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)

It is well known that insulin resistance (IR) and inflammation (IF) are associated with macroangiopathy. However, whether IR and IF are related to cardiac disease (myocardial infarction, angina pectoris, and heart failure), stroke or both remains elusive. The present hospital-based prospective study was designed to investigate this issue. The study subjects were 300 Japanese patients with type 2 diabetes mellitus and negative history of cardiac disease and stroke. IR (K index of insulin tolerance test; K(ITT)) and IF (high-sensitivity C-reactive protein [hs-CRP]) were measured in each patient at baseline. Patients were followed-up for a mean period of 5.5 years. The time of first evidenced cardiac disease or stroke was monitored. During the follow-up, 35 patients developed cardiac disease and 26 patients developed stroke. Age, smoking, K(ITT), and hs-CRP were independently related to cardiac disease, while age, systolic blood pressure, low HDL, and anti-platelet drug use were independently related to stroke. When patients were subdivided into IR(-) and IR(+), and IF(-) and IF(+), Kaplan-Meier survival analysis showed that the rate of cardiac disease, but not of stroke, was significantly higher in IR(+)IF(+) than IR(-)IF(-) patients (p < 0.01). In conclusion, coexistence of IR and IF effectively predicted cardiac disease but not stroke in Japanese patients with type 2 diabetes mellitus.
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PMID:Coexistence of insulin resistance and inflammation effectively predicts cardiac disease but not stroke in Japanese patients with type 2 diabetes mellitus. 1673 Aug 41

The aim of this study was to assess the association between high sensitivity-C-reactive protein (hs-CRP), a sensitive marker of inflammation, and early-stage carotid atherosclerosis, in patients with early-state type 2 diabetes mellitus. The study subjects were 75 patients with type 2 diabetes mellitus without obvious diabetic vascular complications, who were not on any medication, and whose HbA(1c) level was less than 6.5%. We evaluated the mean intima-media thickness (IMT) of the common carotid artery (CCA) by ultrasound B-mode imaging. Then, we investigated various factors associated with CCA-IMT including hs-CRP. Serum hs-CRP levels correlated well with factors strongly associated with insulin resistance such as homeostasis model assessment of insulin resistance (HOMA-IR), fasting insulin level, and body mass index. Serum hs-CRP also correlated with mean CCA-IMT and serum levels of soluble intercellular adhesion molecule-1. Multivariate regression analysis using mean CCA-IMT as the dependent variable identified only age, hs-CRP, and diastolic blood pressure as independent determinants of mean CCA-IMT. While hs-CRP associates with insulin resistance and subclinical atherosclerosis in ealy-state type 2 diabetes, our data suggest that hs-CRP is a useful marker of subclinical atherosclerosis in early-state type 2 diabetes mellitus independent of factors that directly reflect insulin resistance.
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PMID:Association of C-reactive protein with early-stage carotid atherosclerosis in Japanese patients with early-state type 2 diabetes mellitus. 1692 21

