Metabolic syndrome of prediabetic and diabetic subjects in a Bangladeshi population

BackgroundThe metabolic syndrome is a cluster of medical disorder that increases the risk of developing cardiovascular disease and diabetes.Aims and objectiveObjective of the study was to determine the metabolic syndrome in prediabetic subjects to know whether this syndrome, which is common in diabetic subjects, appears in earlier stage of the disease.Materials and methodsA group of 17 IFG, 60 IGT, 29 combined IFG–IGT and 68 type 2 DM subjects were studied along with a group of 56 healthy controls. Anthropometric and clinical characteristics were measured using appropriate methods. Serum glucose was measured using glucose-oxidase method; lipid profile by enzymatic–colorimetric method.ResultsWaist hip ratio (WHR) was significantly higher in IFG–IGT and type 2 DM subjects. Systolic blood pressure was significantly higher in IFG–IGT and diastolic blood pressure is significantly higher in IGT, IFG–IGT and type 2 DM compared to controls. Fasting serum TG (p = 0.008) and cholesterol (p = 0.001) level was significantly higher in type 2 DM subjects but the values were not significantly different in prediabetic subjects compared to controls. HOMA B% and HOMA S% were significantly lower in DM and IFG–IGT subjects, IFG subjects have also shown significantly lower HOMA B% compared to controls.ConclusionThese results indicate that hypertension, central obesity (WHR) and insulin resistance, three major factors for metabolic syndrome are present in prediabetic condition in a Bangladeshi population.     

Natural Course of Fulminant Hepatic Failure: The Scenario in Bangladesh and the Differences from the West

Background/Aim:

Fulminant hepatic failure (FHF) is a devastating complication of acute viral hepatitis, leading to death in most cases. The etiology and predictors of outcome differ according to the geographical region. This study was conducted with the aim of evaluating the etiology, complications, and outcome of FHF in Bangladesh.

Patients and Methods:

In this prospective study, we included 67 consecutive cases of FHF presenting to the Department of Hepatology, Bangabandhu Sheikh Mujib Medical University, Dhaka, between November 2003 and May 2008. Thirty-nine of the patients were male and 28 were female. Data was analyzed using SPSS, version 13.0.

Results:

The mean age of the subjects was 31.9 ± 11.7 years. Hepatitis E virus (HEV) was the commonest etiological factor for FHF (50 cases, 74.6%); of the 50 cases with HEV infection, 43 (64.2%) were not coinfected with any other virus, four cases were Hepatitis B virus (HBV) carriers, and three had coinfection with hepatitis A virus (HAV). HBV was the cause of FHF in nine (13.4%) patients. HCV, paracetamol, and alcohol were not responsible for any of the cases. Most of the patients (57 patients, 85%) developed FHF within 2 weeks of the onset of jaundice. Of the 67 patients, 49 (73.1%) died. Cerebral edema was the single most common cause of death (48 patients, 71.6%). Other complications were renal failure (23 patients, 34.3%), sepsis (15 patients, 22.4%), electrolyte imbalance (12 patients 17.9%), and bleeding tendency (7 patients, 10.4%). Occurrence of cerebral edema, longer prothrombin time, higher grade of encephalopathy, and longer jaundice-to-encephalopathy interval had significant negative influence on outcome.

Conclusions:

The etiology of FHF in Bangladesh is different from that in the West. Prolongation of prothrombin time and occurrence of cerebral edema are predictors of the worst prognosis.     

Polymorphisms in XPD (Asp312Asn and Lys751Gln) genes, sunburn and arsenic-related skin lesions

BACKGROUND: Single-nucleotide polymorphisms in genes related to DNA repair capacity and ultraviolet exposure have not been well investigated in relation to skin lesions associated with arsenic exposure. This population based case-control study, of 600 cases and 600 controls, frequency matched on age and gender in Pabna, Bangladesh, in 2001-2002, investigated the association and potential effect modification between polymorphisms in Xeroderma Pigmentosum complementation group D (XPD) (Lys751Gln and Asp312Asn) genes, tendency to sunburn and arsenic-related skin lesions. METHODS: Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). RESULT: No significant association was observed between skin lesions and the XPD 312 Asp/Asn (adjusted OR = 0.87, 95% CI = 0.65-1.15) Asn/Asn (adjusted OR = 0.76, 95% CI = 0.50-1.15) (referent Asp/Asp); XPD 751 Lys/Gln (adjusted OR = 0.92, 95% CI = 0.69-1.23) Gln/Gln (adjusted OR = 0.98, 95% CI = 0.66-1.45) (referent Lys/Lys). While we did not observe any evidence of effect modification of these polymorphisms on the association between well arsenic concentration and skin lesions, we did observe effect modification between these polymorphisms and sunburn tendency and arsenic-related skin lesions. Individuals with the heterozygote or homozygote variant forms (Asp/Asn or Asn/Asn) had half the risk of skin lesions (OR = 0.45, 95% CI = 0.29-0.68) compared with those with the wild-type XPDAsp312Asn genotype (Asp/Asp) and individuals with heterozygote or homozygote variant forms (Lys/Gln or Gln/Gln) had half the risk of skin lesions (OR = 0.47, 95% CI = 0.31-0.72) compared with those with the wild-type XPDLys751Gln genotype (Lys/Lys), within the least sensitive strata of sunburn severity. We observed effect modification on the multiplicative scale for XPD 751 and XPD 312. CONCLUSION: XPD polymorphisms modified the relationship between tendency to sunburn and skin lesions in an arsenic exposed population. Further study is necessary to explore the effect of XPD polymorphisms and sun exposure on risk of arsenic-related skin lesions.     

