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)

Women with GDM have a greater risk of developing diabetes in the future compared with those women who have normal glucose tolerance during pregnancy. Using life table techniques, 17 years after the initial diagnosis of GDM, 40% of women were diabetic compared with 10% in a matched control group of women who had normal glucose tolerance in pregnancy. The incidence of diabetes was higher among women who were older, more obese, of greater parity and with more severe degrees of glucose intolerance during pregnancy. Diabetes also occurred more commonly among women who had a first-degree relative who was diabetic, in women born in Mediterranean and East Asian countries, and in those who had GDM in two or more pregnancies. Despite differing testing techniques and varying criteria for the diagnosis of GDM, follow-up studies from across the world consistently show a higher rate of subsequent diabetes among GDM mothers. NIDDM is associated with increased morbidity and a higher mortality rate, especially in women. Cardiovascular and cerebrovascular diseases are the leading causes of death. High lipid levels, hypertension and obesity are often already present when diabetes is diagnosed and may antedate the development of overt diabetes; treatment of diabetes at this stage may therefore be too late to prevent complications occurring. A follow-up programme for women with GDM facilitates screening of a group known to be at increased risk of developing diabetes so that the diagnosis can be made before associated risk factors for complications develop. Intervention in the form of counselling regarding cigarette smoking, exercise and a healthy, high-residue, unrefined carbohydrate, low cholesterol diet, given together with weight monitoring, may prevent the onset of both diabetes and its associated cerebrovascular and cardiovascular problems.
 ...
PMID:Long-term implications of gestational diabetes for the mother. 195 23

The attempt has been made to identity the lowest dose of glipizide, a second generation sulphonylurea, capable of improving glucose tolerance in overweight and obese subjects with various degrees of glucose tolerance. Thirty one obese subjects, 12 with non insulin dependent diabetes mellitus (NIDDM), 9 with impaired glucose tolerance (IGT) and 10 with normal glucose tolerance (NGT) each underwent four OGTTS (75 g), at 1 week intervals, after administration in random order of placebo or glipizide 0.5, 1.0 or 2.5 mg 30 min before glucose. Glucose tolerance in all groups was progressively improved by the increasing doses of glipizide and was normalized by 1.0 mg glipizide in impaired glucose tolerance (IGT) and by 2.5 mg glipizide in NIDDM. Insulin release was not significantly affected by glipizide in the three groups of subjects. The data indicate that it is possible, at least in acute experiments, to improve glucose tolerance in overweight and obese subjects with IGT, with NGT and with NIDDM, with doses of glipizide that do not affect insulin release.
 ...
PMID:Acute effect of glipizide on glucose tolerance in obesity and diabetes mellitus (NIDDM). 206 May 41

Glucose intolerance often occurs in liver cirrhosis; therefore a long-term control of plasma glucose levels appears to be important. For this purpose glycated hemoglobin A (HbA1c) determination is proposed as a suitable method, while no data are available on fructosamine test. In 98 cirrhotic patients serum fructosamine and HbA1c levels were compared with those of normal controls and among cirrhotic patients grouped in non glucose-intolerant and with non insulin-dependent (NIDDM) or insulin-dependent diabetes mellitus (IDDM). The mean HbA1c values of cirrhotic patients with normal glycemic control were significantly lower than normal, and only a few IDDM and NIDDM cirrhotic patients showed high values of HbA1c, indicating that HbA1c is often underestimated in these patients. On the contrary, serum fructosamine levels were on the average higher than normal in nondiabetic patients, but they were significantly higher in IDDM and NIDDM patients than in nondiabetics, and the 72% of NIDDM and 85% of IDDM patients had fructosamine levels higher than the upper normal value. In conclusion, in diabetic patients with liver cirrhosis fructosamine seems to be a more suitable test than HbA1c for monitoring blood glucose levels.
 ...
PMID:Fructosamine and glycated hemoglobin as indices of glycemic control in patients with liver cirrhosis. 207 78

