between blood pressure and renal damage in IDDM. In NIDDM the frequent presence of non-diabetic renal lesions, of hypertension at or before the onset of diabetes, and the relative paucity of clinical-pathological correlations currently make it difficult to understand the role of hypertension in the genesis and progression of nephropathy. Again, longitudinal studies of blood pressure and renal structure and function are required in NIDDM patients. Finally, animal models of hypertension and diabetes may aid progress in these areas.
Clin Invest Med 1991 Dec
PMID:Hypertension and diabetic renal disease. 179 13

Lipase activities were measured at pH 4 and pH 8 in the placentas of rats made diabetic by streptozotocin treatment and also in the placentas of women classified as having 1) impaired glucose tolerance or type 2 diabetes, 2) type 1 diabetes with no associated vascular complication, and 3) type 1 diabetes with associated vascular disease. In both sets of experiments, the placentas were compared with normal control groups. The placental lipase activity measured at pH 8 was not significantly different in either streptozotocin-treated rats or impaired glucose tolerance/diabetic women as compared with controls, whereas the lipase activity measured at pH 4 increased significantly as compared with controls in both species. Furthermore, in the women there was a significant correlation between placental lipase activity at pH 4 and birth weight in impaired glucose tolerance/type 2 diabetes. It is suggested that the increased placental lipase activity may contribute to the increased fetal weight in human diabetic pregnancy, by contributing to the increased fat transfer across the placenta from mother to fetus.
Pediatr Res 1991 Dec
PMID:The effects of diabetes on placental lipase activity in the rat and human. 180 50

Although quinidine has been widely used since the beginning of the century, quinidine-induced hepatotoxicity has been recently reported in the literature. We describe a reversible case of quinidine-induced hepatotoxicity. A 62-y-old male with a past medical history of atrial flutter and adult onset diabetes was admitted to the hospital with a 3-d history of diarrhea, nausea, fever, chills and palpitations. Past medications included 7.5 mg glyburide daily for 4 y, 0.25 mg digoxin daily for 3 w, 324 mg quinidine gluconate 3 times daily for 2 w, and 150 mg papaverine daily for 2 y. On admission, liver enzyme levels were elevated (SGOT 606, SGPT 1104). Quinidine was considered an etiologic agent and was discontinued after administration of 1 dose. The patient became afebrile within 48 h, liver enzyme levels gradually decreased, and the patient was discharged on day 6 of hospitalization. Repeat enzyme levels obtained 12 d after discharge were mostly within normal limits. The symptoms were atypical as described in the literature. We conclude that unexplained fever or elevated liver enzyme levels should alert the clinician to the possibility of quinidine-induced hepatotoxicity.
Vet Hum Toxicol 1991 Dec
PMID:Quinidine-induced hepatotoxicity revisited. 180 44

To determine the effectiveness of dietary protein restriction on proteinuria in patients with non-insulin dependent diabetes (NIDDM), 14 diabetic patients with overt nephropathy were placed on either a low protein diet (N = 7) or conventional protein diet (N = 7) for one month. After the study period, daily urinary protein excretion rates decreased significantly, from 3.2 +/- 0.4 to 1.9 +/- 0.4 g/day, and serum albumin levels increased from 3.3 +/- 0.2 to 3.7 +/- 0.5 g/dl only in the low protein diet group, without any significant changes in either serum creatinine levels or creatinine clearance. These findings suggest that dietary protein restriction has a beneficial role in the treatment of NIDDM patients with overt nephropathy.
J Nutr Sci Vitaminol (Tokyo) 1991 Dec
PMID:Effect of dietary protein restriction on proteinuria in non-insulin-dependent diabetic patients with nephropathy. 182 Apr 50

