Lower Fasting Plasma Glucose Levels Research Articles

Increased prevalence of proliferative retinopathy in patients with acromegaly

BackgroundThis pilot study was carried to determine the prevalence of retinopathy, especially proliferative retinopathy, in patients with acromegaly. MethodsWe analyzed 43 acromegalic patients and 129 age- and gender-matched patients with type 2 diabetes. The retinopathy status was determined from the medical records based on the ophthalmologist consultations of patients with acromegaly. Color photographs of the macula- and disc-centered views were obtained at an angle of 45° with a fundus camera after pharmacologic-induced mydriasis in patients with type 2 diabetes. ResultsCompared with age- and gender-matched patients with type 2 diabetes, the acromegalic patients had lower fasting plasma glucose levels and lower systolic and diastolic blood pressures, but were taller and had higher IGF-1 levels. Any degree of retinopathy was present in 9.3% (4 of 43) of patients with acromegaly and 34.9% (45 of 129) of patients with type 2 diabetes (odds ratio [OR] = 0.191; 95% confidence interval [CI] = 0.064–0.570). Proliferative retinopathy was present in 9.3% (4 of 43) of patients with acromegaly and 9.3% (12 of 129) of patients with type 2 diabetes (OR = 1.000; 95% CI = 0.305–3.281). Non-proliferative retinopathy was absent in patients with acromegaly, but present in 25.9% (33 of 129) of patients with type 2 diabetes. ConclusionThe high proliferative, but absence of non-proliferative retinopathy in our patients with acromegaly may reflect the pathogenic effect of IGF-1 on neovascularization. IGF-1 may play an important role in proliferative retinopathy, but may play no role in non-proliferative retinopathy.

Improvement of glucose metabolism via mung bean protein consumption: A clinical trial of GLUCODIATM isolated mung bean protein in Japan

Background: The main component of mung bean protein, accounting for more than 80%, is 8Sα globulin. Its structure closely resembles that of soybean β-conglycinin. Thereby, the mung bean protein is expected to have similar physiological effects to those of β-conglycinin, but there is no clinical evidence for these effects.Purpose of this study: The aim of this study was to confirm the positive effects of mung bean protein (GLUCODIATM) on glucose metabolism in clinical trials.Method: This clinical study was conducted using a double-blind placebo-controlled design with 45 prediabetes patients.Results: Many of the subjects were pre-diabetes with blood glucose levels exceeding 140 mg/dL by 2-hour plasma glucose level. However, the initial mean fasting plasma glucose level was less than 100 mg/dL. Therefore, mung bean protein did not lower fasting plasma glucose levels. The test period extended from summer to autumn, and increased fasting plasma glucose levels in the placebo group were observed due to seasonal factors. However, this increase was suppressed in the test group. Similarly, the mean insulin level increased in the placebo group, but the increase was also suppressed in the test group. Among obese subjects with a high body mass index, significant increases in fasting plasma glucose and insulin levels in the placebo group were observed. In the comparison between the test and the placebo groups with the average elevation value, there was a significant difference in fasting blood glucose level and significant tendencies in insulin level and homeostatic model assessment for insulin resistance value between the two groups.Conclusion: Mung bean protein suppresses fasting plasma glucose and insulin levels. Consequently, it may have an inhibitory effect on insulin resistance, a trigger of metabolic syndrome.Key words: mung bean protein, insulin, obesity, body mass index, randomized clinical trial, seasonal variation.

Severe spasticity in lower extremities is associated with reduced adiposity and lower fasting plasma glucose level in persons with spinal cord injury.