Adiponectin levels are significantly lower in obese adult patients with type 2 diabetes mellitus, essential hypertension, dyslipidemia, and cardiovascular disease. However, the role of hypoadiponectinemia in nonobese healthy adults has not been fully elucidated. In this study, we examined the association between hypoadiponectinemia and cardiovascular risk factors and estimated plasma adiponectin values in nonobese, apparently healthy adults. A total of 204 male and 214 female healthy individuals aged 20 to 80 years, with a body mass index (BMI) of less than 25 kg/m2, were included in this study. We measured patients' plasma adiponectin levels, serum lipid profiles, high-sensitivity C-reactive protein (hs-CRP) levels, fasting glucose levels, and fasting insulin levels. Mean values of plasma adiponectin were 5.45 +/- 3.3 microg/mL in male and 8.16 +/- 4.6 microg/mL in female subjects. The hypoadiponectinemia group (< 4.0 microg/mL) had significantly higher levels (P < .01) of BMI, fasting glucose, fasting insulin, homeostasis model assessment of insulin resistance (HOMA-IR), and triglycerides, but lower levels of high-density lipoprotein cholesterol (HDL-C). In males, plasma adiponectin levels were inversely correlated with BMI (r = -0.32, P < .01), HOMA-IR (r = -0.14, P < .05), triglyceride levels (r = -0.17, P < .05), and hs-CRP levels (r = -0.15, P < .05), and positively correlated with HDL-C (r = 0.24, P < .01). In females, plasma adiponectin levels were negatively correlated with BMI (r = -0.31, P < .01), fasting glucose (r = -0.18, P < .01), fasting insulin (r = -0.23, P < .01), HOMA-IR (r = -0.24, P < .01), and triglyceride (r = -0.18, P < .01) levels, and positively correlated with HDL-C (r = 0.37, P < .01). Sex, age, BMI, and HDL-C (P < .01 for each) were found to be independent factors associated with plasma adiponectin levels in multivariate analysis. Hypoadiponectinemia is significantly associated with cardiovascular risk factors such as insulin resistance and atherogenic lipid profiles in nonobese, apparently healthy subjects.
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PMID:Association between hypoadiponectinemia and cardiovascular risk factors in nonobese healthy adults. 1704 59

During the recent years increasing knowledge has been obtained in the understanding of the coincidence of type 2 diabetes and cardiovascular disease. Insulin resistance and beta cell failure were shown to have a direct impact in the pathogenesis of arteriosclerosis which goes far beyond the effects of elevated glucose levels. The use of additional laboratory parameters for the characterisation of patients with type 2 diabetes on a pathophysiological basis might improve treatment strategies and might help to reduce the cardiovascular risk in patients with type 2 diabetes. Intact proinsulin is secreted from the beta cell and increasing levels of intact proinsulin serve as an indicator of beta cell failure. In addition, increased levels of intact proinsulin were shown to predict insulin resistance with a specificity of 100 % and a sensitivity of about 50 %. On the other side, adiponectin, derived from the visceral adipose tissue, serves as a marker closely correlated to insulin sensitivity. Plasma adiponectin is a very sensitive marker of insulin resistance and might be used for the judgement of therapeutical interventions aimed to improve insulin sensitivity. In addition, both markers are predictive for the estimation of cardiovascular risk in patients with type 2 diabetes. Measurement of inflammation, by high sensitive CRP might add further information about the cardiovascular risk of a patient with type 2 diabetes.
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PMID:[Current laboratory parameters in the differential diagnosis of type 2 diabetes mellitus. Proinsulin, adiponectin and others]. 1713 85

We have investigated predictive value of HbA1c for hospital mortality and length of stay (LOS) in patients with type 2 diabetes admitted because of sepsis. A prospective observational study was implemented in a university hospital, 286 patients with type 2 diabetes admitted with sepsis were included. Leukocyte count, CRP, admission plasma glucose, APACHE II and SOFA score were noted at admission, HbA1c was measured on the first day following admission. Hospital mortality and hospital length of stay (LOS) were the outcome measures. Admission HbA1c was significantly lower in surviving patients than in non-survivors (median 8.2% versus 9.75%, respectively; P<0.001). There was a significant correlation between admission HbA1c and hospital LOS of surviving patients (r=0.29; P<0.001). Logistic regression showed that HbA1c is an independent predictor of hospital mortality (odds ratio 1.36), together with female sex (OR 2.24), APACHE II score (OR 1.08) and SOFA score (OR 1.28). Multiple regression showed that HbA1c and APACHE II score are independently related to hospital LOS. According to our results, HbA1c is an independent predictive factor for hospital mortality and hospital LOS of diabetic patients with sepsis.
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PMID:HbA1c is outcome predictor in diabetic patients with sepsis. 1714 50

