Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the clinical utility of 123I-metaiodobenzylguanidine (MIBG) scintigraphy in evaluating cardiac sympathetic nerve disturbance in diabetic patients, we performed MIBG scintigraphy in 18 diabetic patients and 11 normal controls. Diabetic patients with symptomatic neuropathy (DM2) had a significantly lower heart to mediastinum uptake ratio than did those without neuropathy or normal controls in initial and delayed images (initial image, 1.90 +/- 0.27 vs 2.32 +/- 0.38, 2.41 +/- 0.40, p< 0.01; delayed image, 1.80 +/- 0.31 vs 2.48 +/- 0.35 2.56 +/- 0.28, p < 001, respectively). Defect score, assessed visually, were higher in DM2 patients than in patients in the other two groups (initial image, 7 +/- 2.6 vs 1.5 +/- 1.9, 0.7 +/- 0.9; delayed image 10.6 +/- 3.3 vs 4.0 +/- 2.5, 1.7 +/- 1.6 p < 0.01, respectively). The maximum washout rate in DM2 patients was also higher than those in patients in the other two groups. The findings of these indices obtained from MIBG scintigraphy coincided with the % low-frequency power extracted from heart rate fluctuations using a power spectral analysis and the results of the Schellong test, which were used to evaluate sympathetic function. These results suggest that MIBG scintigraphy may be useful for evaluating cardiac sympathetic nerve disturbance in patients with diabetes.
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PMID:Clinical usefulness of 123I-metaiodobenzylguanidine myocardial scintigraphy in diabetic patients with cardiac sympathetic nerve dysfunction. 750 May 43

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.
Diabetes Res Clin Pract 1994 Dec 31
PMID:Management of type 2 diabetes in Western Australian metropolitan general practice. 773

Blood glucose levels were continuously monitored in 70 subjects during a 75 g oral glucose tolerance test (OGTT). Subjects were divided into normal (N = 15), borderline (N = 31), diabetes with fasting glucose levels below 140 mg/dl (DM1) (N = 15) and diabetes with levels above 140 mg/dl (DM2) (N = 9). Three patterns of blood glucose curves were observed in each subject group; domed, biphasic and upward. The frequency of blood glucose patterns in each class of glucose tolerance group was as follows: in the normal group; domed 33.3%, biphasic 66.7%; in the borderline group; domed 67.7%, biphasic 29.0%, upward 3.2%; in the DM1 group; domed 66.7%, biphasic 13.3%, upward 20.0%; in the DM2 group; domed 77.8%, upward 22.2%. The frequency of patients with a biphasic pattern was significantly higher in the normal group than in the other groups. In the borderline group, almost all patients with a biphasic pattern were young or middle aged (< 60 years old). When the patients with fasting glucose levels below 140 mg/dl were analyzed, the mean peak time and peak value of blood glucose levels were significantly higher in patients with domed patterns than those with biphasic patterns. Indices of early insulin response to glucose load were significantly lower in patients with domed patterns than in those with a biphasic pattern. In conclusion, the pattern of the glucose curve in an OGTT is mainly dependent on the patient's early insulin response. Glucose intolerance with aging resembles diabetes from the standpoint of the pattern of glucose tolerance curves.
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PMID:[Oral glucose tolerance test using a continuous blood sampling technique for analysis of the blood glucose curve]. 793 56

The present study was undertaken to evaluate the effects of a selective thromboxane synthetase inhibitor (OKY-046) on urinary prostaglandins (PGs) excretion and renal parameters such as endogenous creatinine clearance rate (Ccr) and urinary protein excretion in streptozotocin (STZ)-induced diabetic rats. STZ-diabetic rats were divided into two groups; one fed standard chow (DM1) and the other, standard chow mixed with 0.1% OKY-046 (DM2) for 24 weeks. Male Wistar rats were fed standard chow for 24 weeks as control (C). Urinary thromboxane B2 (TXB2) and 6-keto-PGF1 alpha excretions significantly increased in STZ-induced diabetic rats (DM1 and DM2) compared with C after 24 weeks. The increased urinary TXB2 excretion in DM2 was significantly reduced (p < 0.05) compared with that in DM1 (261.1 +/- 18.6 ng/gCr versus 380.0 +/- 48.4 ng/gCr, mean +/- SEM). No significant difference could be found in urinary protein excretion between DM1 and DM2, which was significantly higher in both diabetic groups than C after 12 and 24 weeks. Ccr in both DM1 and DM2 significantly increased (p < 0.05) compared with C after 12 weeks. In contrast, after 24 weeks, Ccr in DM1 fell down to 0.18 +/- 0.02 mL/min 100 g body weight (BW), thus being significantly lower (p < 0.05) than that in C (0.27 +/- 0.03 mL/min 100 g BW) and DM2 (0.25 +/- 0.02 mL/min 100 g BW). Electron microscopic findings in diabetic rats after 24 weeks were the typical change of early diabetic nephropathy, whereas there were no obvious differences between DM1 and DM2.(ABSTRACT TRUNCATED AT 250 WORDS)
J Diabetes Complications
PMID:Effects of thromboxane synthetase inhibitor (OKY-046) on urinary prostaglandin excretion and renal function in streptozotocin-induced diabetic rat. 806 49

