Serum selenium concentrations and diabetes in U.S. adults : National Health and Nutrition Examination Survey (NHANES) 2003–2004

Background: Increasing evidence suggests that high selenium levels are associated with diabetes and other cardiometabolic risk factors. Objectives: We evaluated the association of serum selenium concentrations with fasting plasma glucose, glycosylated hemoglobin levels, and diabetes in the most recently available representative sample of the U.S. population. Methods: We used a cross-sectional analysis of 917 adults ≥ 40 years of age who had a fasting morning blood sample in the National Health and Nutrition Examination Survey 2003–2004. We evaluated the association of serum selenium, measured by inductively coupled plasma-dynamic reaction cell-mass spectrometry, and diabetes, defined as a self-report of current use of hypoglycemic agents or insulin or as fasting plasma glucose ≥ 126 mg/dL. Results: Mean serum selenium was 137.1 μg/L. The multivariable adjusted odds ratio [95% confidence interval (CI)] for diabetes comparing the highest quartile of serum selenium (≥ 147 μg/L) with the lowest (< 124 μg/L) was 7.64 (3.34–17.46). The corresponding average differences (95% CI) in fasting plasma glucose and glycosylated hemoglobin were 9.5 mg/dL (3.4–15.6 mg/dL) and 0.30% (0.14–0.46%), respectively. In spline regression models, the prevalence of diabetes as well as glucose and glycosylated hemoglobin levels increased with increasing selenium concentrations up to 160 μg/L. Conclusions: In U.S. adults, high serum selenium concentrations were associated with higher prevalence of diabetes and higher fasting plasma glucose and glycosylated hemoglobin levels. Given high selenium intake in the U.S. population, further research is needed to determine the role of excess selenium levels in the development or the progression of diabetes

Does Obesity Modify the Relationship between Exposure to Occupational Factors and Musculoskeletal Pain in Men? Results from the GAZEL Cohort Study

Objective: To analyze relationships between physical occupational exposures, post-retirement shoulder/knee pain, and obesity. Methods: 9 415 male participants (aged 63–73 in 2012) from the French GAZEL cohort answered self-administered questionnaires in 2006 and 2012. Occupational exposures retrospectively assessed in 2006 included arm elevation and squatting (never, <10 years, ≥10 years). “Severe” shoulder and knee pain were defined as ≥5 on an 8-point scale. BMI was self-reported. Results: Mean BMI was 26.59 kg/m2 +/−3.5 in 2012. Long-term occupational exposure to arm elevation and squatting predicted severe shoulder and knee pain after retirement. Obesity (BMI≥30 kg/m2) was a risk factor for severe shoulder pain (adjusted OR 1.28; 95% CI 1.03, 1.90). Overweight (adjusted OR 1.71; 1.28,2.29) and obesity (adjusted OR 3.21; 1.90,5.41) were risk factors for severe knee pain. In stratified models, associations between long-term squatting and severe knee pain varied by BMI. Conclusion: Obesity plays a role in relationships between occupational exposures and musculoskeletal pain. Further prospective studies should use BMI in analyses of musculoskeletal pain and occupational factors, and continue to clarify this relationship

Management of the child born small for gestational age through to adulthood: A consensus statement of the international societies of pediatric endocrinology and the Growth Hormone Research Society

Objective: Low birth weight remains a major cause of morbidity and mortality in early infancy and childhood. It is associated with an increased risk of health problems later in life, particularly coronary heart disease and stroke. A meeting was convened to identify the key health issues facing a child born small for gestational age (SGA) and to propose management strategies. Participants: There were 42 participants chosen for their expertise in obstetrics, peri- and neonatal medicine, pediatrics, pediatric and adult endocrinology, epidemiology, and pharmacology. Evidence: Written materials were exchanged, reviewed, revised, and then made available to all. This formed the basis for discussions at the meeting. Where published data were not available or adequate, discussion was based on expert clinical opinions. Consensus Process: Each set of questions was considered by all and then discussed in plenary sessions with consensus and unresolved issues identified. The consensus statement was prepared in plenary sessions and then edited by the group chairs and shared with all participants. Conclusions: The diagnosis of SGA should be based on accurate anthropometry at birth including weight, length, and head circumference. We recommend early surveillance in a growth clinic for those without catch-up. Early neurodevelopment evaluation and interventions are warranted in at-risk children. Endocrine and metabolic disturbances in the SGA child are recognized but infrequent. For the 10% who lack catch-up, GH treatment can increase linear growth. Early intervention with GH for those with severe growth retardation (height SD score, < -2.5; age, 2-4 yr) should be considered at a dose of 35-70 mu g/kg center dot d. Long-term surveillance of treated patients is essential. The associations at a population level between low birth weight, including SGA, and coronary heart disease and stroke in later life are recognized, but there is inadequate evidence to recommend routine health surveillance of all adults born SGA outside of normal clinical practice

Evolution of IGF-1 in children born small for gestational age and with growth retardation, treated by growth hormone adapted to IGF-1 levels after 1 year

