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

Of the many information obtainable from the urine of diabetic patients, urinary C-peptide (CPR), albumin and anti-diuretic hormone (ADH) were representatively described using my clinical and experimental data. C-peptide excretion in 24h collection of urine is a good estimate of insulin secretion from the pancreas and thus low in IDDM patients and even in NIDDM patients at a later stage, but high in pathological conditions including Graves' disease, obesity, liver cirrhosis and Cushing's syndrome. Urinary albumin excretion in small amounts (microalbuminuria) is usually observed in diabetic patients who have been under a poor control state of diabetic hyperglycemia for over 5 years and provides a good tool for monitoring early diabetic nephropathy. The grade of microalbuminuria (30-300 mg/day) is positively correlated with the HbA1 level in diabetic patients, showing that microalbuminuria is reversible along with an improvement of diabetic control at least in an early phase of diabetic nephropathy. As the albumin level measured in a spot urine sample correlates well with the value in the 24h collection of urine, the albumin measurement is conveniently feasible with a spot urine sample at every patient's visit. The amount of ADH excreted in urine is 7-10% of that secreted from the posterior pituitary. The excretion of ADH in a day was in the urine of diabetic patients positively correlated with HbA1, urinary osmolarity and concentration of sodium in urine, although the pathological meaning of the observed ADH hypersecretion in the development of diabetic complications is currently unknown.
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PMID:[Pathophysiological analysis of diabetes mellitus and complications from the urine of diabetic patients]. 150 92

We analyzed O-GTT obtained from 375 children (group A; 7-11 years old) and adolescents (group B; 12-16 years old), including 96 normal non-obese cases, 266 simple obese cases (172 with normal O-GTT, 79 with border line type O-GTT and 15 with diabetic type O-GTT), 8 obese NIDDM cases and 5 non-obese NIDDM cases. The results were as follows; 1) The levels of epsilon CPR (in terms of total sum of the values measured at 0, 30, 60, 120 and 180 minutes on O-GTT) in the obese children and adolescents were only 1.5 and 1.2 times as high as in the control group. The levels of epsilon CPR/epsilon IRI molar ratio in the control group were 2.0 and 2.3 times as high as in the obese children and adolescents. These data suggest that hyperinsulinemia in the obese children and adolescents is caused mainly by decreased hepatic insulin extraction rather than by increased insulin secretion. 2) In the non-obese NIDDM adolescents, the levels of epsilon CPR decreased to about 3/4 of those in the control group; in contrast, the epsilon CPR/epsilon IRI molar ratio increased. Therefore, it seems that there is increased hepatic insulin extraction as well as decreased insulin secretion in the non-obese NIDDM adolescents. 3) In the obese NIDDM adolescents, the levels of epsilon CPR were nearly the same as in the control group and the epsilon CPR/epsilon IRI molar ratios were slightly lower as the disease state of NIDDM counterbalanced obesity.
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PMID:[Studies on insulin secretion and clearance in obese and diabetic children (7-11 years old) and adolescents (12-16 years old) investigation by oral glucose tolerance tests (O-GTT)]. 154 73

The serum ketone response to glucagon was measured in 10 patients with IDDM and 37 with NIDDM. In both groups, serum 3-hydroxybutyrate increased significantly after intravenous injection of 1 mg glucagon. The difference between the serum level of 3-hydroxybutyrate at 30 min and basal level [delta 3-OHBA(30')] was 133 +/- 25 mumol/l in the patients with IDDM, 13 +/- 8 mumol/l in those with NIDDM treated by diet alone or with oral hypoglycemic agents and 23 +/- 13 mumol/l in those with NIDDM treated with insulin. The delta 3-OHBA(30') was significantly greater in IDDM patients than in both groups of NIDDM patients (P less than 0.001). The delta 3-OHBA(30') was greater than 87 mumol/l in eighty percent of IDDM patients, but smaller than 87 mumol/l in both groups of NIDDM patients. The delta 3-OHBA(30') was correlated with the difference between the plasma level of C-peptide at 6 min and basal level [delta CPR(6')] (r = -0.540, P less than 0.001). The delta 3-OHBA(30') was not correlated with fasting plasma levels of glucose, fructosamine or hemoglobin A1c. These observations show that measurement of the serum ketone response to glucagon is a useful marker of insulin dependency. In order to determine insulin dependency, the simultaneous measurement of concentrations of ketones and C-peptide is indicated during the glucagon stimulation test.
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PMID:Serum ketone response to glucagon as a marker of insulin dependency in diabetics. 175 81

