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)

The purpose of this study was: (1) to record GP opinions, practices and outcomes for the care of Type 2 Diabetes Mellitus (DM2), (2) compare practice facilities and process of care with a criterion of recommended competent care and (3) determine if there were any differences between vocationally registered and non-vocationally registered GPs. A random sample of 204 metropolitan doctors from 124 practices was selected and an audit performed on 467 of their patient records. GPs pursued good blood sugar control and advocated lifestyle changes before hypoglycaemic drugs. Over 80% regard uncomplicated DM2 as a condition for general practice management. However, only 15% conducted an annual diabetes check, 9% had a diabetic register, 6% a diabetic recall system and 8% used a diabetic health care checklist for monitoring their patients. The most commonly recorded processes of medical audit in the previous 12 months were: blood pressure (94%), duration of diabetes (72%), blood glucose (70%), diet (66%), body weight (56%), HBA1c (52%) and ophthalmoscopy (50%). The least commonly recorded processes of care were body mass index (5%), inspection of the feet (18%), enquiries about vaginitis or impotence (23%). The amount of exercise, alcohol and tobacco was recorded in only 34% of records. Hypoglycaemic drugs were used appropriately but the most commonly used drugs for treating hypertension in DM2 patients were thiazide diuretics and beta-blockers. Vocationally registered (VR) doctors had better records, higher process of care scores and more were willing to participate in the study than non-vocationally registered (NVR) doctors. However, there was no difference in metabolic control between patients from either group. The use of a Diabetic Health Care Checklist would improve diabetes care especially in the search for early complications and in the recording of HBA1c and other metabolic parameters. The drugs commonly used to control hypertension can have adverse effects on glucose and lipid metabolism and should be replaced with glucose and lipid neutral drugs.
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PMID:Management of type 2 diabetes in Western Australian metropolitan general practice. 773

We examined the ability of an equivalent increase in circulating glucose concentrations to inhibit endogenous glucose production (EGP) and to stimulate glucose metabolism in patients with Type 2 diabetes mellitus (DM2). Somatostatin was infused in the presence of basal replacements of glucoregulatory hormones and plasma glucose was maintained either at 90 or 180 mg/dl. Overnight low-dose insulin was used to normalize the plasma glucose levels in DM2 before initiation of the study protocol. In the presence of identical and constant plasma insulin, glucagon, and growth hormone concentrations, a doubling of the plasma glucose levels inhibited EGP by 42% and stimulated peripheral glucose uptake by 69% in nondiabetic subjects. However, the same increment in the plasma glucose concentrations failed to lower EGP, and stimulated glucose uptake by only 49% in patients with DM2. The rate of glucose infusion required to maintain the same hyperglycemic plateau was 58% lower in DM2 than in nondiabetic individuals. Despite diminished rates of total glucose uptake during hyperglycemia, the ability of glucose per se (at basal insulin) to stimulate whole body glycogen synthesis (glucose uptake minus glycolysis) was comparable in DM2 and in nondiabetic subjects. To examine the mechanisms responsible for the lack of inhibition of EGP by hyperglycemia in DM2 we also assessed the rates of total glucose output (TGO), i.e., flux through glucose-6-phosphatase, and the rate of glucose cycling in a subgroup of the study subjects. In the nondiabetic group, hyperglycemia inhibited TGO by 35%, while glucose cycling did not change significantly. In DM2, neither TGO or glucose cycling was affected by hyperglycemia. The lack of increase in glucose cycling in the face of a doubling in circulating glucose concentrations suggested that hyperglycemia at basal insulin inhibits glucose-6-phosphatase activity in vivo. Conversely, the lack of increase in glucose cycling in the presence of hyperglycemia and unchanged TGO suggest that the increase in the plasma glucose concentration failed to enhance the flux through glucokinase in DM2. In summary, both lack of inhibition of EGP and diminished stimulation of glucose uptake contribute to impaired glucose effectiveness in DM2. The abilities of glucose at basal insulin to both increase the flux through glucokinase and to inhibit the flux through glucose-6-phosphatase are impaired in DM2. Conversely, glycogen synthesis is exquisitely sensitive to changes in plasma glucose in patients with DM2.
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PMID:Regulation of endogenous glucose production by glucose per se is impaired in type 2 diabetes mellitus. 971 Apr 43