Cross-sectional study. To investigate the effects of severe lower extremity spasticity on anthropometric dimensions, body composition and metabolic profiles in persons with chronic motor complete spinal cord injury (SCI). Outpatient clinic. Fifty-five of the 61 participants were divided into two groups (no or mild spasticity group, 28; severe spasticity group, 27) based on the assessment of the extensor muscle spasticity according to the modified Ashworth scale. Anthropometric dimensions (waist circumference (WC), waist-to-height ratio (WtHR)), body composition (fat mass (FM), body fat percentage (BFP), fat-free mass (FFM), fat-free mass percentage (FFMP), bone mineral density (BMD)) and metabolic profiles (leptin, total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride (TG), fasting plasma glucose (FPG) and glycosylated hemoglobin (HbA1c)) were compared between the two groups with different degree of spasticity. Spasticity of the extensor muscle group negatively correlated with BFP (r=-0.458, P<0.001). Patients with severe spasticity showed a lower WC and WtHR than those in the no or mild spasticity group (P=0.038, P=0.006, respectively). The FM, BFP, leptin and FPG of the severe spasticity group were significantly lower than those of the patients in the no or mild spasticity group (P=0.003, P<0.001, P<0.001 and P=0.037, respectively). However, no differences in BMD, total cholesterol, LDL, HDL, TG and HbA1c were observed between the groups. The results of this study suggest that severe spasticity in lower extremities is associated with reduced adiposity and lower FPG levels in persons with chronic motor complete SCI.

Expression study of GLUT4 translocation-related genes in a porcine pre-diabetic model.

Obesity is a world-wide exponentially growing health problem that increases the risk of co-morbidities including metabolic syndrome, pre-diabetes, Type 2 Diabetes Mellitus (T2DM), and cancer. These co-morbidities are all complex conditions constituting a big challenge when searching for susceptibility genes. Identification of relevant genes, which could contribute to an earlier identification of individuals prone to develop diabetes, is urgently needed as many long-term complications can be avoided by preventive measures. Pre-diabetes is mainly associated with hyperglycemia; thus studying this phenotype might provide knowledge on relevant genes implicated in molecular mechanisms underlying pre-diabetes, and contributing to the development of T2DM. In the present study, two groups of pigs with high (HGG, N=6) and low (NGG, N=6) fasting plasma glucose level respectively were selected from a large pig population. Transcriptional levels of seven genes involved in the glucose transporter 4 (GLUT4) translocation pathway were studied by quantitative real-time PCR (qPCR) in diabetes relevant tissues (pancreas, adipose tissue, skeletal muscle, liver and kidney). Three of the genes, TBC (Tre-2, BUB2, CDC16) 1 Domain Family Member 4 (TBC1D4), insulin receptor and GLUT4 showed altered expression in some of the tissues. The expression pattern observed is in agreement with what has previously been reported in pre-diabetic humans confirming the pre-diabetic status of our pigs. Moreover, a novel isoform of TBC1D4 was detected by Western blotting using protein extracted from pancreas. The expression level of this novel isoform was further verified by qPCR in all tissues, showing the highest expression in the pancreas.

AFREZZA® (insulin human) Inhalation Powder: A Review in Diabetes Mellitus.

Afrezza® (insulin human) inhalation powder is a rapid-acting Technosphere® insulin (TI) administered via a breath-powered oral inhaler to patients with diabetes requiring prandial insulin. TI, a dry powdered formulation of recombinant human insulin adsorbed onto a proprietary carrier, is designed to deliver insulin to the deep lung, at the level of the alveoli, where it is absorbed into the systemic circulation. In a randomized, open-label, multinational, phase III trial (trial 171) in type 1 diabetes (T1DM) patients, prandial TI via the Gen2 inhaler provided noninferior glycated haemoglobin (HbA1c) lowering compared with prandial subcutaneous insulin aspart. Although TI was associated with less HbA1c lowering, it provided significantly lower fasting plasma glucose levels and significantly less hypoglycaemia and bodyweight gain compared with insulin aspart. In a randomized, double-blind, placebo-controlled, multinational, phase III trial (trial 175) in type 2 diabetes (T2DM) patients, prandial TI via the Gen2 inhaler provided superior HbA1c lowering compared with inhaled placebo. Cough was the most commonly occurring non-hypoglycaemia adverse event across both studies. In a pooled analysis of tolerability data from phase II and III studies, the most commonly occurring non-hypoglycaemia adverse events in T1DM and T2DM patients were cough and throat pain/irritation. However, cough was generally mild, dry and decreased over time. In addition, treatment with TI was associated with positive patient-reported outcomes. Insulin human inhalation powder is an effective and generally well-tolerated agent for the prandial treatment of hyperglycaemia in T1DM and T2DM patients and may provide a solution to insulin initiation barriers such as injection phobia, concerns of bodyweight gain and concerns of hypoglycaemia.

