Impact of metabolic comorbidity on the association between body mass index and heatlh-related quality of life: a Scotland-wide cross-sectional study of 5,608 participants

<p/>Background: The prevalence of obesity is rising in Scotland and globally. Overall, obesity is associated with increased morbidity, mortality and reduced health-related quality of life. Studies suggest that "healthy obesity" (obesity without metabolic comorbidity) may not be associated with morbidity or mortality. Its impact on health-related quality of life is unknown. <p/>Methods: We extracted data from the Scottish Health Survey on self-reported health-related quality of life, body mass index (BMI), demographic information and comorbidity. SF-12 responses were converted into an overall health utility score. Linear regression analyses were used to explore the association between BMI and health utility, stratified by the presence or absence of metabolic comorbidity (diabetes, hypertension, hypercholesterolemia or cardiovascular disease), and adjusted for potential confounders (age, sex and deprivation quintile). <p/>Results: Of the 5,608 individuals, 3,744 (66.8%) were either overweight or obese and 921 (16.4%) had metabolic comorbidity. There was an inverted U-shaped relationship whereby health utility was highest among overweight individuals and fell with increasing BMI. There was a significant interaction with metabolic comorbidity (p = 0.007). Individuals with metabolic comorbidty had lower utility scores and a steeper decline in utility with increasing BMI (morbidly obese, adjusted coefficient: -0.064, 95% CI -0.115, -0.012, p = 0.015 for metabolic comorbidity versus -0.042, 95% CI -0.067, -0.018, p = 0.001 for no metabolic comorbidity). <p/>Conclusions: The adverse impact of obesity on health-related quality of life is greater among individuals with metabolic comorbidity. However, increased BMI is associated with reduced health-related quality of life even in the absence of metabolic comorbidity, casting doubt on the notion of "healthy obesity"

Effects of in vitro potassium on ammoniagenesis in rat and canine kidney tissue

Effects of in vitro potassium on ammoniagenesis in rat and canine kidney tissue. Decreased ammonium (NH4+) excretion is associated with hyperkalemia. To determine if potassium could directly influence renal ammonia production, we investigated ammoniagenesis by rat and canine renal cortical tissues in vitro at different potassium concentrations. Renal tissue from normal and acidotic rats and normal dogs incubated in glutamine, lactate, and 7 to 10mEq/liters of potassium or 25mEq/liters of potassium produced significantly less ammonia than slices incubating in glutamine, lactate, and 4 to 5mEq of potassium. Glutamate accumulation, which follows glutamine deamidation, did not decrease and even increased at 25mEq/liters of potassium. With glutamine as the sole substrate, decreased ammoniagenesis was seen only at higher potassium concentrations (> 16mEq/liters) than when lactate was also present. The depression to glutamine ammoniagenesis by high concentrations of potassium was partially obliterated in an anaerobic environment. When glutamate replaced glutamine as the precursor, renal ammonia produced by slices in 7 and 25mEq/liters was again significantly lower than by slices incubating in 4mEq/liters. We blocked glutamine synthesis by rat kidney slices with dl-methionine dl-sulfoximine when glutamate was the renal ammonia precursor. This essentially allows glutamate deamination to produce ammonia. Potassium depressed glutamate deamination significantly at 7mEq/liters (↓ 13%) and at 25mEq/liters of potassium (↓ 35%) as compared to 4mEq/liters. The above findings are consistent with a major depressive effect of in vitro potassium on glutamate deamination in rat and canine kidneys. Other evidence, especially from rat tissue studies, suggests that potassium also may affect glutamine deamination directly. Rat kidney slices incubating in the high potassium medium of 7mEq/liter or greater also consumed less oxygen in the presence of glutamine (P < 0.01), oxidatively decarboxylated less glutamine (P < 0.02) and produced less glucose from glutamine (P < 0.01).Effet du potassium in vitro sur l'ammoniogenèse dans tissu rénal de rat et de chien. Une diminution de l'excrétion d'ammoniaque (NH4+) est associée à l'hyperkaliémie. Afin de déterminer si le potassium peut influencer directement la production rénale d'ammoniac, nous avons étudié l'ammoniogenèse dans le tissu rénal cortical de rat et de chien in vitro à différentes concentrations de potassium. Du tissu rénal provenant de rats normaux et en acidose et de chiens normaux incubés dans de la glutamine, du lactate, et 7 à 10mEq/litres de potassium ou 25mEq/litres de potassium produit significativement moins d'ammoniac que des tranches incubées dans de la glutamine, du lactate, et 4 à 5mEq/litres de potassium. L'accumulation de glutamate, consécutive à la deamination de la glutamine, n'a pas diminué et même a augmenté à 25mEq/litres de potassium. Avec la glutamine comme seul substrat, la diminution de l'ammoniogenèse n'a été observée qu'à des concentrations de potassium supérieures (> 16mEq/litres) à celle nécessaire quand le lactate est présent. La dépression de l'ammoniogenèse due à la glutamine au moyen de concentrations élevées de potassium est partiellement abolie par un environnement anaérobique. Quand la glutamine est remplacée par du glutamate, le rénale d'ammoniac produit par des tranches dans des milieux à 7mEq/litres et 25mEq/litres est là encore significativement inférieur à celui produit par des tranches incubées dans un milieu à 4mEq/litres. Nous avons bloqué la synthèse de glutamine dans les tranches de rein de rat au moyen de la dl-méthionine dl-sulfoximine quand le glutamate était le précurseur de rénale d'ammoniac. Ceci permet à la déamination du glutamate de produire de l'ammoniac. Potassium diminue significativement la déamination du glutamate à 7mEq/litres (diminution de 13%), et à 25mEq/litres (diminution de 35%) par comparaison avec les valeurs obtenues à 4mEq/litres. Ces constatations sont compatibles avec un effet dépresseur majeur du potassium in vitro sur la déamination du glutamate dans les reins de rat et de chien. D'autres arguments, tirés essentiellement des études sur le tissu de rat, suggèrent que le potassium peut aussi affecter la déamination du glutamate directement. Des tranches de rein de rat incubées dans un milieu riche en potassium (7mEq/litres ou plus) consomment moins d'oxygène en présence de glutamine (P < 0,01), décarboxylent moins de glutamine par oxydation (P < 0,02) et produisent moins de glucose à partir de la glutamine (P < 0,01)