A high prevalence of upper gastrointestinal symptoms is described in diabetic patients and, at least in part, this has been attributed to abnormal emptying of the stomach. In an unselected small series of dyspeptic patients with Type 2 diabetes mellitus (DM2), we previously described a higher prevalence of Helicobacter pylori (Hp) infection associated with autonomic neuropathy (AN) than in non-diabetic subjects. To evaluate the prevalence of Hp and its relationship with AN, we studied 164 DM2 patients, matched for sex, age ( +/- 5 years) and body weight ( +/- kg) to 164 non-diabetic subjects, all affected with dyspepsia of unknown origin. Results document that the prevalence of peptic ulcer is similar in both groups of patients (20.1 vs 29.3% P = n.s.); chronic gastritis was 50% in the control group and 35.4% in the DN2 group (P < 0.01) and dyspepsia without ulcer and gastritis (simple dyspepsia) was significantly more frequent in DM2 patients than in non-diabetics (44.5 vs 20.7%, P < 0.01). Hp infection was documented by histology of gastrointestinal mucosa in 74.4% of the DM2 patients and in 50% of the controls (P < 0.01) (ulcer: 97 vs 71%, P < 0.05; gastritis: 72 vs 43.5%, P < 0.05; simple dyspepsia: 66 vs 35%, P < 0.01, respectively). Autonomic neuropathy was found in 65.2% of the DM2 patients (90.9% of patients with ulcer, 65.5% with gastritis and 53.4% with simple dyspepsia). A significant concordance (84.7%, P < 0.001) was found between the presence of AN and Hp infection. Data provide, for the first time, direct evidence for a higher frequency of Hp infection in dyspeptic patients affected with DM2 than in non-diabetic subjects. In addition, in diabetic patients the frequency of non-ulcer, non-gastritis dyspepsia is two times higher than in non-diabetics and is strictly associated with autonomic neuropathy, acting as a favoring factor for occurrence and recurrence of gastrointestinal disease.
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PMID:The role of autonomic neuropathy as a risk factor of Helicobacter pylori infection in dyspeptic patients with type 2 diabetes mellitus. 988 32

Protein tyrosine phosphatases (PTPs) are required for the dephosphorylation of the insulin receptor (IR) and its initial cellular substrates, and it has recently been reported that PTP-1B may play a role in the pathogenesis of insulin resistance in obesity and type 2 diabetes mellitus (DM). We therefore determined the amount and activity of PTP-1B in abdominal adipose tissue obtained from lean nondiabetic subjects (lean control (LC)), obese nondiabetic subjects (obese control (OC)), and subjects with both type 2 DM (DM2) and obesity (obese diabetic (OD)). PTP-1B protein levels were 3-fold higher in OC than in LC (1444 +/- 195 U vs 500 +/- 146 U (mean +/- SEM), P < .015), while OD exhibited a 5.5-fold increase (2728 +/- 286 U, P < .01). PTP activity was assayed by measuring the dephosphorylating activity toward a phosphorus 32-labeled synthetic dodecapeptide. In contrast to the increased PTP-1B protein levels, PTP-1B activity per unit of PTP-1B protein was markedly reduced, by 71% and 88% in OC and OD, respectively. Non-PTP-1B tyrosine phosphatase activity was comparable in all three groups. Similar results were obtained when PTP-1B activity was measured against intact human IR. A significant correlation was found between body mass index (BMI) and PTP-1B level (r = 0.672, P < .02), whereas BMI and PTP-1B activity per unit of PTP-1B showed a strong inverse correlation (r = -0.801, P < .002). These data suggest that the insulin resistance of obesity and DM2 is characterized by the increased expression of a catalytically impaired PTP-1B in adipose tissue and that impaired PTP-1B activity may be pathogenic for insulin resistance in these conditions.
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PMID:Marked impairment of protein tyrosine phosphatase 1B activity in adipose tissue of obese subjects with and without type 2 diabetes mellitus. 1044 21