The aim of the study was to investigate, whether the degree of metabolic risk factors for atherosclerotic complications in a very rare kind of obesity, the Multiple Symmetrical Lipomatosis, also known as the Launois-Bensaude Syndrome (LBS), are comparable or different from "simple" truncal obesity. 10 patients with LBS (Body mass index 34.4 +/- 1.8 kg/m(2), age: 62 +/- 3 yrs) were compared with 19 BMI - matched patients with "simple" truncal obesity and obstructive sleep apnoea syndrome (OSAS) and 20 BMI- matched patients with "simple" truncal obesity without OSAS. Markers of subclinical inflammation and thrombocyte activation (sCD62p = soluble p-selectin, highly sensitive C-Reactive protein = CRP, Interleukin-6 = IL-6, ICAM-1 = Intracellular Adhesion Molecule-1, Vascular Cell Adhesion Molecule = VCAM -1, leptin), as well as adiponectin and resistin were studied. The prevalence of atherogenic risk factors as hypertension (80%), type 2 diabetes (30%), OSAS (50%), smoking (30%) and alcohol abuse (80%) was high in the (obese) LBS group. The markers of subclinical inflammation and thrombocyte activation showed an indifferent picture with lower levels of circulating IL-6 and sCD62p, comparable CRP and higher ICAM-1 and VCAM-1 than in controls. Leptin and adiponectin were higher than in controls. However, the accumulation of "classic" cardiovascular risk factors in the LBS group was well reflected by the presence of symptomatic cardiovascular disease in 3 of the 10 LBS patients, putting LBS patients - if obese - at an atherosclerotic risk at least comparable to obese persons.
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PMID:Adiponectin, resistin and subclinical inflammation--the metabolic burden in Launois Bensaude Syndrome, a rare form of obesity. 1744 28

The goal was to investigate the effect of micronized fenofibrate, a hypolipidemic drug, on inflammatory markers and proinsulin in patients with type 2 diabetes who had hyperlipidemia. Thirty-nine patients were treated with micronized fenofibrate (200 mg/day for 12 wk). Erythrocyte sedimentation rate (ESR), fibrinogen, high-sensitivity C-reactive protein (hs CRP), and proinsulin levels were measured at baseline and after 12 wk of therapy. Micronized fenofibrate significantly reduced serum triglyceride, cholesterol, and uric acid levels (all p <0.0001) and increased high-density lipoprotein (HDL)-cholesterol (p <0.001) and creatinine levels (p <0.0001). Micronized fenofibrate also significantly decreased fibrinogen (421 +/- 152 vs 344 +/- 81 mg/dl, p <0.001), hs-CRP (3.3 +/- 3.3 vs 2.1 +/- 1.8 mg/L, p <0.01), and ESR (19.1 +/- 24.8 vs 9.7 +/- 8.7 mm/hr, p <0.01), but did not change proinsulin levels. The correlations among changes of hs-CRP, fibrinogen, and ESR were high. Although correlation among the decreases in inflammatory markers (ESR, fibrinogen, and hs-CRP) was significant, there was no significant correlation between the changes of lipid profile and inflammatory markers. In conclusion, after 12 wk, micronized fenofibrate therapy significantly decreased 3 inflammatory markers (hs-CRP, ESR, and fibrinogen) and improved the lipid profile by decreasing serum triglyceride, cholesterol, and non-HDL-cholesterol levels and increasing HDL-cholesterol; however, it did not change serum proinsulin level, a pancreatic stress marker.
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PMID:Decrease in inflammatory cardiovascular risk markers in hyperlipidemic diabetic patients treated with fenofibrate. 1752 72