Improved glucose control with reduced hypoglycaemic risk when linagliptin is added to basal insulin in elderly patients with type 2 diabetes.

To assess the efficacy, hypoglycaemia risk and other safety markers of linagliptin as an additional therapy in older patients (aged ≥70 years) inadequately controlled with basal insulin. A prespecified safety analysis from the linagliptin trials programme was carried out to explore the hypoglycaemia risk when linagliptin was added to background basal insulin therapy in elderly patients (≥70 years). To do this, two eligible, randomized, placebo-controlled, clinical trials (NCT00954447 and NCT01084005) of 24 and ≥52 weeks, respectively, were analysed. A total of 247 elderly individuals [mean ± standard deviation (s.d.) age 74 ± 4 years, glycated haemoglobin (HbA1c) 8.2 ± 0.8%] on basal insulin (mean ± s.d. baseline dose 36 ± 25 IU/day) were identified. Alongside placebo-adjusted change in HbA1c with linagliptin of -0.77% [95% confidence interval (CI) -0.95 to 0.59; p < 0.0001] after 24 weeks, the hazard ratios (HRs) of both overall and confirmed hypoglycaemia [blood glucose ≤3.9 mmol/l (70 mg/dl)], were significantly lower with linagliptin than with placebo: HR 0.61 (95% CI 0.39-0.97) versus 0.59 (95% CI 0.37-0.94), respectively (both p < 0.05). Moreover, significantly less confirmed hypoglycaemia was present in linagliptin-treated patients with renal impairment [HR 0.45 (95% CI 0.27-0.76)], moderate hyperglycaemia [HbA1c 7.5 to <9.0%; HR 0.51 (95% CI 0.27-0.99)], lower fasting plasma glucose levels [<152 mg/dl; HR 0.49 (95% CI 0.28-0.86)] and those treated with higher insulin doses [insulin ≥35.6 IU/day; HR 0.46 (95% CI 0.23-0.91); p < 0.05 for all]. Severe hypoglycaemia was rare and the incidence was lower with linagliptin (0.8%) versus placebo (2.5%): HR 0.21 (95% CI 0.02-2.30). Despite improvements in hyperglycaemia and no relevant on-trial insulin dose reductions, adding linagliptin to basal insulin appears to decrease hypoglycaemia risk. The biological basis of this phenomenon warrants further research but may involve counter-regulatory effects of incretin hormones.

Effects of acute exercise on pancreatic endocrine function in subjects with type 2 diabetes.

We determined the effects of exercise on pancreatic endocrine responses to metabolic stimuli in subjects with type 2 diabetes (T2D) and examined the influence of subjects' diabetic status. Fourteen subjects underwent a hyperglycaemic clamp with glucagon-like peptide-1 (GLP-1) infusion and arginine injection, the morning after a 1-h walk or no exercise. Subjects were stratified by high and low fasting plasma glucose (FPG) levels and by glycated haemoglobin (HbA1c) levels, as well as by current use/non-use of antidiabetic medication. In the entire cohort, exercise did not alter insulin secretion, while glucagon levels were increased in all clamp phases (p < 0.05 to <0.01). In subjects with low FPG levels, exercise increased GLP-1-stimulated insulin secretion (p < 0.05), with the same trend being observed for arginine (p = 0.08). The same trends were seen for subjects with low HbA1c levels. Furthermore, exercise increased GLP-1- and arginine-stimulated insulin secretion (p < 0.05) in subjects who were antidiabetic drug-naïve. Exercise-induced increases in insulin secretion are blunted in subjects with T2D with high rates of hyperglycaemia and in those using antidiabetic drugs.

