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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 bioelectrical characteristics correspond well to body water compartments, this study investigated bioelectrical differences between type 1 and type 2 diabetic subjects that could reflect differences in body water compartments. We investigated cross-sectionally 612 adult subjects, classified into 10 groups according to sex and disease (control, obese normal glucose tolerant, non-obese type 2 diabetes, obese type 2 diabetes, type 1 diabetes). Resistance (R), reactance (Xc) and phase angle (PA) were measured (800 microA - 50 kHz alternating current). The bioelectrical vector was obtained by plotting R and Xc normalized for height (ht), it is easily identified on the basis of the length (inversely related to the total body water, likewise R) and direction, given by the PA (inversely related to the extra-/intra-cellular water - ECW/ICW -). Results show that disease and sex had a significant (ANOVA: P<0.0001 for both F disease and F sex) and independent effect on both R/ht and Xc/ht; no difference was found between type 2 and type 1 diabetic groups. A bioelectrical vector with a lower PA characterized both type 2 and type 1 diabetic groups. An independent positive correlation between fasting plasma glucose and R/ht and a negative correlation between fasting plasma glucose and PA were observed. These findings suggest a non-different body water content and distribution between type 2 and type 1 diabetic subjects; the bioelectrical vector indicates a higher ECW/ICW in type 2 and type 1 diabetic compared to nondiabetic subjects.
Acta Diabetol 1998 Dec
PMID:Bioelectrical characteristics of type 1 and type 2 diabetic subjects with reference to body water compartments. 993 22

We and others have shown that insulin acutely suppresses glucose production in fasting nondiabetic humans and dogs, by both a direct hepatic effect and an indirect (extrahepatic) effect, and in diabetic dogs by an indirect effect alone. In type 2 diabetes, there is resistance to insulin's ability to suppress hepatic glucose production, but it has not previously been determined whether the resistance is primarily at the level of the hepatocyte or the peripheral tissues. To determine whether the diabetic state reduces the direct effect of insulin in humans, we studied nine patients with untreated type 2 diabetes who underwent three studies each, 4-6 weeks apart. 1) Portal study (POR): intravenous tolbutamide was infused for 3 h with calculation of pancreatic insulin secretion from peripheral plasma C-peptide. 2) Peripheral study (PER): equidose insulin was infused by peripheral vein. 3) Half-dose peripheral insulin study (1/2 PER): matched peripheral insulin levels with study 1. In all studies, glucose was clamped at euglycemia, glucose turnover was measured with the constant specific activity method, and 3-[3H]glucose was purified by high-performance liquid chromatography. Peripheral insulin was lower in POR versus PER but slightly higher in POR versus 1/2 PER, although most of the difference could be accounted for by higher proinsulin levels in POR (stimulated by tolbutamide). Calculated portal insulin was approximately 1.3-fold higher in POR versus PER and approximately 2.2-fold higher in POR versus 1/2 PER. In the final 30 min of the clamp, glucose production reached a lower steady-state level in PER than in POR (4.0 +/- 0.4 vs. 5.3 +/- 0.5 pmol(-1) x kg(-1) x min(-1), P < 0.05), despite the higher hepatic insulin level in POR. In contrast with our studies in nondiabetic individuals, glucose production was not more suppressed at steady state in POR versus 1/2 PER (5.3 +/- 0.4 micromol x kg(-1) x min(-1)), despite much higher hepatic insulin levels in POR. In conclusion, this is the first study in patients with type 2 diabetes to characterize insulin resistance to the acute direct suppressive effect of insulin on hepatic glucose production.
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PMID:Resistance to insulin's acute direct hepatic effect in suppressing steady-state glucose production in individuals with type 2 diabetes. 1007 58