To determine quantitative and qualitative differences in insulin secretion equimolar amounts of glucose and arginine were infused in 9 healthy subjects, in 8 individuals each with obesity without and with impaired glucose tolerance, and in non-obese and obese non-insulin-dependent diabetic patients (NIDDM). Insulin secretion was calculated after individual determination of metabolic clearance rate of C-peptide (MCRcp) both as the area under the C-peptide concentration curve times MCRcp, and by a mono-compartment mathematical model, both yielding identical results. MCRcp fell consistently with increasing C-peptide infusion rate (e.g.: healthy subjects: C-peptide, 10 nmol/h, 4.2 +/- 0.4; 20 nmol/h, 3.3 +/- 0.3; 30 nmol/h, 3.1 +/- 0.2 ml/kg.min; p less than 0.05 to p less than 0.01). Basal insulin secretion was 2.1-fold greater in the obese with impaired glucose tolerance than in healthy subjects, but was unchanged in non-obese NIDDM. Glucose and arginine triggered insulin release was greater than in healthy subjects at almost identical area under the respective substrate concentration curve (AUC/kg body weight) in obese subjects without (2-fold) and with impaired glucose tolerance (4-fold), and in NIDDMs following i.v. arginine (2-fold). The mean ratio of incremental insulin release to i.v. glucose and arginine was smaller in NIDDM (normal weight, 1.3 +/- 0.4; obese, 1.0 +/- 0.2) than in healthy (2.0 +/- 0.3), or obese subjects with impaired glucose tolerance (2.8 +/- 0.7). Stimulated C-peptide/insulin ratio was reduced in all patients vs that in healthy subjects (p less than 0.05). We conclude that (a) MCR of C-peptide is in part a saturable process; (b) insulin clearance may be impaired in obesity and NIDDM; and (c) insulin secretion differs in obese states and NIDDM both quantitatively and qualitatively, and thereby separates the two disorders as different entities. In addition, quantitation of insulin release in obese states may also help (d) to better define primary algorithms for insulin replacement in normal- and overweight insulin-dependent diabetic patients.
 ...
PMID:Quantitative and qualitative differences in basal and glucose- and arginine-stimulated insulin secretion in healthy subjects and different stages of NIDDM. 207 83

Diabetic relatives and obese subjects are at increased risk for development of diabetes mellitus, and therefore are classed as potential abnormality of glucose tolerance (POT-AGT). Disturbances of lipid and purine metabolisms have been reported in diabetic and obese non-diabetic subjects. In obese subjects above alterations are probably due to hyperinsulinemia. This study aimed at verifying whether similar metabolic abnormalities could be found in relatives of non-insulin dependent diabetic patients and whether they could be related to possible glucose intolerance. We have studied 10706 outpatients and 95 hospitalized subjects, aged between 20 and 50 years. We have selected 4 groups according to diabetic relationship and body mass index: A (normal weight subjects), B (obese subjects), C (normal weight NIDDM-relatives), D (overweight NIDDM-relatives). The NIDDM-relatives showed higher prevalence of hyperglycemia, as expected; furthermore the relatives with normal glucose tolerance had higher glucose area during OGTT. Serum levels of uric acid and insulin response to oral glucose were increased in all obese subjects, but abnormalities of lipid metabolism and fasting hyperinsulinemia were found only in obese NIDDM-relatives. These results suggest that family history of diabetes mellitus can be a risk for metabolic disturbance even in absence of glucose intolerance. Furthermore some metabolic disorders observed in obese subjects could be due to an associated and not sufficiently investigated family history of diabetes.
 ...
PMID:Metabolic abnormalities in first-degree relatives of type 2 diabetics. 208 58

In vivo studies indicate that patients with NIDDM have defects in both insulin secretion and insulin action. The decrease in insulin action is due to both hepatic and extrahepatic insulin resistance. The impairment in glucose uptake is associated with alterations in both oxidative and nonoxidative disposal. Defective glucose transport may limit both of these processes. NIDDM also is associated with increased concentrations and rates of oxidation of plasma free fatty acids. Insulin resistance appears to be familial and in at least some individuals antedates glucose intolerance. In vitro studies indicate that insulin resistance can involve a variety of insulin sensitive tissues including adipocytes, muscle and liver. While most studies note that insulin binding and insulin receptor kinase activity are decreased in insulin sensitive tissues in obese patients with NIDDM, further delineation of the contribution of obesity and diabetes is required. Alterations in glucose transporter number and function likely account at least in part for impaired glucose transport. The cause of the alterations in other insulin responsive pathways and the role of an abnormal metabolic milieu versus intrinsic cellular defects remain to be established.
 ...
PMID:Insulin resistance in type II diabetes mellitus. 216 26

Overt diabetes (NIDDM) was induced by overeating in neonatally streptozocin (60 mg/kg.BW) treated impaired glucose tolerant mice. We imposed a food restriction and a high fiber diet to evaluate the effects of dietary treatment in this NIDDM model mouse. Furthermore, insulin secretion after the dietary treatment was studied using the perfused pancreas technique. One group of IGT mice (SZ) was maintained on ordinary mouse chow during 6 to 14 weeks of age. The others received a cookie and chocolate mashed diet (C.C. diet) to induce overt diabetes during 6 to 10 weeks of age. Thereafter, the mice with induced overt diabetes were divided according to their diet treatment. The C.C. diet was continued in one group (SZC) for 4 weeks, and the others were divided into a food restriction group (SZR: 4 g/mouse/day of ordinary mouse chow, for 4 weeks) and a high fiber diet group (SZF: 20% W/W of cellulose in ordinary mouse chow, for 8 weeks). The mean caloric intake/mouse/day in SZC, SZR and SZF were 140, 80 and 98% of that in SZ, respectively. Amelioration of hyperglycemia and impaired glucose tolerance was noted in SZR and SZF. A better glycemic control was obtained in SZF with keeping a normal growth rate. On the pancreas perfusion, the insulin secretion to 30 mM glucose was improved in SZR and SZF. Furthermore, the incremental first phase peak insulin release to 30 mM glucose in SZF was significantly greater than that in SZC (SZF, 10.5 +/- 1.0 vs. SZC, 4.5 +/- 1.9 microU/min).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Dietary treatment ameliorates overt diabetes and decreased insulin secretion to glucose, induced by overeating in impaired glucose tolerant mice. 217 33

