Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the role of glucagon in the pathogenesis of diabetes, we observed change of plasma glucagon concentrations during glucose loading in normal subjects and patients with impaired glucose tolerance (IGT) and non-insulin dependent diabetes mellitus (NIDDM) using specific radioimmunoassay. The results showed that the fasting plasma glucagon levels in patients with IGT and NIDDM were similar to those of the normal subjects. The nadir of plasma glucagon level in the normal control occurred at 1-h after glucose loading and the changes of glucagon, glucose and insulin levels synchronized; but peaks of plasma glucose and insulin levels in the IGT and NIDDM patients were delayed at 2-h after glucose loading with the lowest glucagon level at 3-h. It was suggested that there were relative hyperglucagonemia and decrease of sensitivity of islet A cell to glucose in IGT and NIDDM patients. The present study also showed that hyperglucagonemia is related to the reduction of insulin secretion and might play an important role in the development of postprandial hyperglycemia in NIDDM.
 ...
PMID:[Changes in plasma glucagon concentration in patients with diabetes mellitus and its clinical significance]. 132 51

Insulin resistance contributes to the pathogenesis of NIDDM. We have investigated the molecular mechanisms of insulin resistance in patients with genetic syndromes caused by mutations in the insulin-receptor gene. In general, patients with two mutant alleles of the insulin-receptor gene are more severely insulin-resistant than are patients who are heterozygous for a single mutant allele. These mutations can be put into five classes, depending upon the mechanisms by which they impair receptor function. Some mutations lead to a decrease in the number of insulin receptors on the cell surface. For example, some mutations decrease the level of insulin receptor mRNA or impair receptor biosynthesis by introducing a premature chain termination codon (class 1). Class 2 mutations impair the transport of receptors through the endoplasmic reticulum and Golgi apparatus to the plasma membrane. Mutations that accelerate the rate of receptor degradation (class 5) also decrease the number of receptors on the cell surface. Other mutations cause insulin resistance by impairing receptor function--either by decreasing the affinity to bind insulin (class 3) or by impairing receptor tyrosine kinase activity (class 4). The prevalence of mutations in the insulin receptor gene is not known. However, theoretical calculations suggest that approximately 0.1-1% of the general population are heterozygous for a mutation in the insulin-receptor gene; the prevalence is likely to be higher among people with NIDDM. Accordingly, it is likely that mutations in the insulin-receptor gene may be a contributory cause of insulin resistance in a subpopulation with NIDDM.
Diabetes 1992 Nov
PMID:Lilly Lecture: molecular mechanisms of insulin resistance. Lessons from patients with mutations in the insulin-receptor gene. 132 27

The prevalence of diabetes mellitus among patients treated for end-stage renal failure was studied using a questionnaire mailed to all dialysis units of mainland France in 1989. With a response rate of 80.8%, the study population amounted to 12,903 dialysed patients of whom 884 were declared diabetic (6.9%). In a second phase, the study focused on the diabetic patients treated in the 63 largest units (those with at least four diabetic patients). Seven specially trained physicians completed questionnaires after having interviewed the patients and checked their medical records. All this material was reviewed by the same diabetologist. The conflict of diabetes type declared by both sources of information (the nephrologists and the diabetologist) showed a misclassification rate of 31.2%. Using these new data, the prevalence of type 1 diabetes mellitus was estimated at 1.4% of patients on dialysis therapy in mainland France, and 5.5% for type 2 diabetes mellitus. A north-south declining trend was suggested for type 2 diabetes mellitus. Diabetic nephropathy was the only primary renal diagnosis among 93.9% of type 1 diabetic patients, but only for 36.8% of type 2 diabetic patients. Of the latter, 51.6% had a non-diabetic cause of renal failure. These data show that the proportion of diabetics among patients receiving dialysis, while steadily increasing in France, remains lower than in other countries in Europe and in North America. However, the validity of international comparisons depends on diabetes ascertainment. Heterogeneity in selection of patients and in diabetes type classification by dialysis units may account to a considerable degree for the differences between diabetes mellitus prevalence across countries.
 ...
PMID:Diabetes mellitus prevalence among dialysed patients in France (UREMIDIAB study). 133 35