The stimulatory effect of the glucagon-like peptide (GLP)-1(7-36) amide on electrical activity in pancreatic b-cells recorded in vivo was studied. The injection of GLP-1 produces a lengthening of the active phase with respect to the silent phase, leading to a stimulation of insulin release, which produces a secondary decrease in blood glucose concentration and eventually, to the hyperpolarization of the membrane at a blood glucose level of approximately 5 mmol/l. The injection of GLP-1 at a glycemic level <5 mmol/l does not stimulate electrical activity. This is in contrast to the effect of tolbutamide, which stimulates electrical activity at low glucose concentrations. These results demonstrate that in vivo, the stimulatory effect of GLP-1 on insulin secretion is at least partially mediated by its effect on beta-cell electrical activity. Furthermore, the glucose dependence of the effect confers to GLP-1, a security factor that supports its potential use in the treatment of type 2 diabetes.
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PMID:Glucose-dependent stimulatory effect of glucagon-like peptide 1(7-36) amide on the electrical activity of pancreatic beta-cells recorded in vivo. 1010 91

The main action of SU in the treatment of diabetes mellitus is the stimulation of insulin secretion, and the extrapancreatic action including stimulation of insulin actions in glycogen synthesis and inhibition of glucose production in liver is also reported. The indication of SU in the treatment of diabetes mellitus is for NIDDM usually after diet therapy or suitable exercise therapy. In IDDM and several special cases including diabetic ketoacidosis, severe infection, pregnancy, poor-controlled NIDDM, gangrane, surgery operation, severe renal or hepatic failure et al. insulin therapy should be started. In mild NIDDM, gliclazide, tolbutamide or acetohexamide is used, and in more severe NIDDM glibenclamide is used. The action time of chlorpropamide is very long, usually from 20 to 60 hours, therefore special care should be taken for hypoglycemia. As the causes for secondary failure, transition from NIDDM to IDDM, failure of diet therapy, glucose toxity and others are considered.
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PMID:[Use of sulfonylurea (SU) in the treatment of diabetes mellitus]. 1019 51

Both defective insulin secretion and insulin resistance have been reported in relatives of type 2 diabetic subjects. We tested 120 members of 26 families with a type 2 diabetic sibling pair with a tolbutamide-modified, frequently sampled i.v. glucose tolerance test to determine the insulin sensitivity index (S(I)) and acute insulin response to glucose (AIRglucose). A measure of beta-cell compensation for insulin sensitivity was calculated as the product S(I) x AIRglucose, based on the demonstrated hyperbolic relationship between insulin sensitivity and insulin secretion. A percentile score for this compensation was assigned based on published values. Of the 120 family members, 26 had previously diagnosed impaired glucose tolerance on oral testing, and 94 had normal glucose tolerance tests. As a group, family members showed a significantly lower S(I) x AIRglucose than a similar, previously reported, control population, even when impaired glucose tolerance members were excluded. We performed a multivariate analysis of diabetes status, S(I), AIRglucose and to estimate the heritability of each trait and the genetic and environmental correlations between traits. We estimated the heritability of S(I) x AIRglucose to be 67 +/- 3% when all members were included and 70 +/- 4% when only normal glucose tolerance members were considered. Both AIRglucose and S(I) were also familial, albeit with lower heritabilities (38 +/- 1% and 38 +/- 2%, respectively, for all family members). Both S(I) x AIRglucose and S(I) showed strong negative genetic correlations with diabetes (-85 +/- 3% and -87 +/- 2%, respectively, all family members), whereas AIRglucose did not correlate with diabetes. We conclude that insulin secretion, as measured by S(I) x AIRglucose, is decreased in nondiabetic members of familial type 2 diabetic kindreds, that S(I) x AIRglucose in these high risk families is highly heritable, and that the same polygenes may determine diabetes status and a low S(I) x AIRglucose. Our data suggest that insulin secretion, when expressed as an index normalized for insulin sensitivity, is more familial than either insulin sensitivity or first phase insulin secretion alone and may be a very useful trait for identifying genetic predisposition to type 2 diabetes.
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PMID:Heritability of pancreatic beta-cell function among nondiabetic members of Caucasian familial type 2 diabetic kindreds. 1019 85