Growth hormone (GH) signaling via the growth hormone receptor (GHR) forms a major part of the GH-IGF-I axis, which is crucial for controlling metabolism and anabolism. Two common variants of the GHR differ by the presence (full length or GHR(fl)) or absence of exon 3 (exon 3 deleted or GHR(d3)), the function of which is unknown. However, differential response to GH treatment has been observed with carriers of the GHR(d3) variant conferring a greater growth rate. This study investigates these GHR variants in subjects with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT), including Type 2 diabetes mellitus (T2DM). DNA was extracted from blood samples from subjects with NGT (n=158), IGT (n=116) and T2DM (n=194). The T2DM subjects in set 1 (n= 39) were newly diagnosed, whilst those in set 2 (n=155) had a mean duration of 7 years. Set 1 also included NGT and IGT subjects. Genotyping by standard PCR and gel electrophoresis were carried out. A significant difference was observed between T2DM and NGT (p<0.0001) with a significantly lower frequency of GHR(d3) in T2DM (3.6% compared to 17% in NGT). Both sets of T2DM subjects with at least one GHR(d3) allele had significantly higher BMI. In the larger subset of T2DM, GHR(d3) was associated with higher CRP levels as well as age adjusted IGF-I, with a trend of higher C-peptide secretion and impaired lipid levels, indicating a phenotype with metabolic disorder when compared to the GHR(fl/fl) T2DM subjects. In conclusion, homozygosity for the GHR(d3) allele appears to be preventive of T2DM. However, when other factors cause overt T2DM, the GHR(d3) allele confers a phenotype indicative of metabolic disorder. This study supports the hypothesis that the two GHR alleles by their inclusion or exclusion of exon 3 are functionally different.
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PMID:GHR exon 3 polymorphism: association with type 2 diabetes mellitus and metabolic disorder. 1753 58

The recognition that inflammation plays a fundamental role in atherothrombosis has led to the measurement of circulating inflammatory biomarkers such as high-sensitivity C-reactive protein (hs-CRP) as a means of improving cardiovascular disease detection and prevention. Clinically, levels of hs-CRP >3 mg/L indicate elevated risk for myocardial infarction and stroke, even among apparently healthy individuals with low-to-normal lipid levels. Emerging laboratory and epidemiologic data now link inflammation and hs-CRP to insulin resistance in that hs-CRP levels have been associated with impaired insulin sensitivity and the development of dysglycemic conditions, including the cardiometabolic syndrome and incident type 2 diabetes. hs-CRP has also been associated with each of the individual components of the cardiometabolic syndrome. Furthermore, in large prospective studies, hs-CRP adds prognostic information about cardiovascular risk beyond that provided by the cardiometabolic syndrome. These findings have led to discussion about the addition of hs-CRP measurement to the current definition of the cardiometabolic syndrome to improve detection of risk for both diabetes and cardiovascular events in patients. Multiple clinical studies are now underway that are evaluating whether agents traditionally used to improve glycemic control may also significantly reduce hs-CRP.
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PMID:Interrelationships between inflammation, C-reactive protein, and insulin resistance. 1767 26

Although the epidemic of obesity has been accompanied by an increase in the prevalence of the metabolic syndrome, not all obese develop the syndrome and even lean individuals can be insulin resistant. Both lean and obese insulin resistant individuals have an excess of fat in the liver which is not attributable to alcohol or other known causes of liver disease, a condition defined as nonalcoholic fatty liver disease (NAFLD) by gastroenterologists. The fatty liver is insulin resistant. Liver fat is highly significantly and linearly correlated with all components of the metabolic syndrome independent of obesity. Overproduction of glucose, VLDL, CRP, and coagulation factors by the fatty liver could contribute to the excess risk of cardiovascular disease associated with the metabolic syndrome and NAFLD. Both of the latter conditions also increase the risk of type 2 diabetes and advanced liver disease. The reason why some deposit fat in the liver whereas others do not is poorly understood. Individuals with a fatty liver are more likely to have excess intraabdominal fat and inflammatory changes in adipose tissue. Intervention studies have shown that liver fat can be decreased by weight loss, PPARgamma agonists, and insulin therapy.
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PMID:Fatty liver: a novel component of the metabolic syndrome. 1769 Mar 17


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