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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 prevalence of nephropathy in black patients with type 2 diabetes mellitus is poorly defined. We performed a cross-sectional analysis of 98 unrelated and unselected black type 2 diabetic patients treated in indigent care internal medicine clinics to determine the prevalence of proteinuria and nephropathy. Serum creatinine, blood urea nitrogen, urine albumin and urine creatinine concentrations were measured. A Spearman's rank correlation was computed to test for a relationship between diabetes duration and continuous outcomes. For binary outcomes, an odds ratio and 95% confidence interval were computed for a change of 10 years diabetes duration based on logistic regression. Cases were 61% female, and had mean (+/- SD) age 59.9 +/- 12.5 years, diabetes duration 12.6 +/- 9.4 years, body mass index 32.4 +/- 9.3 kg/m(2), hemoglobin A1C (HbA1C) 9.2 +/- 2.3%, and serum creatinine concentration 1.60 +/- 1.1 mg/dl. For continuous variables, diabetes duration was positively associated with albuminuria (r = 0.31; p = 0.0017), serum creatinine (r = 0.36; p = 0.0003) and blood urea nitrogen concentration (r = 0.36; p = 0.0003). For binary variables, cases with longer diabetes duration were at increased risk for urinary albumin:creatinine >300 microg/mg (p = 0.006), elevated serum creatinine concentration (> or = 1.4 mg/dl in women or > or = 1.6 mg/dl in men; p = 0.045), elevated blood urea nitrogen concentration (> or = 20 mg/dl; p = 0.026), and clinical cerebrovascular disease (p = 0.028). HbA1C, body mass index, and blood pressure did not correlate with diabetes duration in this population. Among the cases, 33.7% had elevated serum creatinine concentration and 71.5% had abnormal levels of albuminuria (27.6% > 300 microg albumin/mg Cr and 43.9% 30-300 microg albumin/mg Cr). Abnormal proteinuria was seen in the majority of black patients with poorly controlled type 2 diabetes mellitus treated in indigent care clinics. This prevalence may be conservative, due to the widespread use of angiotensin-converting enzyme inhibitor therapy and exclusion of cases treated only by nephrologists. Approximately 70% of black patients with type 2 diabetes cared for in indigent care clinics have abnormal proteinuria and are at heightened risk for ESRD and death.
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PMID:Prevalence of nephropathy in black patients with type 2 diabetes mellitus. 1191 1

In patients with type 2 diabetes mellitus, we used nevibolol, a lipophilic high-selective beta 1-blocker. It has been found out that the drug, while augmenting the synthesis of nitrogen oxide, improves antioxidant properties. Therefore, it can be recommended for use in patients with type 2 diabetes mellitus concurrent with arterial hypertension to achieve normalization of arterial pressure and accomplish a correction of endothelial dysfunction.
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PMID:[Effects of nebivolol on serum levels of NO2 and NO3 oxides in patients with type 2 diabetes mellitus]. 1194 52

We report tamoxifen-induced hypertriglyceridemia and asymptomatic acute pancreatitis in a 51 year-old women with type 2 diabetes mellitus and stage III-b infiltrative ductal carcinoma, admitted to the hospital with weakness, oliguria and glucose dysregulation. On admission, there was no fever, abdominal or back pain, rebound tenderness, nausea, or vomiting. Following 1 year of tamoxifen treatment, triglycerides increased from 400 to 1344 mg/dl (blood urea nitrogen 52 mg/dl, creatinine 2.0 mg/dl, glucose 341 mg/dl). Hypertriglyceridemia was considered to be due to either diabetic dyslipidemia and/or tamoxifen. On computerized tomography, pancreatic enlargement, heterogenity, hypodensity and a pancreatic pseudocyst (5 x 7.5 cm diameter) were found. Acute pancreatitis was suspected, and serum amylase level was found to be increased (273 IU/L). Tamoxifen was discontinued and gemfibrozil was started. Triglycerides decreased to 301 mg/dl and amylase decreased to 66 IU/L a week later and remained normal thereafter. This case indicates that tamoxifen-induced hypertriglyceridemia may cause acute pancreatitis without classical symptoms which might be due to autonomic neuropathy in diabetic patients. Effects on lipid metabolism should be considered and triglycerides should be closely followed in patients on tamoxifen.
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PMID:Asymptomatic acute pancreatitis due to tamoxifen-induced severe hypertriglyceridemia in a patient with diabetes mellitus and breast cancer. 1212 Aug 88