Type 2 diabetes mellitus (NIDDM) is a complex disorder encompassing multiple metabolic defects. There exists strong evidence for a genetic component to NIDDM; however, to date there have been few reports of linkage between genetic markers along the genome and NIDDM or NIDDM-related quantitative traits. We sought to determine whether individual quantitative traits which determine glucose tolerance exhibit familiality in Finnish families with at least one NIDDM-affected sibling pair. Tolbutamide-modified frequently sampled intravenous glucose tolerance tests (FSIGT) were performed on unaffected offspring (n = 431) and spouses (n = 154) of affected sibling pairs sampled for the Finland-United States Investigation of NIDDM Genetics (FUSION) study. FSIGT data were analyzed using the Minimal Model to obtain quantitative measures of insulin sensitivity (SI), glucose effectiveness (SG), and insulin secretion assessed as the acute insulin response to glucose (AIR). The disposition index (DI), a measure of insulin resistance-corrected beta-cell function, was also derived as the product of SI and AIR. Variance components analysis was used to determine for each trait, the heritability (h2), the proportion of the total trait variance accounted for by additive genes. After adjustment for age, gender, and body mass index, h2 estimates were: SG: 18 +/- 9%, SI: 28 +/- 8%, AIR: 35 +/- 8%, and DI: 23 +/- 8%. We conclude that there is strong evidence for modest heritability of Minimal-Model-derived NIDDM-related quantitative traits in unaffected spouses and offspring of Finnish affected sibling pairs.
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PMID:Familiality of quantitative metabolic traits in Finnish families with non-insulin-dependent diabetes mellitus. Finland-United States Investigation of NIDDM Genetics (FUSION) Study investigators. 1036 81

Several conditions have been described to cause osteoporosis, including diabetes mellitus. While the relationship between type 1 diabetes and osteopenia is well documented in the literature, data on the presence of this complication in type 2 diabetes have not been well established. We studied a population composed of 66 post-menopausal women with type 2 diabetes and a control population. We examined bone mineral density with the dual-energy X-ray absorptiometry (DXA) technique at the lumbar and femoral levels and, in a subgroup of patients, we also measured the levels of markers of bone remodelling. We found significantly higher levels of bone mineral density at the femoral (but not lumbar) level in the diabetic subjects compared with the control population in all the examined subregions, except Ward's triangle. Moreover, we found higher levels of some markers of bone resorption (urinary calcium and hydroxyproline, telopeptide) in the patients with diabetes, while urinary crosslinks were higher in the controls. On the basis of these results, we suggest that osteoporosis cannot be considered a complication of type 2 diabetes and that, from a metabolic point of view, bone resorption is greater in diabetic patients than in normal subjects, as suggested by the high levels of most of the markers of osteoclastic activity.
Acta Diabetol 1999 Jun
PMID:Bone metabolism in type 2 diabetes mellitus. 1043 50

In the present study we assessed and compared the effectiveness and safety of preconstituted, fixed, combinations of low-dose glyburide plus metformin with higher-dose glyburide monotherapy in patients with type 2 diabetes. This randomized, double-blind, cross-over study comprised 40 patients. After a 30-day run-in period of dietary treatment, patients received combined glyburide (5, 7.5 or 10 mg/day) and metformin (800, 1,200 or 1,600 mg/day) as preconstitued, fixed combinations, or glyburide alone (5, 10 or 15 mg/day). The dose was increased stepwise so as to have 1 (T1), 2 (T2) and 3 (T3) months of treatment for any given regimen (6 months in total). After 2 weeks of washout (T4), the groups were then crossed over (T5, T6, T7 periods). Body weight, fasting plasma glucose, HbA(1c), blood lactate, total cholesterol and HDL-cholesterol, and triglycerides were measured at the beginning and end of T1 and T5, and end of T2, T3, T6 and T7; postprandial plasma glucose, fasting and postprandial plasma insulin and C-peptide were evaluated at the beginning of T1 and T5, and end of T3 and T7. At these latter time points additional assessments included routine clinical chemistry measurements, ECG, and ophthalmoscopic examination. Statistical analysis was performed by the paired Student's t-test and analysis of variance for cross-over studies. Thirty-three patients completed the study. Fasting plasma glucose, postprandial plasma glucose and HbA(1c) levels improved significantly during combined treatment with glyburide at lower doses plus metformin. This effect was achieved without any major change of insulin and C-peptide concentrations. Circulating lactate concentrations increased during the regimen including metformin, but they remained well within the reference values for normal subjects. Plasma total cholesterol and triglycerides levels remained substantielly unchanged throughout the study, whereas HDL-cholesterol concentrations increased slightly, but significantly, with glyburide plus metformin therapy. Routine clinical chemistry measurements, ECG and ophthalmoscopic examinations did not change during the study. These results demonstrate that improved metabolic control can be achieved with preconstituted, fixed combinations of low-dose glyburide plus metformin in patients with type 2 diabetes, compared to higher doses of the sulphonylurea alone.
Acta Diabetol 1999 Jun
PMID:A comparison of preconstituted, fixed combinations of low-dose glyburide plus metformin versus high-dose glyburide alone in the treatment of type 2 diabetic patients. 1043 54