Epicardial adipose tissue in patients with heart failure

<p>Abstract</p> <p>Purpose</p> <p>The aim of this study was to evaluate the extent of epicardial adipose tissue (EAT) and its relationship with left ventricular (LV) parameters assessed by cardiovascular magnetic resonance (CMR) in patients with congestive heart failure (CHF) and healthy controls.</p> <p>Background</p> <p>EAT is the true visceral fat deposited around the heart which generates various bioactive molecules. Previous studies found that EAT is related to left ventricular mass (LVM) in healthy subjects. Further studies showed a constant EAT to myocardial mass ratio in normal, ischemic and hypertrophied hearts.</p> <p>Methods</p> <p>CMR was performed in 66 patients with CHF due to ischemic cardiomyopathy (ICM), or dilated cardiomyopathy (DCM) and 32 healthy controls. Ventricular volumes, dimensions and LV function were assessed. The amount of EAT was determined volumetrically and expressed as mass indexed to body surface area. Additionally, the EAT/LVM and the EAT/left ventricular remodelling index (LVRI) ratios were calculated.</p> <p>Results</p> <p>Patients with CHF had less indexed EAT mass than controls (22 ± 5 g/m²versus 34 ± 4 g/m², p < 0.0001). In the subgroup analysis there were no significant differences in indexed EAT mass between patients with ICM and DCM (21 ± 4 g/m²versus 23 ± 6 g/m², p = 0.14). Linear regression analysis showed that with increasing LV end-diastolic diameter (LV-EDD) (r = 0.42, p = 0.0004) and LV end-diastolic mass (LV-EDM) (r = 0.59, p < 0.0001), there was a significantly increased amount of EAT in patients with CHF. However, the ratio of EAT mass/LV-EDM was significantly reduced in patients with CHF compared to healthy controls (0.54 ± 0.1 versus 0.21 ± 0.1, p < 0.0001). In CHF patients higher indexed EAT/LVRI-ratios in CHF patients correlated best with a reduced LV-EF (r = 0.49, p < 0.0001).</p> <p>Conclusion</p> <p>Patients with CHF revealed significantly reduced amounts of EAT. An increase in LVM is significantly related to an increase in EAT in both patients with CHF and controls. However, different from previous reports the EAT/LVEDM-ratio in patients with CHF was significantly reduced compared to healthy controls. Furthermore, the LV function correlated best with the indexed EAT/LVRI ratio in CHF patients. Metabolic abnormalities and/or anatomic alterations due to disturbed cardiac function and geometry seem to play a key role and are a possible explanation for these findings.</p

Genetic and environmental influence on thyroid gland volume and thickness of thyroid isthmus: a twin study.