The clinical efficacy of bezafibrate was examined with special reference to glucose metabolism in patients with type 2 diabetes mellitus (DM2). In protocol 1, 342 patients with DM2 and hyperlipidemias were randomly divided into 2 groups, 16-week bezafibrate treatment (n = 174) and no bezafibrate treatment (n = 168). In protocol 2, 20 DM2 patients were randomly divided into 2 groups, 8-week bezafibrate treatment (n = 10) and no bezafibrate treatment (n = 10), and a meal tolerance test (MTT) was performed. In protocol 1, bezafibrate treatment significantly reduced the fasting levels of triglyceride (TG) by 50% +/- 1.6%, total cholesterol (TC) by 12% +/- 1.1%, plasma glucose (PG) from 151.3 +/- 3.5 to 128.6 +/- 3.4 mg/dL, and hemoglobin A1c (HbA1c) from 7.2% +/- 0.1% to 6.9% +/- 0.1%, and significantly increased high-density lipoprotein cholesterol (HDL-C) by 20% +/- 0.8%. In protocol 2, fasting TG, PG, and insulin levels were significantly reduced by bezafibrate treatment. Moreover, in the MTT, postprandial increments of TG were significantly blunted after bezafibrate treatment, whereas postprandial PG and insulin levels were not significantly changed. Leptin levels were significantly decreased, while tumor necrosis factor alpha (TNF-alpha) levels were not changed. In conclusion, both hyperglycemia and hyperlipidemia can be improved by bezafibrate treatment in DM2.
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PMID:Bezafibrate reduces blood glucose in type 2 diabetes mellitus. 1072 10

Both type 2 diabetes mellitus (DM2) and left ventricular hypertrophy are associated with an increased risk of cardiovascular diseases (CVD). A strong association between hyperinsulinemia, which is the hallmark of DM2 and of insulin resistance syndrome (a cohort of metabolic abnormalities such as DM2, dyslipidemia, hyperuricemia, obesity, hypertension, hyperfibrinogenemia), and left ventricular (LV) hypertrophy was found in several studies. We studied 140 consecutive (both normo- and hypertensive) DM2 patients to determine a possible link between metabolic features and the degree of LV mass, calculated by the ECG method of Cornell voltage. The Cornell voltage value was 12.9+/-0.5 mm in the DM2 population as a whole, and 13.6+/-0.7 vs 11.7+/-0.9 mm (p=NS) in hypertensive and normotensive DM2 subgroups, respectively. Among all the metabolic parameters taken into account, the multivariate analysis shows that the fasting plasma insulin level is the strongest independent predictor of LV mass, both in the whole population (p=0.0005) and in the normo (p=0.0460) and hypertensive DM2 (p=0.0184) subgroups.
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PMID:Left ventricular mass in type 2 diabetes mellitus. A study employing a simple ECG index: the Cornell voltage. 1080 69