We evaluated the relationship between plasma fibrinogen concentration and the serum levels of interleukin-6 (IL-6), its soluble receptor, and their complex in patients with type 2 diabetes mellitus. The study comprised 57 patients with type 2 diabetes and 15 normal healthy controls. Serum levels of IL-6, soluble IL-6 receptor (IL-6R), and circulating IL-6/IL-6R complex were determined by enzyme-linked immunosorbent assays. Correlations between the different study parameters and serum IL-6, IL-6R, or IL-6/IL-6R complex levels were determined by multiple linear regression analysis. Any association between the different study parameters and the serum levels of IL-6, IL-6R, or IL-6/IL-6R complex were determined by stepwise linear regression analysis. The serum IL-6 level in diabetic subjects was significantly higher than in normal healthy controls (3.48 +/- 3.29 pg/ml vs 0.784 +/- 0.90 pg/ml, mean +/- SD, respectively, P = 0.0001). The specific optical density of the serum IL-6/IL-6R complex in diabetic patients was also significantly higher than in normal healthy controls, although there was no significant difference in the serum IL-6R level between diabetic patients and controls. The serum IL-6 concentration was correlated significantly with the HbA(1C) level (beta = 0.58, P = 0. 04) by multiple regression analysis. Stepwise regression analysis revealed that the levels of serum IL-6 (F = 8.251), HbA(1C) (F = 1. 08), and serum urea nitrogen (F = 5.603) were associated with the plasma fibrino gen concentration. These results suggest that hyperglycaemia and increased levels of serum IL-6 can increase the plasma fibrinogen concentration, one of the known risk factors for atherosclerosis in patients with type 2 diabetes mellitus.
Acta Diabetol 1999 Jun
PMID:Circulating levels of interleukin-6, its soluble receptor and interleukin-6/interleukin-6 receptor complexes in patients with type 2 diabetes mellitus. 1043 55

Type 2 diabetes mellitus is a chronic disease which causes neurologic, cardiac, vascular, ocular and renal complications. The present study documented the prevalence of diabetes and associated risk factors in 1774 adults who were older than 30 years. An oral glucose tolerance test (OGTT) was conducted according to the World Health Organization (WHO) criteria. Of the 1452 subjects, 58 (4%) had diagnosed diabetes, 41 (2.9%) undiagnosed diabetes and 130 (9%) had impaired glucose tolerance. The total glucose intolerance was 15. 9%. The prevalences of type 2 diabetes mellitus (9.7%-4.1%) were significantly different in low occupational and high occupational activity groups, respectively (P<0.0001). The prevalence of type 2 diabetes mellitus was 17.9% among the hypertensive group (P<0.0001). The prevalence of type 2 diabetes mellitus was higher in smokers (P<0.05). Patients with diagnosed diabetes, undiagnosed diabetes and IGT were older, more obese and have higher blood glucose values, triglyceride values, systolic and diastolic blood pressures than healthy subjects (P<0.001). We conclude that type 2 diabetes mellitus and IGT prevalences are quite high in the urban area of Kayseri, central Anatolia and multivariate analysis indicated that low occupational activity, low leisure activity, family history for diabetes, hypertension and obesity were significant independent risk factors for diabetes mellitus.
Acta Diabetol 1999 Jun
PMID:The prevalence and identification of risk factors for type 2 diabetes mellitus and impaired glucose tolerance in Kayseri, central Anatolia, Turkey. 1043 58


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