In this study, 16 overweight or obese NIDDM patients with a long period of stable weight and dietary surveillance were treated with 150 mg t.i.d. of Benfluorex per os for 3 months. A significant improvement occurred in the fasting and post-meal glucose levels and in the HbA1C values, regardless of weight changes that occurred throughout the study. No significant changes were found in the fasting or meal-stimulated insulin (IRI) levels and in the glucose:IRI molar ratios. On the contrary, there were no significant variations in C-peptide levels while the glucose:CPR ratio appeared to decrease while on Benfluorex. In basal conditions, 11 patients presented insulin insensitivity (as measured by the glucose-insulin-somatostatin technique) which was unaffected by the pharmacological treatment. Benfluorex may therefore ameliorate metabolic control in overweight or obese NIDDM patients, but our data do not clarify whether its effects are mediated by an improvement in the action of insulin in peripheral tissues.
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PMID:Benfluorex action on metabolic control and insulin sensitivity in type 2 non-insulin dependent diabetics. 268 69

In order to better understand the role of A- and B-cell function in diabetic pregnancy, we studied four groups of pregnant women at week 34-36 of gestation. Seventeen were healthy controls (C), 24 had gestational diabetes (GD), 16 had type 2 diabetes (NIDD) and 37 had type 1 diabetes (IDD). At times -20, 0, 20, 30, 45, 60, 90 and 120 min from the beginning of a 30 min infusion of 30 g of arginine intravenously, plasma glucose, glucagon (IRG) and C-peptide (CPR) were measured. Plasma glucose was higher in diabetic than in control subjects. IRG values were also higher in the GD and the NIDD women. CPR values were similar to, or slightly higher than control values in the GD and the NIDD and were much lower in the IDD women. All three variables increased during the arginine infusion in all groups, with the exception that CPR remained unchanged in the IDD. The CPR/IRG molar ratio was similar in control, GD and NIDD women; in the IDD, it was much smaller than in the other groups and was not affected by arginine. In all the diabetic patients, IRG was negatively correlated with the maternal weight gain and in the IDD IRG was positively correlated with the increase in the insulin need and with the CPR levels. In conclusion diabetes appeared to enhance the A-cell function also in pregnancy, possibly impairing the 'facilitated anabolism' and stressing the 'accelerated starvation' which are typical of normal pregnancy. Glucagon was confirmed as one possible determinant of the insulin resistance seen in diabetic pregnancy.
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PMID:Endocrine pancreatic function in insulin-dependent diabetic pregnant women. 353 67

The overall annual IDDM incidence rates by area in Japan for 1985-1989 for children 0-14 years of age at diagnosis were from 1.65 to 2.07 per 100,000. The incidence in males and females did not show any temporal trends during the period between 1980 and 1989. The prevalence of IDDM was about 1 per 10,000. The clinical features at diagnosis among Japanese IDDM children identified during the 2-year period between 1979 and 1980 were as follows. Fourteen percent of the cases were in coma and 12% of the cases were asymptomatic at diagnosis. There is a suggestion that slow onset IDDM is often seen in Japan. In these children, the decline of serum CPR levels and the prevalence of ICA (islet cell antibodies) over the course of diabetes was slower than in those with an abrupt onset classical IDDM. During the period from 1975 through 1990 the incidence rates of NIDDM in school children showed as much as an approximate 1.5-fold increase along with a similar increase in the prevalence of obesity. About eighty percent of these NIDDM children were obese. A predominance of female children developing diabetes was seen in both type of diabetes, IDDM and NIDDM, in Japan. Non-obese type NIDDM in children was more common in females than in males. It is interesting to note that the mean height of Japanese children with IDDM was not different from the national average, but children with NIDDM were significantly taller than the national average.
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PMID:Epidemiology of type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetes mellitus in Japanese children. 785 37

A pedigree with maternally transmitted diabetes mellitus, deafness, and cardiomyopathy is described. A A-->G mutation at nucleotide pair 3243 in mitochondrial gene was detected by Apa I digestion of PCR amplified genomic DNA from 3 brothers and their mother. The proband, suffering from CHF, showed unique fine granular pattern of hyperechogenic cardiomyopathy as his brother and their mother did. Although he is recently treated with insulin, he was initially NIDDM treated by sulfonylurea. His urinary CPR excretion decreased gradually to as low as less than 10 micrograms/day in these 3 years. The insulin response to oral glucose was decreased in all other family members with the mutation. It is suggested that the defective insulin secretion exists in this family with the mutation and the progressive decrease in insulin secretion might resulted in IDDM in the proband.
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PMID:[A pedigree with maternally transmitted diabetes mellitus, deafness and cardiomyopathy]. 798 86