Post-prandial glucose excursions remain elevated in most patients with diabetes even when normal fasting plasma glucose levels have been achieved. In 39 patients with type 2 diabetes who had attained basal normoglycaemia by therapy with diet alone, a sulphonylurea, a basal insulin supplement or basal plus prandial insulin the mean glycosylated haemoglobin (HbA1) values were at the upper end (mean +/- 1SD, 8.1 +/- 1.1%) of the normal range (5.0-8.2%). Miglitol, an alpha-glucosidase inhibitor, given in a dose of 50 mg three times a day was studied in a double blind randomized crossover study. In diet and sulphonylurea treated patients, a mean 25% reduction of the post-prandial plasma glucose excursions was obtained whereas in ultralente treated patients miglitol appeared to reduce basal plasma glucose levels (p < 0.006). Side effects were limited to minor gastrointestinal disturbances, usually ameliorating after the first week of therapy. Alpha-glucosidase inhibition to prevent post-prandial glycaemia may have a role in patients in whom sulphonylurea or diet therapy has been used to obtain normal basal glucose concentrations.
Diabetes Res 1991 Dec
PMID:Post-prandial glycaemic reduction by an alpha-glucosidase inhibitor in type 2 diabetic patients with therapeutically attained basal normoglycaemia. 184 49

We have previously reported on plant mixture extract comprising of Nigella sativa, Myrrh, Gum Olibanum, Gum Asafoetida and Aloe to have a blood glucose lowering effect. The present study with streptozotocin diabetic rats is focussed on the mechanism of action, specifically on a) hepatic gluconeogenesis b) activity of key gluconeogenic enzymes, pyruvate carboxylase (PC) and phosphoenol-pyruvate carboxykinase (PEPCK). Similar studies using a biguanide, phenformin, have been conducted to compare the mode of action of these two compounds. The blood glucose levels (mean +/- SEM) before and after treatment with the plants extract were (16.7 +/- 1.7 mmol/L and 8.5 +/- 1.3 mmol/L) and with phenformin (15.1 +/- 1.3 mmol/L and 10.7 +/- 1.5 mmol/L). The rate of gluconeogenesis in isolated hepatocytes as well as activity of PC and PEPCK in liver homogenates is significantly lowered following treatment with the plants extract. Although phenformin also lowers blood glucose, it does not affect hepatic gluconeogenesis under stated experimental conditions. It is concluded that the anti-diabetic action of the plants extract may, at least partly, be mediated through decreased hepatic gluconeogenesis. The extract may prove to be a useful therapeutic agent in the treatment of non-insulin dependent diabetes mellitus (NIDDM).
Diabetes Res 1991 Dec
PMID:The effect of a plants mixture extract on liver gluconeogenesis in streptozotocin induced diabetic rats. 184 51

A cohort of 132 well-documented White Welsh non-insulin-dependent diabetic (NIDDM) subjects were genotyped for 5 restriction-fragment-length polymorphisms (RFLPs) at the insulin-receptor gene (IRG) locus and a polymorphic locus 5' to the insulin gene. There was no significant difference in RFLP frequencies between the NIDDM subjects and a group of 87 matched White control subjects. Paired haplotype analysis of the IRG RFLPs suggested a difference between NIDDM and control groups for the endonuclease combinations Bgl II-Rsa I and Bgl II-Xba I. Analysis of implied haplotypes defined by the endonucleases Bgl II, Rsa I, and Xba I revealed one haplotype to be more prevalent in the NIDDM group; whereas, another haplotype was associated with the control group (P less than 0.02). Subset analysis within the NIDDM cohort compared the metabolic response of NIDDM subjects with the differing IRG haplotypes to a standard meal tolerance test. Both groups showed equivalent basal and postprandial glucose excursions, but one group revealed a significantly exaggerated plasma insulin response compared with the other (P less than 0.05). This may reflect the influence of genetic variation at the IRG locus on insulin sensitivity in patients with NIDDM.
Diabetes 1990 Dec
PMID:Allelic variants at insulin-receptor and insulin gene loci and susceptibility to NIDDM in Welsh population. 197 26


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