Young female obese (cp/cp) and lean littermates (?/+) of the recently developed congenic strain, SHR/NIH-corpulent (SHR/N-cp), were fed for 6.5 months isocaloric diets containing 54 percent carbohydrate as either sucrose or starch. Glycemic, lipidemic and renal parameters were determined after 1, 3 and 6 months. Systolic blood pressure and plasma corticosterone levels were determined after 3 months. After 6.5 months rats were killed for histological examination. Obese rats were hyperglycemic following an oral glucose challenge (1 hour response greater than 11.1 mmol/l) (200 mg/dl), hyperinsulinemic, hypertriglyceridemic, and developed proteinuria and mild hypertension. Feeding sucrose, as compared to starch, further increased serum glucose, insulin and triglyceride levels and urinary protein excretion in obese rats and serum triglyceride levels in lean rats. An amelioration of glucose intolerance was observed in sucrose-fed obese rats by 6 months. In contrast to serum insulin levels, serum triglyceride levels increased with age in obese rats. Obese rats exhibited hypertrophy of the kidney and adrenal cortex with abnormal histology. The study demonstrates that obese female SHR/N-cp rats exhibit some of the metabolic and histopathological changes associated with NIDDM in humans and that feeding sucrose, as the source of dietary carbohydrate, further magnifies the expression of diabetes in this model.
 ...
PMID:Influence of genetic obesity, dietary carbohydrate and age on parameters of glucose tolerance and kidney and adrenal gland histology in female SHR/N-corpulent rats. 217 55

We tested the hypothesis that insulin resistance, rather than high insulin level, is associated with lipid and lipoprotein changes favoring atherosclerosis independently of the glucose tolerance status. To this aim, 50 subjects with normal glucose tolerance, 28 subjects with impaired glucose tolerance, and 54 subjects with noninsulin-dependent diabetes (NIDDM) were studied. Subjects with low glucose disposal rate (GDR) or a high degree of insulin resistance as measured by the euglycemic hyperinsulinemic clamp technique had lower high density lipoprotein (HDL) cholesterol and higher total and very low density lipoprotein (VLDL) triglycerides than did subjects with high GDR (highest GDR tertile). These associations were independent of fasting insulin level and other confounding factors. In stepwise multiple linear regression analysis, GDR was the most important single variable associated with HDL cholesterol and VLDL triglyceride level independently of age, obesity, distribution of obesity (waist/hip ratio), 2-hour glucose level, and free fatty acid concentration. We conclude: 1) insulin resistance measured by the euglycemic clamp technique is associated with adverse lipid and lipoprotein changes favoring atherosclerosis not only in nondiabetic subjects (as shown in previous studies) but also in impaired glucose tolerance and NIDDM subjects; 2) the association of high insulin level with adverse lipid and lipoprotein changes indirectly reflects the association of insulin resistance with lipid and lipoprotein levels; and 3) HDL cholesterol and VLDL triglycerides are independently associated with insulin-mediated glucose uptake, which may indicate that these lipoproteins have separate sites of interaction with insulin action.
 ...
PMID:Insulin resistance is associated with lipid and lipoprotein abnormalities in subjects with varying degrees of glucose tolerance. 218 Mar 96

Islet amyloid polypeptide (IAPP) has been implicated by in vitro studies as an inhibitor of insulin-stimulated glucose utilization by skeletal muscle cells and also as an inhibitor of insulin-stimulated insulin secretion by beta cells. Increased expression and production of IAPP by beta cells, as has been suggested to occur in cats with impaired glucose tolerance, could thus contribute substantially to the development of the insulin resistance and impaired insulin release which are the hallmarks of Type 2 diabetes mellitus. The effects of IAPP with respect to glucose metabolism in living animals, however, have not been previously reported. In the present in vivo study we show that synthetic amidated IAPP induced impaired glucose tolerance in each of the 3 cats studied, with dramatic impairment (increases in glucose to T1/2 values of 124% and 234%) in 2 of the 3 cats. Impaired insulin responses were also evident in the 2 cats with the most dramatic states of glucose intolerance. These results provide the most direct evidence to-date that IAPP may have an important role in the development of Type 2 diabetes mellitus.
 ...
PMID:The putative hormone islet amyloid polypeptide (IAPP) induces impaired glucose tolerance in cats. 218 15


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