With the aim of investigating glucose-mediated glucose disposal (glucose effectiveness [GE]) in 15 (3 female and 12 male subjects) insulin-resistant normoglycemic relatives of patients with type 2 diabetes (DM2), and 15 age-, sex-, and BMI-matched control subjects without a family history of DM2, we performed 2 studies: 1) a 5-h euglycemic near-normoinsulinemic pancreatic clamp with somatostatin (360 microg/h), insulin (0.25 mU x kg(-1) x min(-1)), glucagon (0.5 ng x kg(-1) x min(-1)), growth hormone (6 ng x kg(-1) x min(-1)), and tritiated glucose infusion and indirect calorimetry; and 2) on a separate day, an identical 5-h clamp but at hyperglycemia (approximately 12 mmol/l) over the last 2 h. Fasting plasma insulin (PI) concentrations were elevated in the relatives compared with control subjects (49 +/- 6 vs. 32 +/- 5 pmol/l, P < 0.04), whereas plasma glucose (PG) was not (5.6 +/- 0.1 vs. 5.5 +/-0.1 mmol/l). At the end (i.e., 4.5-5.0 h) of the euglycemic clamp (PG, 6.1 +/- 0.4 vs. 5.6 +/- 0.1 mmol/l; PI, 78 +/- 5 vs. 73 +/-6 pmol/l), peripheral glucose uptake (Rd(euglycemia)) was decreased in the relatives (2.93 +/- 0.08 vs. 3.70 +/-0.23 mg x min(-1) x kg(-1) fat free mass [FFM], P < 0.005), due to a decreased nonoxidative glucose disposal (0.83 +/-0.21 vs. 1.62 +/- 0.19 mg x min(-1) x kg(-1) FFM, P < 0.01), but hepatic glucose production (HGP) was increased (1.97 +/-0.19 vs. 1.50 +/- 0.13 mg x min(-1) x kg(-1) FFM, P < 0.05). At the matched end of the hyperglycemic clamp (PG, 12.7 +/-0.2 vs. 12.6 +/- 0.2 mmol/l; PI, 87 +/- 5 vs. 78 +/- 7 pmol/l), peripheral glucose disposal (Rd(hyperglycemia)) (5.52 +/- 0.22 vs. 5.92 +/- 0.29 mg x min(-1) x kg(-1) FFM, NS), nonoxidative glucose disposal (2.93 +/- 0.18 vs. 2.78 +/- 0.25 mg x min(-1) x kg(-1) FFM, NS), and HGP(hyperglycemia) (1.20 +/- 0.09 vs. 1.37 +/-0.23 mg x min(-1) x kg(-1) FFM, NS) were all identical. When the effectiveness of glucose itself on glucose uptake and production [(Rd(hyperglycemia) - Rd(euglycemia))/deltaPG and (HGP(euglycemia)- HGP(hyperglycemia))/deltaPG] was calculated, the relatives had a 22% increase in peripheral uptake (0.022 +/- 0.002 vs. 0.018 +/- 0.002 mg x min(-1) x kg(-1) FFM per mg/dl), due to a significantly increased nonoxidative glucose metabolism and enhanced suppression of HGP (0.0076 +/- 0.0021 vs. 0.0011 +/- 0.0022 mg x min(-1) x kg(-1) FFM per mg/dl, P < 0.05). In conclusion, in insulin-resistant relatives of DM2 patients, whole-body glucose-mediated glucose disposal is increased by GE enhancement of the muscle nonoxidative glucose pathway and by GE enhancement of the suppression of HGP. These mechanisms may represent a compensatory mechanism to the ongoing insulin resistance of these relatives.
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PMID:Glucose-mediated glucose disposal in insulin-resistant normoglycemic relatives of type 2 diabetic patients. 1090 80

The aim of this study was to estimate the prevalence of type 2 diabetes mellitus (DM2), impaired glucose tolerance (IGT), and the frequency of dyslipidemia, obesity, and hypertension in the rural Aymara population from Northern Chile. In this cross-sectional study, 196 Aymara adult subjects were characterized with respect to their reported physical activity, fasting plasma glucose levels, insulin concentrations, blood pressures, body mass indexes, and plasma lipid profiles. The participants also underwent a 2-h oral glucose tolerance test. The diagnostic criteria for DM2 and IGT followed those of the World Health Organization. The overall prevalence of DM2 was estimated as 1.5% (95% confidence interval: 0.3--4.5). Overall prevalence of IGT was calculated as 3.6% (1.5--7.3). The occurrence of obesity and dyslipidemia was relatively high in the Aymara population, although the frequency of sedentary habits, and the prevalence of hypertension were low. In conclusion, the prevalence of DM2 in the rural Aymara population living at high altitudes in Northern Chile, was much lower than that of other Amerindian groups that adopted lifestyles from industrialized Western societies. Despite a relatively high prevalence of a body mass index of at least 30 kg/m(2), especially in women (23.5%), high physical activity levels and low plasma-insulin concentrations may have been responsible in part for the low prevalence of DM2 in the Aymara population.
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PMID:Low prevalence of type 2 diabetes despite a high average body mass index in the Aymara natives from Chile. 1136 69