Improvement of glycemic status by insulin is associated with profound changes in amino acid metabolism in type 1 diabetes. In contrast, a dissociation of insulin effect on glucose and amino acid metabolism has been reported in type 2 diabetes. Type 2 diabetic patients are reported to have reduced muscle oxidative enzymes and VO(2max). We investigated the effect of 11 days of intensive insulin treatment (T(2)D+) on whole-body amino acid kinetics, muscle protein synthesis rates, and muscle functions in eight type 2 diabetic subjects after withdrawing all treatments for 2 weeks (T(2)D-) and compared the results with those of weight-matched lean control subjects using stable isotopes of the amino acids. Whole-body leucine, phenylalanine and tyrosine fluxes, leucine oxidation, and plasma amino acid levels were similar in all groups, although plasma glucose levels were significantly higher in T(2)D-. Insulin treatment reduced leucine nitrogen flux and transamination rates in subjects with type 2 diabetes. Synthesis rates of muscle mitochondrial, sarcoplasmic, and mixed muscle proteins were not affected by glycemic status or insulin treatment in subjects with type 2 diabetes. Muscle strength was also unaffected by diabetes or glycemic status. In contrast, the diabetic patients showed increased tendency for muscle fatigability. Insulin treatment also failed to stimulate muscle cytochrome C oxidase activity in the diabetic patients, although it modestly elevated citrate synthase. In conclusion, improvement of glycemic status by insulin treatment did not alter whole-body amino acid turnover in type 2 diabetic subjects, but leucine nitrogen flux, transamination rates, and plasma ketoisocaproate level were decreased. Insulin treatments in subjects with type 2 diabetes had no effect on muscle mitochondrial protein synthesis and cytochrome C oxidase, a key enzyme for ATP production.
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PMID:Synthesis rate of muscle proteins, muscle functions, and amino acid kinetics in type 2 diabetes. 1214 50

In diabetic patients, a number of studies have suggested an impairment of vascular reactivity in response to vasodilatory stimuli. The pattern of dysregulation at the coronary microcirculatory level, however, has not been clearly defined. Thus, it was the aim of this study to characterise coronary microvascular function non-invasively in a homogeneous group of asymptomatic type 2 diabetic patients. In 46 patients with type 2 diabetes, myocardial blood flow (MBF) was quantified at baseline, in response to cold pressor test (CPT) and during adenosine-mediated vasodilation using positron emission tomography and nitrogen-13 ammonia. None of the patients had been treated with insulin, and none had symptoms of cardiac disease. Decreased MBF during CPT, indicating microvascular dysregulation, was observed in 16 patients (CPT-), while 30 patients demonstrated increased MBF during CPT (CPT+). Response to CPT was mildly, but significantly correlated with response to adenosine ( r=0.44, P=0.0035). There was no difference in HbA1c, serum lipid levels or serum endothelial markers between the groups. Microvascular dysregulation in the CPT- group was associated with elevated baseline MBF ( P<0.0001), reduced baseline vascular resistance ( P=0.0026) and an abnormal increase in resistance during CPT ( P=0.0002). In conclusion, coronary microvascular dysregulation is present in approximately one-third of asymptomatic, non-insulin-treated type 2 diabetic patients. Elevated baseline blood flow and reduced microvascular resistance at rest are characteristics of this dysregulation. These data suggest a state of activation of endothelial-dependent vasodilation at baseline which appears to limit the flow response to stress conditions.
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PMID:Dysregulation of coronary microvascular reactivity in asymptomatic patients with type 2 diabetes mellitus. 1245 3

In both type 1 and type 2 diabetes, diabetic complications in target organs arise from chronic elevations of glucose. The pathogenic effect of high glucose, possibly in concert with fatty acids, is mediated to a significant extent via increased production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and subsequent oxidative stress. ROS and RNS directly oxidize and damage DNA, proteins, and lipids. In addition to their ability to directly inflict damage on macromolecules, ROS and RNS indirectly induce damage to tissues by activating a number of cellular stress-sensitive pathways. These pathways include nuclear factor-kappaB, p38 mitogen-activated protein kinase, NH(2)-terminal Jun kinases/stress-activated protein kinases, hexosamines, and others. In addition, there is evidence that in type 2 diabetes, the activation of these same pathways by elevations in glucose and free fatty acid (FFA) levels leads to both insulin resistance and impaired insulin secretion. Therefore, we propose here that the hyperglycemia-induced, and possibly FFA-induced, activation of stress pathways plays a key role in the development of not only the late complications in type 1 and type 2 diabetes, but also the insulin resistance and impaired insulin secretion seen in type 2 diabetes.
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PMID:Are oxidative stress-activated signaling pathways mediators of insulin resistance and beta-cell dysfunction? 1250 86