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.
Diabetes Res Clin Pract 1998 Oct
PMID:The role of autonomic neuropathy as a risk factor of Helicobacter pylori infection in dyspeptic patients with type 2 diabetes mellitus. 988 32

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.
Diabetes 2000 Jul
PMID:Glucose-mediated glucose disposal in insulin-resistant normoglycemic relatives of type 2 diabetic patients. 1090 80

Obesity and type 2 diabetes mellitus (DM2) are 2 closely related syndromes, with obesity occurring in 70% to 80% of DM2 patients. Both syndromes are characterized by insulin resistance (IR). However, the metabolic characteristics of lean DM2 patients are not clearly defined, a fact attributed to the heterogeneity of the diabetes syndrome. Our objective was to study glucose metabolism in lean DM2 patients, in terms both of the basal and the insulin-stimulated states, and particularly, to investigate whether 2 subpopulations of diabetic patients are identifiable on the basis of degree of IR. Sixteen nonobese (body mass index [BMI] less than 27 kg. m(-2)) DM2 subjects with light to moderate fasting hyperglycemia were studied. Ten healthy subjects were used as a control group, with no family history of DM2 and matched by age, sex, and BMI in the diabetic group. All participants underwent an intravenous glucose tolerance test with frequent sampling over 180 minutes. Insulin sensitivity (IS) and glucose effectiveness at zero insulin (GEZI) were calculated using Bergman's minimal model. Non-insulin-mediated glucose uptakes (NIMGU) and insulin-mediated glucose uptakes (IMGU) were calculated for the basal (F) and insulin-stimulated states at 11.1 mmol/L of glucose (11.1). The beta-cell function was calculated via the acute insulin response to glucose (AIRg). Clustering techniques were used to identify subpopulations of DM2 patients on the basis of insulin sensitivity. The group of DM2 patients was characterized by both IR (IS index, 6.23 +/- 4.68 v 12.75 +/- 7.74 x 10(-5). min(-1). (pmol. L(-1))(-1), P <.01) and insulin secretion abnormalities (AIRg, 336 +/- 456 v 1,912 +/- 1,293 pmol/L. min, P <.0001), but showed similar values for GEZI (0.011 +/- 0.005 v 0.011 +/- 0.007 min(-1), not significant [NS]) in comparison to the control group. For the basal state, no differences were found between the DM2 patients and control subjects for NIMGU(F) (0.13 +/- 0.07 v 0.08 +/- 0.05 mmol/kg. min, NS) or for IMGU(F) (0.05 +/- 0.04 v 0.05 +/- 0.02 mmol/kg. min, NS). For the insulin-stimulated state, the DM2 patients showed a reduction of approximately 50% in the IMGU(11.1) value (0.20 +/- 0.17 v 0.38 +/- 0.24 mmol/kg. min, P <.05), but no significant differences were found for NIMGU(11.1) (0.19 +/- 0.09 v 0.20 +/- 0.12 mmol/kg. min, NS) in relation to the control group. Using the clustering technique, it was possible to identify 2 subpopulations of DM2 patients, a DM-IS group (n = 6) that was insulin sensitive (IS index, 11.70 +/- 2.40 x 10(-5). min(-1). (pmol. L(-1))(-1)) and a DM-IR group (n = 10) that was insulin resistant (IS index, 3.02 +/- 1.60 x 10(-5). min(-1). (pmol. L(-1))(-1)). The DM-IS group was characterized by an absence of IR, diminished GEZI, and a reduction in AIRg; whereas the DM-IR group was characterized by IR and a reduction in AIRg, but normal GEZI. We conclude that (1) as a group, DM2 patients are characterized by IR and beta-cell dysfunction, but normal NIMGU; (2) two subpopulations of DM2 patients can be identified on the basis of insulin sensitivity, with the DM-IS group further characterized by diminished GEZI; and finally, (3) deterioration in the pancreatic response to glucose stimulus is a sine qua non condition for a profound alteration in glucose metabolism in DM2 patients.
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PMID:Glucose metabolism in lean patients with mild type 2 diabetes mellitus: evidence for insulin-sensitive and insulin-resistant variants. 1214 80