Pleiotropic Effects of Lipid Genes on Plasma Glucose, HbA1c, and HOMA-IR Levels

Dyslipidemia is strongly associated with raised plasma glucose levels and insulin resistance (IR), and genome-wide association studies have identified 95 loci that explain a substantial proportion of the variance in blood lipids. However, the loci's effects on glucose-related traits are largely unknown. We have studied these lipid loci and tested their association collectively and individually with fasting plasma glucose (FPG), glycated hemoglobin (HbA1c), and IR in two independent cohorts: 10,995 subjects from LifeLines Cohort Study and 2,438 subjects from Prevention of Renal and Vascular Endstage Disease (PREVEND) study. In contrast to the positive relationship between dyslipidemia and glucose traits, the genetic predisposition to dyslipidemia showed a pleiotropic lowering effect on glucose traits. Specifically, the genetic risk score related to higher triglyceride level was correlated with lower levels of FPG (P = 9.6 × 10(-10) and P = 0.03 in LifeLines and PREVEND, respectively), HbA1c (P = 4.2 × 10(-7) in LifeLines), and HOMA of estimated IR (P = 6.2 × 10(-4) in PREVEND), after adjusting for blood lipid levels. At the single nucleotide polymorphism level, 15 lipid loci showed a pleiotropic association with glucose traits (P < 0.01), of which eight (CETP, MLXIPL, PLTP, GCKR, APOB, APOE-C1-C2, CYP7A1, and TIMD4) had opposite allelic directions of effect on dyslipidemia and glucose levels. Our findings suggest a complex genetic regulation and metabolic interplay between lipids and glucose.

Revising the fasting glucose threshold for detection of cardiovascular risk factors: analysing two representative population-based studies of more than 50 000 Iranians in 3 years: The National Survey of Risk Factors for Non-Communicable Diseases of Iran

Objectives: To study the prevalence of cardiovascular risk factors across different glycaemia strata and to assess the optimal cut-off value of fasting plasma glucose (FPG) to identify the constellation of cardiovascular risk factors.Methods: Data of the National Survey of Risk Factors for Non-Communicable Diseases of Iran (SURFNCD 2005–2007) were analysed. Prevalence rates of obesity, central obesity, hypertension and hypercholesterolemia of individuals with Impaired Fasting Glucose (IFG) were compared with those of individuals with normal fasting glycaemia and newly diagnosed diabetes. Optimal FPG cut-point to diagnose subjects with cardiovascular risk factors was assessed.Results: Prevalence of each and combinations of cardiovascular risk factors were higher among subjects with IFG compared to those with normal fasting glycaemia. The areas under the curve (AUC) for detecting cardiovascular risk were highest at FPG values of 90 mg/dL. FPG of 90 mg/dL was the optimal cut-off and, in comparison to 100 mg/dL, corresponds to correct detection of 26–29% of obese, 22–27% of centrally obese, 26–29% of hypertensive and 25–30% of hypercholesterolemic individuals.Conclusions: IFG and even lower levels of FPG are associated with high prevalence of cardiovascular risk factors in Iranian adults. This study suggests the FPG cut-off to be revised at 90 mg/dL to identify people with increased cardiovascular risk.

Low fasting plasma glucose level predicts morbidity and mortality in symptomatic adults with congenital heart disease