The obvious syntropy of obesity and type II (non-insulin dependent) diabetes mellitus has always suggested a causal inter-relationship between the two diseases. However, the actual pathophysiological connection still remains to be elucidated. Recent findings have suggested that insulin resistance and hyperinsulinaemia might link glucose intolerance/type II diabetes mellitus, hypertension and hyperlipoproteinaemia in the context of a hypothetical 'syndrome X' characterized by an excessive risk constellation for the development of atherosclerosis. However, as to the practical consequences of the ('diabesity') syndrome of type II diabetes mellitus and structured programmes for effective therapy, very little new information has been gathered during the past 100 years.
 ...
PMID:Risk of obesity in type II diabetes mellitus. 133 84

Diabetes mellitus (DM) is frequently associated with hypertension for which an independent pathomechanism has been suggested. We studied 26 patients with insulin-dependent (IDDM) and 18 patients with non-insulin-dependent (NIDDM) uncomplicated DM; all patients were in metabolic balance and none of them had hypertension. Exchangeable body sodium (NaE was estimated by isotope dilution, using appr. 1.1 Mbq 24NA. In a subset of 8 IDDM and 8 NIDDM patients atrial natriuretic peptide (ANP) plasma concentration was determined prior to and after the infusion of 2000 ml physiological saline over 2 hr. NaE was significantly increased both in IDDM and NIDDM patients (104.4 +/- 11.4% and 109.9 +/- 8.0% of the normal value for healthy subjects of identical body surface area; p < 0.05 and < 0.001 resp.). Mean blood pressure (MBP) correlated significantly with NaE in both groups (r = 0.364 and r = 0.520; p < 0.05 and < 0.025, resp.) but not in healthy control subjects (r = 0.112; N.S.). Resting ANP levels were not significantly different in IDDM (34.9 +/- 11.3 pg/ml), NIDDM (42.6 +/- 11.7 pg/ml) or control subjects (40.9 +/- 17.2 pg/ml) however the infusion of saline resulted in a significantly greater increase of plasma ANP in the NIDDM patients (to 82.9 +/- 43.2 pg/ml; P < 0.01) than in the controls (55.6 +/- 23.7 pg/ml; P < 0.01) which was associated with a significantly less increase in sodium excretion (UNAV) in the NIDDM patients (+86% vs. 3170%; P < 0.02) indicating down-regulation of ANP receptors in the kidney of NIDDM patients.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Body sodium, atrial natriuretic peptide and blood pressure in diabetes mellitus. 134 Jun 60

Conflicting evidence has been reported on the metabolic fate of glucose following oral ingestion. We measured the metabolic pattern of gluconeogenic substrates as alanine, predominantly produced by muscle, and lactate after an oral glucose load in ten normal subjects and in eighteen non-insulin dependent diabetes mellitus (NIDDM) subjects. Neither in normal or NIDDM subjects were significant increases in plasma alanine observed, whereas a significant increase in plasma lactate was observed at 60, 90 and 120 min after a glucose load. Although a similar behaviour in plasma alanine and lactate between normal and NIDDM subjects was found, in NIDDM significantly higher levels of plasma alanine and lactate were found at each time. From these observations we conclude: 1) when glucose is ingested under post-absorptive conditions, since plasma alanine levels do not change concurrently with lactate increase, muscle tissue does not play a predominant role in glucose disposal 2) after an oral glucose load, the pattern of gluconeogenic precursors (alanine and lactate) is similar in normal and NIDDM subjects 3) the main cause of fasting and post-prandial hyperglycemia in NIDDM subjects may be due to an overproduction of alanine as well as lactate.
Diabetes Res 1992
PMID:Plasma alanine and lactate concentrations following glucose ingestion in normal and NIDDM subjects. 134 5