Objectives Decreased thyroid volume has been related to increased prevalence of thyroid cancer.Subjects and methods One hundred and fourteen Hungarian adult twin pairs (69 monozygotic, 45 dizygotic) with or without known thyroid disorders underwent thyroid ultrasound. Thickness of the thyroid isthmus was measured at the thickest portion of the gland in the midline using electronic calipers at the time of scanning. Volume of the thyroid lobe was computed according to the following formula: thyroid height*width*depth*correction factor (0.63).Results Age-, sex-, body mass index- and smoking-adjusted heritability of the thickness of thyroid isthmus was 50% (95% confidence interval [CI], 35 to 66%). Neither left nor right thyroid volume showed additive genetic effects, but shared environments were 68% (95% CI, 48 to 80%) and 79% (95% CI, 72 to 87%), respectively. Magnitudes of monozygotic and dizygotic co-twin correlations were not substantially impacted by the correction of covariates of body mass index and smoking. Unshared environmental effects showed a moderate influence on dependent parameters (24-50%).Conclusions Our analysis support that familial factors are important for thyroid measures in a general twin population. A larger sample size is needed to show whether this is because of common environmental (e.g. intrauterine effects, regional nutrition habits, iodine supply) or genetic effects

An urban traffic network model by first order hybrid Petri nets

The paper proposes a model for real time control of urban traffic networks. A modular framework based on first order hybrid Petri nets models the vehicle flows by a first order fluid approximation. Moreover, the lane interruptions and the signal timing plan controlling the area are described by the discrete event dynamics using timed Petri nets. The proposed model is applied to a real intersection located in Bari, Italy. Simulation of different scenarios shows the technique efficiency: validation is performed by comparison with a previously proposed alternative approach employing colored Petri net

Amino acids contribute to adaptive thermogenesis. New insights into the mechanisms of action of recent drugs for metabolic disorders are emerging

Adaptive thermogenesis is the heat production by muscle contractions (shivering thermogenesis) or brown adipose tissue (BAT) and beige fat (non-shivering thermogenesis) in response to external stimuli, including cold exposure. BAT and beige fat communicate with peripheral organs and the brain through a variegate secretory and absorption processes − controlling adipokines, microRNAs, extracellular vesicles, and metabolites − and have received much attention as potential therapeutic targets for managing obesity-related disorders. The sympathetic nervous system and norepinephrine-releasing adipose tissue macrophages (ATM) activate uncoupling protein 1 (UCP1), expressed explicitly in brown and beige adipocytes, dissolving the electrochemical gradient and uncoupling tricarboxylic acid cycle and the electron transport chain from ATP production. Mounting evidence has attracted attention to the multiple effects of dietary and endogenously synthesised amino acids in BAT thermogenesis and metabolic phenotype in animals and humans. However, the mechanisms implicated in these processes have yet to be conclusively characterized. In the present review article, we aim to define the principal investigation areas in this context, including intestinal microbiota constitution, adipose autophagy modulation, and secretome and metabolic fluxes control, which lead to increased brown/beige thermogenesis. Finally, also based on our recent epicardial adipose tissue results, we summarise the evidence supporting the notion that the new dual and triple agonists of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and glucagon (GCG) receptor − with never before seen weight loss and insulin-sensitizing efficacy − promote thermogenic-like amino acid profiles in BAT with robust heat production and likely trigger sympathetic activation and adaptive thermogenesis by controlling amino acid metabolism and ATM expansion in BAT and beige fat

The apple of daddy’s eye: Parental overvaluation links the narcissistic traits of father and child

This study contributes to the literature on the parental correlates of children’s narcissism. It addresses whether parental overvaluation may drive the putative link between parents’ narcissism and children’s narcissism and self-esteem. The cross-sectional design involved a community sample of 519 school-age children (age ranging from 9 to 11 years old) and their parents from an Italian urban context. Child-reported measures included narcissistic traits and self-esteem, while parent-reported measures included narcissistic traits and overvaluation, as well as parenting styles. A series of structural equation models, run separately for mothers and fathers, showed that both parents’ narcissism was directly and positively related to overvaluation and the children’s narcissistic traits; overvaluation partially mediated the indirect link between the fathers’ and children’s narcissistic traits. None of the parenting-style dimensions were related to the children’s outcomes, with the exception of the mothers’ positive parenting being directly and positively related to children’s self-esteem. These findings shed new light upon the parental correlates of child narcissism by suggesting that mothers and fathers convey their narcissism to their offspring through differential pathways. Our findings may be understood from universal as well as cultural specifics regarding the parenting roles of mothers and fathers. Clinical implications for the treatment of youth narcissism suggest the potential of targeting not only children but also their parents