BackgroundAdults with complex congenital heart disease (ACHD) have a high prevalence of abnormal glucose regulation (AGR: impaired glucose tolerance and diabetes mellitus). However, the impact of AGR on the prognosis remains unclear. PurposeOur purpose was to clarify the prognostic value of AGR in ACHD. Methods and resultsWe performed a 75g oral glucose tolerance test in 438 consecutive patients with ACHD (age 26±8years), including 38 unrepaired, 148 Fontan, 252 biventricular, and 27 healthy subjects and investigated associations between AGR and clinical events that required hospitalization or caused deaths from all-causes. When compared with the healthy group, fasting blood glucose level (FPG, mg/dl) was lower in the unrepaired and Fontan subjects (p<0.05–0.01) and the prevalence of low FPG (≤80mg/dl) was also higher in the unrepaired (58%), Fontan (47%), and biventricular group (33%) than in the healthy control (11%) (p<0.0001). Postprandial hyperglycemia (area under the curve of glucose: PG-AUC) was higher in all ACHD groups (p<0.0001 for all). New York Heart Association class and lower FPG independently predicted the hospitalization (FPG≤84mg/dl) and mortality (FPG≤80mg/dl) (p<0.05–0.0001), while the PG-AUC was not an independent predictor. When compared with the asymptomatic ACHD, symptomatic ACHD with lower FPG had high hazard ratios of 2.2 (95% confidence interval [CI]: 1.3–3.8, p<0.002) and 3.3 (95% CI: 1.2–11.9, p<0.03) for the hospitalizations and all-cause mortality, respectively. ConclusionsLow FPG is not uncommon in ACHD and the low FPG predicts the morbidity and all-cause mortality in symptomatic ACHD.

The relationship between estimated average glucose and fasting plasma glucose

Estimated average glucose (eAG) is a value calculated from hemoglobin A1c (HbA1c) that reflects average glycemic status over the preceding few months. A linear relationship between HbA1c and eAG was demonstrated by the International HbA1c-Derived Average Glucose (ADAG) Trial in 2008. We investigated the relationship between fasting plasma glucose (FPG) and eAG. This retrospective study was conducted by reviewing the medical records of 6443 subjects, including 5567 diabetic patients and 876 non-diabetic subjects. The levels of HbA1c and FPG were reviewed and eAG was calculated using the regression equation published by the ADAG trial: eAGmmol/L=1.59×HbA1c(NGSP, %)-2.59[eAGmg/dL= 28.7×HbA1c(NGSP, %)-46.7]. In all subjects, FPG showed a moderate correlation with eAG (r=0.672, p<0.001). When diabetic and non-diabetic subjects were divided into subgroups according to FPG level, the correlation between eAG and FPG decreased in both diabetic [FPG ≥10.0 mmol/L (180 mg/dL), r=0.425; FPG 7.2-9.9 mmol/L (130-179 mg/dL), r=0.373; FPG <7.2 mmol/L (130 mg/dL), r=0.202] and non-diabetic [FPG 5.6-6.9 mmol/L (100-125 mg/dL), r=0.363; FPG <5.6 mmol/L (100 mg/dL), r=0.186] subgroups as the FPG level decreased. The differences between eAG and FPG were statistically significant (p<0.001). Only 81% (4487/5567) of diabetic patients had a lower FPG level than eAG level. Our results suggest that the relationship between eAG and FPG may depend on glycemic control, thereby enhancing our understanding of eAG.

Association of Dysglycemia and All-Cause Mortality Across the Spectrum of Coronary Artery Disease

ObjectiveTo assess the association between fasting plasma glucose (FPG) and all-cause mortality across the spectrum of coronary artery disease (CAD). Patients and MethodsThe study included 18,999 patients during a study period of April 1, 2004, through October 31, 2010. The primary end points were in-hospital and follow-up all-cause mortality. According to the quartiles of FPG levels, patients were categorized into 4 groups: quartile 1, less than 5.1 mmol/L; quartile 2, 5.1 to less than 5.9 mmol/L; quartile 3, 5.9 to less than 7.5 mmol/L; and quartile 4, 7.5 mmol/L or greater. The conversion factor for units of plasma glucose is 1.00 mmol/L equals 18 mg/dL. Presented as mg/dL, the 4 quartile ranges of plasma glucose concentrations used in our data analysis are ≤90.0 mg/dL, 90.1-106.0 mg/dL, 106.1 mg/dL-135.0 mg/dL and ≥135.1 mg/dL. Quartile 1 was recognized as the lower glycemic group, quartiles 2 and 3 as the normoglycemic groups, and quartile 4 as the higher glycemic group. ResultsIn patients with acute myocardial infarction, all-cause mortality for the dysglycemic groups was higher than for the normoglycemic groups: in-hospital mortality for quartiles 1, 2, 3, and 4 was 1.0%, 0.9%, 0.2%, and 1.5%, respectively (P=.001); follow-up mortality for quartiles 1, 2, 3, and 4 was 1.7%, 0.9%, 0.3%, and 1.8%, respectively (P<.001). In patients with stable CAD, no significant differences in mortality were found among groups. However, in patients with unstable angina pectoris, the normoglycemic groups had lower follow-up mortality and roughly equal in-hospital mortality compared with the dysglycemic groups. After adjusting for confounding factors, this observation persisted. ConclusionThe association between lower FPG level and mortality differed across the spectrum of CAD. In patients with acute myocardial infarction, there was a U-shaped relationship. In patients with stable CAD or unstable angina pectoris, mildly to moderately decreasing FPG level was associated with neither higher nor lower all-cause mortality.