Association of methylenetetrahydrofolate reductase (C677T) polymorphism with hyperuricemia

Background and aimsHomozygosity for the thermolabile variant of 5,10-methylene tetrahydrofolate reductase (C677T) has been suggested to be positively associated with the risk of vascular disease and neural tube defects. In addition, recent studies have suggested that elevated serum uric acid predicts ischemic heart disease, and epidemiological data on ethnic groups have suggested that genetic factors are determinants of serum uric acid levels. In this study, we tested the hypothesis that 5,10-methylenetetrahydrofolate reductase (C677T) polymorphism may be associated with hyperuricemia.Methods and resultsSamples from 518 healthy individuals (268 men and 250 women) were analyzed for MTHFR genotyping and serum uric acid. The participants were categorized to homozygous wild type (CC), heterozygous for wild type and thermolabile (CT), or homozygous for the thermolabile (TT) variant. Serum uric acid was significantly higher in males and females with TT genotype than those with either CC or CT genotype (p = 0.0001, ANOVA). Univariate and multivariate analysis showed that 5,10-methylenetetrahydrofolate reductase (C677T) polymorphism was a strong correlate and predictor of uric acid in males (r = 0.28, p = 0.0001, β = 0.673, p = <0.001) and in females (r = 0.27, p = 0.0001, β = 0.599, p = <0.001). Odds ratio analysis has also shown that the risk of hyperuricemia was greater in males (OR 3.1, CI 1.8–5.2, p = 0.001) and females (OR 3.3, CI 1.9–5.7, p = <0.001) with CT genotypes and in males (OR 3.7, CI 1.3–10.7, p = 0.014) and females (OR 3.2, CI 1.1–9.7, p = 0.032) with TT genotypes than in those with CC genotypes.ConclusionResults from this study suggest that mutation of 5-MTHFR C677T contributes to the higher uric acid levels in both males and females and may be a risk factor for hyperuricemia.     

<Emphasis Type="Italic">GSTM1</Emphasis> and <Emphasis Type="Italic">APE1</Emphasis> genotypes affect arsenic-induced oxidative stress: a repeated measures study

Background  

Chronic arsenic exposure is associated with an increased risk of skin, bladder and lung cancers. Generation of oxidative stress may contribute to arsenic carcinogenesis.     

Association of red blood cell 5-methyltetrahydrofolate and severity of coronary artery disease: a cross-sectional study from Shiraz, southern Iran

In this study we tested the hypothesis that red blood cell 5-methyltetrahydrofolate, a long-term marker of the folate status, is associated with the severity of coronary artery disease and whether this association is independent of homocysteine, vitamin B₁₂, plasma 5-methyltetrahydrofolate, 5,10-methyltetrahyrofolate reductase C677T genotype, and other cardiovascular risk factors. Two hundred and fifty-one angiographically documented patients aged <70 years with single, double, or triple coronary artery disease were investigated. Red blood cell 5-methyltetrahydrofolate concentrations were significantly decreased with the increasing number of diseased vessels (analysis of variance, P < 0.001). Red blood cell 5-methyltetrahydrofolate was also inversely and significantly correlated with the number of diseased vessels (r = −0.36, P < 0.001). Stepwise multiple regression analysis showed that red cell 5-methyltetrahydrofolate was a strong predictor of number of diseased vessels independent of plasma total homocysteine, 5,10-methyltetrahyrofolate reductase C677T genotype, and all other coronary artery risk factors (β = −0.002, P < 0.001, r² = 0.128). The results of this study suggest that low red blood cell 5-methyltetrahydrofolate is associated with the severity of coronary artery disease independent from plasma homocysteine and other cardiovascular risk factors.     

Cardiac function in mice lacking the glucagon-like peptide-1 receptor

Glucagon-like peptide-1 (GLP-1) acts via its G protein-coupled receptor (GLP-1R) to regulate blood glucose. Although the GLP-1R is widely expressed in peripheral tissues, including the heart, and exogenous GLP-1 administration increases heart rate and blood pressure in rodents, the physiological importance of GLP-1R action in the cardiovascular system remains unclear. We now show that 2-month-old mice with genetic deletion of the GLP-1R (GLP-1R(-/-)) exhibit reduced resting heart rate and elevated left ventricular (LV) end diastolic pressure compared with CD-1 wild-type controls. At the age of 5 months, echocardiography and histology demonstrate increased LV thickness in GLP-1R(-/-) mice. Although baseline hemodynamic parameters of GLP-1R(-/-) did not differ significantly from those of wild type, GLP-1R(-/-) mice displayed impaired LV contractility and diastolic function after insulin administration. The defective cardiovascular response to insulin was not attributable to a generalized defect in the stress response, because GLP-1R(-/-) mice responded appropriately to insulin with increased c-fos expression in the hypothalamus and increased circulating levels of glucagon and epinephrine. Furthermore, LV contractility after exogenous epinephrine infusion was also reduced in GLP-1R(-/-) mice. These findings provide new evidence implicating an essential role for GLP-1R in the control of murine cardiac structure and function in vivo.