Lipoprotein(a) [Lp(a)] has been added to the list of independent risk factors for cardiovascular disease (CVD), whose incidence is greater in obese subjects. There are few data available on the serum Lp(a) concentrations in obese individuals with or without insulin dependent diabetes mellitus (NIDDM). We selected 31 obese men with normal glucose tolerance (NGT) tests, 15 obese diabetic men, 14 non obese diabetic men and 17 healthy men as controls. We measured serum total cholesterol, HDL cholesterol, triglycerides, glucose, insulin and Lp(a). The mean Lp(a) levels in NGT obese men were 70.00 +/- 13.40 mg/l, which were similar to those found in normal controls (75.98 +/- 24.70 mg/l); significantly higher mean Lp(a) levels were found in obese diabetic men (168.84 +/- 56.43 mg/l) and in non obese diabetic men (240.85 +/- 63.35 mg/l). No significant correlation between Lp(a) levels and age, body mass index (BMI), total cholesterol, HDL cholesterol, triglycerides, insulin, was found; only a significant positive correlation between Lp(a) levels and glucose could be revealed (P < 0.05). Since higher levels of Lp(a) were found in NIDDM subjects with or without obesity, we conclude that hyperglycemia may influence the levels of serum Lp(a) facilitating its glycosylation in the liver with the consequence of a decline in its catabolic rate.
Diabetes Res 1992
PMID:Serum lipoprotein Lp(a) in obesity. 134 6

78 diabetics and a healthy control group of 100 were evaluated according to their haemorrheological parameters (whole blood viscosity, plasma viscosity, aggregability and rigidity of erythrocytes). Diabetics were divided according to type of diabetes, quality of metabolic control and expression of microangiopathy. Hyperviscosity was noted in both groups of diabetics as compared to the control group. Changes in patients with IDDM were more pronounced in erythrocyte rigidity, while in patients with NIDDM they were more expressed in cell aggregability. These changes were present even before the clinical onset of the late complications of diabetes, although they were more expressed in patients with complications. Changes in patients with good metabolic control, were less expressed in comparison to those with poor metabolic control. The conclusion is that metabolic derangements in diabetes have an important influence on haemorrheological properties. Thus, reducing blood viscosity in these patients, may be a promising approach to improving microcirculation and delaying the progression of microangiopathy.
 ...
PMID:[Hemorheologic changes in diabetes mellitus]. 134 47

1. To determine the effects of gene dilution on development of IGT, NIDDM and in vitro glucose oxidation, heterozygous lean LA/N-cp female and SHR/N-cp male rats were mated, and F1 offspring studied at periodic intervals to determine the prevalence of obese and diabetic traits. 2. Obesity occurred in 25% of offspring by 5 weeks of age, consistent with inheritance of the autosomal recessive cp trait. 3. IGT occurred in all obese male F1, 67% of obese female F1, and 18% of the lean male F1 rats by 5 months of age, and diabetes occurred in 80% of male obese and 17% of female obese rats from 6 months of age. Glycosuria occurred with glucose intolerance, and was more severe in rats with NIDDM than IGT. 4. Rates of in vitro glucose oxidation were greater in diaphragm and adipose tissue, and were greater in the presence of insulin (100 mu Units/ml) in obese female but not obese male F1 rats. 5. These results indicate that the development of glucose intolerance is more prominent in male than in female F1 rats, that the progression of IGT to NIDDM occurs later in life in the F1 hybrid than in the SHR/N-cp strain from which the diabetic trait was transmitted, and that genetic dilution of the diabetic trait via hybrid breeding results in a delay in the expression of NIDDM which is chronologically more similar to that which occurs in man.
 ...
PMID:Effect of genetic dilution on development of diabetes, impaired glucose tolerance and in vitro glucose oxidation in LA/N-cp x SHR/N-cp F1 hybrid rats. 134 69

Maturity-onset diabetes of the young (MODY) is a subtype of type 2 diabetes that presents from the second decade and has an autosomal dominant mode of inheritance. We have investigated the glucokinase gene, a candidate gene for diabetes, in two MODY pedigrees. In a large 5-generation pedigree (BX) with 15 diabetic members, use of a microsatellite polymorphism revealed linkage of diabetes to the glucokinase locus on chromosome 7p. A peak lod score of 4.60 was obtained at a recombination fraction (theta) of zero. This finding suggests that a defective glucokinase gene contributes to the diabetes phenotype in this pedigree. This is not universal in MODY since linkage to the glucokinase locus was excluded in a second pedigree M (lod score = -7.36 at theta = 0). The affected members in pedigree BX were diagnosed either when young (in pregnancy or on screening) or when they presented symptomatically in middle and old age; most of them were treated by diet alone. Defects in the glucokinase gene may play an important part in the pathogenesis of type 2 diabetes.
 ...
PMID:Linkage of type 2 diabetes to the glucokinase gene. 135 30


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>