Pharmacotherapy in Type 1 Diabetes

Pharmacotherapy in Type 1 Diabetes

Physically active vs. inactive lifestyle, muscle properties, and glucose homeostasis in middle-aged and older twins.

Exercise-induced positive changes in skeletal muscle properties and metabolism decrease the risk for disability, cardiometabolic diseases and mortality. Here, we studied muscle properties and glucose homeostasis in a non-exercise stage in twin pairs with co-twins discordant for physical activity habits for at least 32 years of their adult lives. Isometric knee extension force, MR imaging of midthigh tissue composition and muscle volume, and fasting blood samples were acquired from 16 same-sex (seven monozygotic, nine dizygotic) middle-aged and older twin pairs. The consistently active twins had 20 % higher knee extension forces than their inactive co-twins (p = 0.006) although the active twins had only 4 % higher midthigh muscle cross-sectional areas (p = 0.072). These results were similar in intrapair analysis in which only the seven identical twin pairs were included. The ratio between the area of midthigh fat and muscle tissues was significantly lower among the active twins (0.65 vs. 0.48, p = 0.006). The active twins had also lower fasting plasma glucose levels (5.1 vs 5.6 mmol/l, p = 0.041). The area of midthigh intramuscular (extramyocellular) fat was associated with the markers of glucose homeostasis, especially with glycated hemoglobin, and these associations were emphasized by the diabetic and inactive twins. Regular exercise throughout the adult life retains muscle strength and quality but not necessarily mass. The regular use of muscles also prevents from the accumulation of intramuscular fat which might be related to maintained glucose metabolism and, thus, prevention of metabolic disorders.

Lower fasting plasma glucose levels in patients with stress-related exhaustion

Lower fasting plasma glucose levels in patients with stress-related exhaustion

Exenatide Twice Daily: Analysis of Effectiveness and Safety Data Stratified by Age, Sex, Race, Duration of Diabetes, and Body Mass Index

Background: Exenatide, a glucagon–like peptide–1 receptor agonist, is used twice daily (BID) as monotherapy or adjunctive therapy for the improvement of glycemic control in patients with type 2 diabetes mellitus. The purpose of this pooled analysis was to evaluate the safety and efficacy of exenatide BID in patients stratified by various demographic characteristics. Methods: This post hoc analysis included data from 16 randomized controlled trials in which patients with type 2 diabetes mellitus were treated with 10–μg exenatide BID. Each patient was classified into subgroups on the basis of his or her baseline values for age (< 65 or ≥ 65 years), sex (male or female), race (white, black, Asian, or Hispanic), duration of diabetes (< 10 years or ≥ 10 years), and body mass index (BMI; ≥ 20 to < 25, ≥ 25 to < 30, ≥ 30 to < 35, or ≥ 35 kg/m2). Results: A total of 2067 patients were included. All groups experienced significant improvements in glycated hemoglobin, fasting plasma glucose levels (other than black patients, who had a relatively low baseline fasting plasma glucose level), and body weight from baseline to endpoint. Most groups had significant improvements in systolic blood pressure. All of the age, sex, and duration of diabetes groups experienced significant improvements in lipid levels (other than high–density lipoprotein cholesterol). Whites and Asians generally experienced significant improvements in lipid levels, whereas blacks and Hispanics did not. Significant improvements in lipid levels were generally seen across BMI groups. The most common adverse events overall were nausea (38.6%), hypoglycemia (28.4%), and vomiting (14.0%). Hypoglycemia was more common overall in patients who were taking a concomitant sulfonylurea than it was in patients who were not. Conclusion: In this pooled analysis, exenatide BID improved glycemic control and body weight, and had generally beneficial effects on blood pressure and lipid levels in patients regardless of baseline age, sex, race, duration of diabetes, or BMI. Gastrointestinal events were the most common adverse events.

