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The objective of the study was to assess associations of the rs9939609 FTO allele to glucose tolerance, hepatic and total insulin sensitivity (IS) in individuals with obesity. From a low-dose hyperinsulinemic euglycemic clamp with glucose-tracer, hepatic IS was assessed by rates of basal and suppressed glucose appearance (Ra), a measure of endogenous glucose production (EGP), and the hepatic insulin resistance index (HIR). Total IS was assessed by rates of glucose infusion (GIR), disappearance (Rd), and metabolic clearance (MCR). From a meal test we assessed IS by the Matsuda index and glucose tolerance by glucose and insulin measurements in the fasted state and postprandially for 2.5 h. The meal test was performed in 97 healthy individuals with BMI ≥35 in similar-sized risk-allele groups (n = 32 T/T, 31 A/T, and 34 A/A), and 79 of them performed the clamp. We analyzed outcomes separately for males and females, and adjusted glucose Ra, Rd, MCR, GIR, and HIR for fat mass. We did not find genotype effects on EGP. Among males, genotype A/A was associated with a significantly lower glucose Rd, MCR, and Matsuda index score relative to genotype T/T. Glucose tolerance was significantly lower in males with genotype A/T vs. T/T and A/A. For females, there were no genotype effects on hepatic or total IS, or on glucose tolerance. Independently of genotypes, females displayed a significantly better hepatic and total IS, and better glucose tolerance than males. We conclude that in subjects with similar obesity we did not register any FTO risk-allele effect on hepatic IS. A FTO risk-allele effect on total IS was registered in males only, findings which need to be reproduced in further studies. Results confirm marked differences in IS between the biological sexes and extend present knowledge by demonstrating a lower endogenous glucose production in females vs. males in uniformly obese individuals. Copyright: © 2021 de Soysa et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Scholars of public health identify globalization as a major cause of obesity. Free markets are blamed for spreading high calorie, nutrient-poor diets, and sedentary lifestyles across the globe. Global trade and investment agreements apparently curtail government action in the interest of public health. Globalization is also blamed for raising income inequality and social insecurities, which contribute to “obesogenic” environments. Contrary to recent empirical studies, this study demonstrates that globalization and several component parts, such as trade openness, FDI flows, and an index of economic freedom, reduce weight gain and obesity among children and youth, the most likely age cohort to be affected by the past three decades of globalization and attendant lifestyle changes. The results suggest strongly that local-level factors possibly matter much more than do global-level factors for explaining why some people remain thin and others put on weight. The proposition that globalization is homogen...

Purpose The metabolic consequences of carrying a FTO obesity-promoting risk allele have not been fully elucidated and may be confounded by obesity per se. Against this background, we investigated the impact of FTO allele (SNP rs9939609) on fasting and postprandial energy expenditure and fasting substrate expenditure in a study population of uniformly and similarly obese individuals. Procedures We studied a similar number of participants with BMI classes 2–3 (median BMI 42.8 kg/m2) who were either homozygote for the non-risk allele TT (n = 33, numbers increased by enrichment), heterozygote (AT) (n = 32), or homozygote for the risk allele AA (n = 35). Major findings Basal metabolic rate and postprandial energy expenditure did not differ between FTO-groups. However, fasting respiratory quotient (RQ) was increased in those carrying ≥1 risk allele (p = 0.008), whereas postprandial RQ was not. Conclusion In this study population, the FTO-risk allele associates with fasting reduced fat and increased carbohydrate oxidation., Highlights • Fasting RQ associates with FTO risk allele in comparably obese subjects. • The association remained after adjusting for gender effects. • FTO risk not associated with meal-related energy utilization.

Summary Background & aims Malnutrition is an important issue in patient outcome. Screening tools to find risk patients need to be evaluated. This study looks at the validity and reliability of nutritional risk screening (named NRS-2002) in hospitalized patients with chronic heart failure. Methods In this cross-sectional study nutritional screening was performed using NRS-2002 in 131 patients with chronic heart failure. The predictive validity was evaluated in relation to whether NRS-2002 predicted the incidence of complications and length of hospital stay. NRS-2002's ability to locate nutritional risk in patients with edema was evaluated. The inter-rater reliability was measured between three investigators screening 45 patients each. Results The prevalence of nutritional risk was 57%. The incidence of complications and the median length of hospital stay were significantly higher in patients at nutritional risk compared to patients not at nutritional risk. Only the component of severity of disease in NRS-2002 and not the component of the nutritional status was associated with increased length of hospital stay in multivariate analysis. Patients with edema were classified correctly regarding nutritional risk status by NRS-2002 in all but one occasion. The inter-rater reliability was documented, kappa >0.60. Conclusion NRS-2002 was a reliable screening tool in an in-patient sample with chronic heart failure. The validity of NRS-2002 needs further investigation in a larger sample of hospitalized patients with chronic heart failure.

Cardiovascular disease, obesity, and type 2 diabetes are conditions characterized by low-grade systemic inflammation, strongly influenced by lifestyle, but the mechanisms that link these characteristics are poorly understood. Our first objective was to investigate if a normocaloric diet with a calorically balanced macronutrient composition influenced immunological gene expression. Findings regarding the suitability of blood as biological material in nutrigenomics and gene expression profiling have been inconclusive. Our second objective was to compare blood and adipose tissue sample quality in terms of adequacy for DNA-microarray analyses, and to determine tissue-specific gene expression patterns. Blood and adipose tissue samples were collected for gene expression profiling from three obese men before, during, and after a 28-day normocaloric diet intervention where each meal contained an approximately equal caloric load of macronutrients. Time series analyses of blood gene expression revealed a cluster of downregulated genes involved in immunological processes. Blood RNA quality and yield were satisfactory, and DNA-microarray analysis reproducibility was similar in blood and adipose tissue. Gene expression correlation between blood and adipose tissue varied according to gene function, and was especially low for genes involved in immunological and metabolic processes. This suggests that diet composition is of importance in inflammatory processes in blood cells. The findings also suggest that a systems biology approach, in which tissues are studied in parallel, should be employed to fully understand the impact of dietary challenges on the human body.

SummaryBackground & aimsMortality among patients with chronic heart failure (CHF) is still high despite progress in medical and surgical treatment. The patients' nutritional condition may play an important role, and needs further investigation. The aim of this study was to evaluate whether nutritional risk in hospitalized patients with CHF was associated with three-year mortality.MethodsA prospective study was conducted in 131 hospitalized Norwegian patients with CHF. Nutritional screening was performed using Nutritional Risk Screening (NRS-2002). The primary clinical outcome was death from any cause.ResultsThe prevalence of nutritional risk was 57% (NRS-2002 score ≥ 3). The overall mortality rate was 52.6% within three-year follow up. More patients at nutritional risk (N = 51) died compared to patients not at nutritional risk (N = 18) (P