Elevated plasma levels of plasminogen activator inhibitor-1 (PAI-1) have been shown to be a risk factor for the development of vascular complications in obese and hyperinsulinemic non-insulin-dependent diabetes (NIDDM) patients. To clarify whether PAI-1 also plays an essential role in the development of such complications in NIDDM patients without obesity or hyperinsulinemia, PAI-1 was analyzed in relation to blood pressure, fasting plasma levels of glucose (FPG), hemoglobin A1C (HbA1c), immunoreactive insulin (F-IRI), C-peptide (CPR), total cholesterol (TC), triglyceride (TGL), and HDL-cholesterol (HDL-C) in 77 NIDDM patients and 10 healthy control subjects. The NIDDM patients were not obese (body mass index [BMI]:<26 kg/m2) or hyperinsulinemic, and BMI in the controls was between 19 and 24 kg/m2. In addition, parameters of insulin secretion reserve, including sigmaIRI, insulinogenic index, and CPR at 5 min after glucagon loading, were evaluated simultaneously. Plasma levels of PAI-1 were higher in the NIDDM group (9.3+/-0.9 ng/ml) than in the controls (4.3+/-0.7 ng/ml;P<0.01). Levels of FPG and HbA1c were also elevated in the NIDDM group (P<0.05 for each), but F-IRI did not differ between the two groups. However, multiple regression analysis revealed no significant correlation in the NIDDM between PAI-1 and F-IRI or the parameters of insulin secretion reserve. Regardless of the presence or absence of vascular complications, PAI-1 did not vary significantly in the NIDDM. These findings suggest that the effects of PAI-1 on the development of diabetic complications in NIDDM patients may not proceed in the same way in those with versus those without obesity or hyperinsulinemia, because no correlation was found between PAI-1 and insulin secretion reserve, while plasma levels of PAI-1 were higher in the NIDDM group than in the controls.
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PMID:Plasminogen activator inhibitor-1 in nonobese subjects with non-insulin-dependent diabetes mellitus. 863 10

We report a 79-year-old woman case of slowly progressive IDDM (SPIDDM) with rheumatoid arthritis (RA) and Hashimoto disease. High titer of anti-glutamic acid decarboxylase antibody (GAD) with a value of 16,400 U/ml (normal value: less than 5 U/ml) and deteriorated secretion of insulin, and clinical course led to the diagnosis of SPIDDM. Both anti-islet cell and anti-insulin antibodies were negative. One year prior to the diagnosis, at 78 years of age, she was newly diagnosed with NIDDM and had been medicated with sulfonylurea and voglibose, resulting her glucose levels well-controlled. Four months before admission, a gradual increase of plasma glucose was noticed, while oral hypoglycemic agents were fully administrated. On admission, her glycemic control was revealed as follows; a fasting blood glucose level of 458 mg/dl and an HbA1 C level of 14.3%. Urinary CPR was 22.5 micrograms day. Her insulin secretion was proved not to be induced with intravenous glucagon injection. Hyperinsulinemic euglycemic glucose clamp test showed the normal glucose uptake ratio; 9.5 mg/kg/min. Moderate doses of subcutaneous insulin (20 units daily) were effective on her diabetes control. She was newly diagnosed with Hashimoto disease that required thyroid hormone replacement 50 micrograms per day after having developed NIDDM. High titer of anti-thyroglobulin antibody (46.9 U/ml) and anti-thyroid peroxidase antibody (81.5 U/ml) were observed. The patient had been medicated for RA with anti-inflammatory drugs since her early seventieth. Rheumatoid factor was elevated to 127.7 IU/L and, anti-nuclear antibody (x 80) and anti-DNA antibody (x 80) were present. It may be of interest that a specific phenotype of HLA; A24 (9) and DR9 recognized to be susceptible to IDDM was detected in the high-elderly onset SPIDDM. Taken together HLA typing with her history of both RA and Hashimoto disease, our case may provide the information to the mechanism of pathogenesis of SPIDDM. Furthermore, to out knowledge, this is the first case of SPIDDM in the aged; 75-year-old or more.
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PMID:[Slowly progressive IDDM with rheumatoid arthritis and Hashimoto disease in high elderly]. 977 59

The clinical significance of anti-pituitary antibodies (APA) was examined by enzyme-linked immunosorbent assay (ELISA) in individuals with non-insulin dependent diabetes mellitus (NIDDM). Serum samples were obtained from 150 NIDDM patients and 45 normal subjects. Urinary C-peptide (U-CPR) was also measured for the NIDDM patients. APA-positive serum was incubated with porcine pancreas, liver, kidney, or spleen powder and analyzed by immunoblot. The prevalence of APA was found to be significantly (P<0.05) higher in NIDDM patients (24.7%) than in the controls (6.7%) by ELISA. The index values for APA were inversely related to the levels of U-CPR (P<0.005). The levels of U-CPR were significantly (P<0.0001) lower and the prevalence of insulin deficiency was significantly (P<0.05) higher in NIDDM patients who were APA positive than in those who were APA negative. The presence of APA may therefore be related to reduced secretion of insulin in NIDDM patients. In Western blot analysis, preincubation of APA-positive sera with porcine pancreas powder prevented recognition of the 22-kD protein (APA). The possibility of a common autoantigenicity in the pancreas and the pituitary was indicated.
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PMID:Studies on circulating anti-pituitary antibodies in NIDDM patients. 979 Feb 68


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