CYBA C242T polymorphism is associated with obesity and diabetes mellitus in Brazilian hypertensive patients

The CYBA C242T polymorphism has been associated with cardiovascular phenotypes such as hypertension and atherosclerosis, but available data are conflicting. This report investigated the impact of this variant on hypertension and metabolic determinants of cardiovascular risk in a large Brazilian sample. We cross-sectionally evaluated 1856 subjects (826 normotensive subjects and 1030 hypertensive patients) by clinical history, anthropometry, laboratory analysis and genotyping of the CYBA C242T polymorphism. Genotype frequencies in the whole population were consistent with the Hardy-Weinberg equilibrium and genotype distributions were not different between hypertensive and normotensive subjects. Hypertensive patients with the CC genotype presented lower fasting plasma glucose levels (5.9 ± 0.1 vs. 6.2 ± 0.1 mmol/l, P = 0.020) and waist circumference (94.5 ± 0.6 vs. 96.3 ± 0.6 cm, P = 0.028) than CT + TT ones. Similarly, the prevalence of diabetes mellitus and obesity was also lower in hypertensive patients carrying the CC genotype (16% vs. 21%, P = 0.041; 36% vs. 43%, P = 0.029, respectively). In addition, multiple and logistic regression analysis demonstrated that the CYBA C242T polymorphism was associated with glucose levels, waist circumference, obesity and diabetes mellitus in hypertensive patients independently of potential confounders. Conversely, in normotensive subjects, no significant difference in studied variables was detected between the genotype groups. These data suggest that the T allele of the CYBA C242T polymorphism may be used as a marker for adverse metabolic features in Brazilian subjects with systemic hypertension.

Increased Serum Bilirubin Level is Related to Good Collateral Development in Patients with Chronic Total Coronary Occlusion

Bilirubin is a bile pigment with potent anti-oxidant properties; in previous studies it has been reported to be negatively associated with coronary artery disease (CAD). Although elevated serum bilirubin concentrations may protect against endothelial dysfunction, it is not clear whether higher serum bilirubin levels (SBLs) in physiological ranges may work in favor of good collateral development in patients with chronic total coronary occlusion (CTO). The study population consisted of patients who underwent coronary angiography with a suspicion of CAD. Patients who had CTO in at least one major coronary artery were included. Coronary angiograms of 179 eligible patients from our database were reanalyzed and 110 of them had good collateral development and 69 had poor collateral development according to the Cohen-Rentrop method. Patients with good collateral development had a lower fasting plasma glucose level (FPG) (p=0.024) and higher SBLs in comparison to patients with poor collateral development (p<0.001). The number of CTO vessels (p=0.013) and left ventricular ejection fraction (EF%) were higher in good collateral group than poor collateral group (p=0.017). In multivariate analysis, FPG negatively (odds ratio [OR]: 0.981, p=0.003) and SBL (OR for per 0.1-mg/dL increase: 1.832, p<0.001) and the number of CTO vessels (OR: 5.642, p=0.007) were positively related to coronary collateral development. This study suggests that higher bilirubin levels within relatively normal ranges were related with favorable coronary collateral growth in patients with CTO. SBL may be responsible for the difference in coronary collateral vessel development among different patients with coronary artery disease. The anti-inflammatory and anti-oxidant properties of bilirubin may mediate this effect.