To investigate the changes of the arteries in extremities in patients with type 2 diabetes(DM2), fifty patients with DM2(35 women and 15 men, mean aged 57.54 +/- 14.19 years old, time of DM2 diagnosed one week-26 years, without the histories of hypertension and smoking) were studied. Radial, finger, anterior tibial and dorsum pedis arteries of all subjects were examined using color Doppler Ultrasonography, 30 of 50 patients had the symptoms of extremities (e.g., numbness, coldness and pain). The Doppler examination revealed: 1. In the patient group, arterial wall became thick, rough and rigid. The atherosclerotic plaques were found inside vascular cavities in 14/50 in patient group with one patient being asymptomatic of extremities. 2. The vascular cavities in patients remarkably narrowed compared with the control group (P < 0.05). The vascular lesion worsened along with the development of the symptoms. 3. Doppler spectra in the majority of patients displayed single-peak, whereas it displayed three peaks in normal subjects with significant differences (P < 0.05). 4. The peak flow velocities in the patients increased, and this increase was related to the development of the symptoms, but no significant differences were found. Color Doppler Ultrasound examination is valuable in the evaluation of the arterial lesion of the extremities, especially at the early stage of artery diseases in patients with DM2.
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PMID:[A study of color Doppler ultrasound on arteries of the extremities in patients with type 2 diabetes]. 1138 64

Elevated plasma angiotensinogen (AGT) levels have been demonstrated in insulin-resistant states such as obesity and type 2 diabetes mellitus (DM2), conditions that are directly correlated to hypertension. We examined whether hyperinsulinemia or hyperglycemia may modulate fat and liver AGT gene expression and whether obesity and insulin resistance are associated with abnormal AGT regulation. In addition, because the hexosamine biosynthetic pathway is considered to function as a biochemical sensor of intracellular nutrient availability, we hypothesized that activation of this pathway would acutely mediate in vivo the induction of AGT gene expression in fat and liver. We studied chronically catheterized lean (approximately 300 g) and obese (approximately 450 g) Sprague-Dawley rats in four clamp studies (n = 3/group), creating physiological hyperinsulinemia (approximately 60 microU/ml, by an insulin clamp), hyperglycemia (approximately 18 mM, by a pancreatic clamp using somatostatin to prevent endogenous insulin secretion), or euglycemia with glucosamine infusion (GlcN; 30 micromol. kg(-1). min(-1)) and equivalent saline infusions (as a control). Although insulin infusion suppressed AGT gene expression in fat and liver of lean rats, the obese rats demonstrated resistance to this effect of insulin. In contrast, hyperglycemia at basal insulin levels activated AGT gene expression in fat and liver by approximately threefold in both lean and obese rats (P < 0.001). Finally, GlcN infusion simulated the effects of hyperglycemia on fat and liver AGT gene expression (2-fold increase, P < 0.001). Our results support the hypothesis that physiological nutrient "pulses" may acutely induce AGT gene expression in both adipose tissue and liver through the activation of the hexosamine biosynthetic pathway. Resistance to the suppressive effect of insulin on AGT expression in obese rats may potentiate the effect of nutrients on AGT gene expression. We propose that increased AGT gene expression and possibly its production may provide another link between obesity/insulin resistance and hypertension.
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PMID:Hyperglycemia modulates angiotensinogen gene expression. 1150 94


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