In persons with diabetes, moderate hyperglycemia can contribute to an increased turnover of protein. To maintain body composition and nitrogen balance requires metabolic control and sufficient protein and energy intakes. However, because most adults eat at least 50% more protein than is required, people with diabetes appear to be protected from protein malnutrition when consuming a usual diet. Although nonessential amino acids undergo hepatic gluconeogenesis, peripheral glucose concentrations do not increase after protein ingestion. The fate of produced glucose is unknown. Protein does not contribute to sustained elevations of glucose levels, slow absorption of carbohydrate, or help in the treatment of hypoglycemia--advice often given to persons with diabetes. Protein is, however, just as potent a stimulant of insulin secretion as glucose. No long-term research is available to document that high-protein, low-carbohydrate diets are continued long-term or that weight lost initially is maintained better from these diets than from traditional weight loss diets. Furthermore, in persons with type 2 diabetes, weight loss is reported to be related to energy restriction and not to the protein-to-carbohydrate ratio of the diet.
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PMID:Protein and diabetes: much advice, little research. 1264 72

To determine the effect of a low-dose angiotensin receptor blocker, candesartan, on early kidney damage associated with diabetes. Fifty-two patients with type 2 diabetes with normo- and microalbuminuria participated in this study. Nineteen patients with high-normal and mildly high blood pressure received low-dose candesartan cilexetil at 4 mg daily (candesartan group), and 33 patients did not receive candesartan (control group). Blood pressure, urinary excretion of albumin, transferrin, and type IV collagen (expressed as urinary creatinine index) and plasma parameters were determined at baseline and at 2, 6, 12 and 18 months after the start of candesartan therapy. Baseline urinary albumin, transferrin, and type IV collagen excretions was similar in the control and candesartan groups. The higher baseline systolic blood pressure was decreased by candesartan treatment to a level similar to that in the control group, such that blood pressure was comparable between the control and candesartan groups during the run-in period. In the control group, urinary albumin excretion was significantly increased at 18 months when compared with baseline, while urinary albumin excretion did not increase in the candesartan group throughout the study. Urinary transferrin excretion was significantly increased at 6, 12, and 18 months when compared with baseline in the control group, while it did not increase in the candesartan group during the study. In both groups, urinary type IV collagen excretion did not change significantly during the study. Hemoglobin A1c, serum urea nitrogen, creatinine, albumin, and lipids were comparable between the two groups throughout the study. In conclusion, low-dose candesartan can prevent early kidney damage in type 2 diabetic patients with mildly higher blood pressure independently of its hypotensive action.
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PMID:Low-dose candesartan cilexetil prevents early kidney damage in type 2 diabetic patients with mildly elevated blood pressure. 1286 1

In a randomized, crossover 5-wk study design, we recently reported that a weight-maintaining diet in which the percentage of total food energy as protein was increased from 15-30% resulted in a decrease in postprandial glucose and glycohemoglobin in people with untreated type 2 diabetes without a significant change in insulin. Protein was substituted for carbohydrate in the diet. The fat content remained unchanged. In this publication, we present data on other hormones and metabolites that were considered to potentially be affected by substitution of protein for carbohydrate in the diet. The mean fasting plasma GH and total IGF-I concentrations were elevated on the 30% protein diet. The urinary free cortisol also was increased. However, the urinary aldosterone was unchanged. Although urinary pH was decreased, calcium excretion was not significantly increased. The plasma postprandial alpha-amino nitrogen concentrations were increased, but the 24-h integrated concentration was unchanged, indicating an accelerated amino acid removal rate. The plasma urea nitrogen was increased as expected. The urea production rate also was increased such that a new steady-state fasting value was present. The calculated urea production rate accounted for 97% of the protein ingested on the 15% protein diet, but only 80% on the 30% protein diet, suggesting net nitrogen retention on the high-protein diet. In conclusion, an increase in dietary protein results in a number of metabolic adaptations in addition to reducing the circulating glucose concentration. Serum TSH, total T(3), free T(4), B(12), folate, homocysteine, uric acid, and creatinine concentrations were unchanged.
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PMID:The metabolic response of subjects with type 2 diabetes to a high-protein, weight-maintenance diet. 1291 39

A series of benzoxazinones has been synthesized and tested for PPARgamma agonist activity. Synthetic approaches were developed to provide either racemic or chiral compounds. In vitro functional potency could be measured through induction of the aP2 gene, a target of PPARgamma. These studies revealed that compounds with large aliphatic chains at the nitrogen of the benzoxazinone were the most potent. Substitution of the chain was tolerated and in many cases enhanced the in vitro potency of the compound. Select compounds were further tested for metabolic stability, oral bioavailability in rats, and efficacy in db/db mice after 11 days of dosing. In vivo analysis with 13 and 57 demonstrated that the series has potential for the treatment of type 2 diabetes.
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PMID:Benzoxazinones as PPARgamma agonists. 2. SAR of the amide substituent and in vivo results in a type 2 diabetes model. 1469 33


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