Fasting plasma glucose is an independent predictor for severity of H1N1 pneumonia

BackgroundThe pandemic influenza A (H1N1) virus emerged during 2009 and has spread worldwide. This virus can cause injuries to the lungs, liver, and heart. However, data regarding whether this influenza virus can affect pancreatic islets are limited. We investigated the effects of influenza A (H1N1) pneumonia on fasting plasma glucose (FPG) and islet function, and evaluated possible correlations between biochemical test results and the severity of H1N1 pneumonia.MethodsWe performed a retrospective analysis of patients either diagnosed with or suspected of having H1N1 pneumonia who were admitted to our hospital in 2009. Possible associations between FPG levels and H1N1 virus infection were assessed by logistic regression. Correlation and regression analyses were used to assess relationships between FPG and biochemical test results. Associations between admission days and significant data were assessed by single factor linear regression. To evaluate effects of H1N1 on pancreatic β-cell function, results of a resistance index (homa-IR), insulin function index (homa-β), and insulin sensitivity index (IAI) were compared between a H1N1 group and a non-H1N1 group by t-tests.ResultsFPG was significantly positively associated with H1N1 virus infection (OR = 1.377, 95%CI: 1.062-1.786; p = 0.016). FPG was significantly correlated with AST (r = 0.215; p = 0.039), LDH (r = 0.400; p = 0.000), BUN (r = 0.28; p = 0.005), and arterial Oxygen Saturation (SaO2; r = -0.416; p = 0.000) in the H1N1 group. H1N1 patients who were hypoxemic (SaO2<93%) had higher FPG levels than those who were not hypoxic (9.82 ± 4.14 vs. 6.64 ± 1.78; p < 0.05). FPG was negatively correlated with SaO2 in the H1N1 group with hypoxia (SaO2<93; r = -0.497; p = 0.041). SaO2 levels in patients with high FPG levels (≥7 mmol/L) were significantly lower than those of H1N1 patients with low FPG levels (<5.6 mmol/L). There were no significant differences in homa-IR, homa-β, or IAI between the H1N1 and non-H1N1 groups after adjusting for age, sex, and BMI.ConclusionsFPG on admission could be an independent predictor for the severity of H1N1 pneumonia. Elevated FPG induced by H1N1 pneumonia is not a result of direct damage to pancreatic β-cells, but arises from various factors' combinations caused by H1N1 virus infection.

Functional glucokinase regulator gene variants have inverse effects on triglyceride and glucose levels, and decrease the risk of obesity in children

ObjectiveRecently, the association of the natural variants rs1260326 and rs780094 of the glucokinase regulatory protein (GCKR) gene with increased fasting triglycerides and decreased fasting plasma glucose in diabetic adults was reported; the minor alleles were also found to reduce the risk of type 2 diabetes. The present study examined the possible associations of these variants with triglycerides and glucose levels, their allele distribution and their possible effects on childhood obesity. Methods and resultsA total of 221 obese children and 115 healthy normal-weight children as controls were genotyped using PCR–RFLP methods. Both functional GCKR variants were found in association with elevated serum triglycerides and lower fasting plasma glucose levels. Results of logistic regression revealed that, despite higher triglyceride levels, the carriers of the GCKR variants were more protected against the development of obesity; the adjusted models confirmed the lower risk of obesity for both variants (rs1260326: OR, 0.46; 95% CI, 0.25–0.83; rs780094: OR, 0.41; 95% CI, 0.23–0.74). ConclusionOur findings confirm the inverse modulating effect of functional GCKR variants on triglycerides and glucose levels in obese paediatric patients and healthy normal-weight controls. The results of our study strongly suggest that the minor alleles confer protection against the development of obesity in children. The findings also suggest that the minor alleles of functional GCKR may protect against diabetes and the metabolic syndrome in adults.