Type 2 diabetes mellitus (DM2) is characterized metabolically by defects in both insulin secretion and insulin action, resulting in hyperglycemia. Histopathologically, DM2 is characterized by depositions of protein in the pancreatic islets. This 'islet amyloid' is present in >90% of patients with DM2, as well as in monkeys and cats with DM2. The pathogenesis of DM2 is heterogeneous and multifactorial, although insulin resistance seems to be the predominant initiating factor for development of the disease. In the longer term, an insulin secretion defect is also revealed (referred to as 'beta-cell failure'), resulting in clinically manifest diabetes. Recent data, particularly from transgenic mouse studies, indicate that islet amyloidosis is a diabetogenic factor, which is both consequence (of insulin resistance) and cause (of beta-cell failure) of DM2. Available transgenic mouse models with islet amyloid formation in vivo will provide the opportunity to assess the effectiveness of novel anti-amyloidogenic therapies, for which promising results are emerging.
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PMID:Role of islet amyloid in type 2 diabetes mellitus: consequence or cause? 1243 14

190 patients with diabetes mellitus (DM) were examined: 24 patients with DM type 1 and 166 with DM type 2. Frequency of arterial hypertension (AH) in diabetics is higher than in population. AH in different DM types varies by pathogenesis. Symptomatic renal AH is typical for DM1, essential AH combining with renal one in 1/3 of cases--for DM2. Treatment of AH and DM often provokes hypothyroidism which can be iatrogenic because of continuous intake of sugar reducing and antihypertensive drugs with antithyroid and strumogenic actions. Hypothyroidism aggravates an AH course: arterial pressure becomes high and resistant to hypotensive therapy. DM makes difficulties in selection of hypotensive drugs as many of them alter metabolism and due to negative attitude of the patients to continuous intake of sugar reducing, antihypertensive drugs, thyroid hormones. Therefore, hypertensive diabetics should be prepared for treatment psychologically and receive only prolonged hypotensive drugs. In DM with AH medication of choice is ACE inhibitors as they are nephroprotective, had no negative effect on carbohydrate, fat metabolism and thyroid system.
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PMID:[Role of thyroid pathology in pathogenesis of arterial hypertension in diabetes]. 1247 32

Accelerated glycoxidation takes part in the development of diabetic complications. We determined advanced glycation end-products (AGEs) and advanced oxidation protein products (AOPP) in the sera of 52 patients with diabetes mellitus (DM) - 18 with DM Type 1 and 34 with DM Type 2 and examined their relationship to the compensation of the disease. AGEs were estimated spectrofluorimetrically (350 nm/440 nm) whereas AOPP were determined spectro-photometrically (340 nm). AGEs were elevated only in DM Type 2 (DM2 5.11+/-1.15 x 10(3) AU/g vs controls 4.08+/-0.71 x 10(3) AU/g, p<0.001, vs DM1 4.14+/-0.86 x 10(3) AU/g, p<0.005, DM1 vs controls were not significant). AOPP were elevated significantly in both types of DM with higher levels in DM Type 2 (DM2 157.50+/-75.15 micromol/l vs healthy subjects 79.80+/-23.72 micromol/l, p<0.001, vs DM1 97.50+/-30.91 micromol/l, p<0.005, DM1 vs controls p<0.05). There was a tight correlation between AGEs and AOPP in both types of DM (DM1 r=0.75, DM2 r=0.47 (p<0.05)) and both AGEs and AOPP correlated with triglycerides. In DM Type 1 only, AGEs correlated with HbA1c r=0.47 (p<0.05) and with blood glucose. Slight but not significant differences in AGEs and AOPP levels were observed in patients with or without diabetic complications. Oxidative stress is increased in both types of DM, more in Type 2 where it contributes to the formation of glycoxidation products.
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PMID:Advanced glycation end-products and advanced oxidation protein products in patients with diabetes mellitus. 1251 Nov 84


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