AIM: This study was designed to estimate the percentage of growth hormone (GH)-treated children born small for gestational age (SGA), with serum IGF-1 &gt;2 SDS before and after GH dose adaptation. METHODS: SGA boys aged 4-9 and girls aged 4-7 with a height &lt;-2 SDS and an annual growth rate below the mean received a subcutaneous GH dose of 57 mug/kg/day for 2 years. The GH dose was to be decreased by 30% in children with serum IGF-1 &gt;2 SDS at 12 months and on the previous sample. The GH dose could be reduced a second time to 35 mug/kg.day. IGF-1 and IGFBP-3 dosages were centralized. RESULTS: Among the 49 (21 boys) children included in the study, 8 (16.3%) had an IGF-1 &gt;2 SDS consecutively at 9 and 12 months (95% CI 7.3, 29.7). The GH dose was decreased in 6/8 children. However, IGF-1 levels were elevated at several nonconsecutive determinations in 45% (95% CI 28.4, 56.6) of the patients. CONCLUSION: A high IGF-1 level is observed in 45% of the GH SGA-treated children with a relatively high dose of GH. A 30% reduction in the GH dose causes a decrease in IGF-1 below 2 SDS in most children

Obesity and the microvasculature

Overweight and obesity are thought to significantly influence a person's risk of cardiovascular disease, possibly via its effect on the microvasculature. Retinal vascular caliber is a surrogate marker of microvascular disease and a predictor of cardiovascular events. The aim of this systematic review and meta-analysis was to determine the association between body mass index (BMI) and retinal vascular caliber. Relevant studies were identified by searches of the MEDLINE and EMBASE databases from 1966 to August 2011. Standardized forms were used for data extraction. Among over 44,000 individuals, obese subjects had narrower arteriolar and wider venular calibers when compared with normal weight subjects, independent of conventional cardiovascular risk factors. In adults, a 1 kg/m(2) increase in BMI was associated with a difference of 0.07 μm [95% CI: -0.08; -0.06] in arteriolar caliber and 0.22 μm [95% CI: 0.21; 0.23] in venular caliber. Similar results were found for children. Higher BMI is associated with narrower retinal arteriolar and wider venular calibers. Further prospective studies are needed to examine whether a causative relationship between BMI and retinal microcirculation exists

Development of a conditionally immortalized human pancreatic β cell line

International audienceDiabetic patients exhibit a reduction in β cells, which secrete insulin to help regulate glucose homeostasis; however, little is known about the factors that regulate proliferation of these cells in human pancreas. Access to primary human β cells is limited and a challenge for both functional studies and drug discovery progress. We previously reported the generation of a human β cell line (EndoC-βH1) that was generated from human fetal pancreas by targeted oncogenesis followed by in vivo cell differentiation in mice. EndoC-βH1 cells display many functional properties of adult β cells, including expression of β cell markers and insulin secretion following glucose stimulation; however, unlike primary β cells, EndoC-βH1 cells continuously proliferate. Here, we devised a strategy to generate conditionally immortalized human β cell lines based on Cre-mediated excision of the immortalizing transgenes. The resulting cell line (EndoC-βH2) could be massively amplified in vitro. After expansion, transgenes were efficiently excised upon Cre expression, leading to an arrest of cell proliferation and pronounced enhancement of β cell–specific features such as insulin expression, content, and secretion. Our data indicate that excised EndoC-βH2 cells are highly representative of human β cells and should be a valuable tool for further analysis of human β cells

Risk factors for metabolic syndrome independently predict arterial stiffness and endothelial dysfunction in patients with chronic kidney disease and minimal comorbidity

OBJECTIVE: Metabolic syndrome (MS) is common in patients with chronic kidney disease (CKD), but its contribution to arterial stiffness and endothelial dysfunction in CKD is not well defined. We hypothesized that risk factors for MS would independently predict arterial stiffness and endothelial dysfunction in CKD patients. RESEARCH DESIGN AND METHODS: Risk factors for MS, carotid-femoral pulse wave velocity (CF-PWV) and flow-mediated dilation (FMD) as measures of arterial stiffness and endothelial dysfunction, respectively, were assessed in 113 minimally comorbid CKD patients and in 23 matched control subjects. RESULTS: CF-PWV correlated with systolic blood pressure (SBP), waist circumference, and plasma glucose (r(2) = 0.25, 0.09, and 0.09; P < 0.01 for all). FMD correlated with SBP (r(2) = 0.09; P < 0.01) and waist circumference (r(2) = 0.03; P < 0.05). CF-PWV increased progressively (r(2) = 0.07; P < 0.01) with increasing number of risk factors for MS. In multiple linear regression, SBP and waist circumference were independent determinants of CF-PWV, whereas only SBP predicted FMD. CONCLUSIONS: The number of MS risk factors is an important determinant of arterial stiffness in CKD patients irrespective of the degree of renal impairment. Although BP remains the major determinant of arterial stiffness and endothelial dysfunction, waist circumference independently predicts arterial stiffness. MS risk factors, particularly abdominal girth, are potential targets for future interventional studies in patients with CKD

Adiposity has differing associations with incident coronary heart disease and mortality in the Scottish population: cross-sectional surveys with follow-up

Objective: Investigation of the association of excess adiposity with three different outcomes: all-cause mortality, coronary heart disease (CHD) mortality and incident CHD. Design: Cross-sectional surveys linked to hospital admissions and death records. Subjects: 19 329 adults (aged 18–86 years) from a representative sample of the Scottish population. Measurements: Gender-stratified Cox proportional hazards models were used to estimate hazard ratios (HRs) for all-cause mortality, CHD mortality and incident CHD. Separate models incorporating the anthropometric measurements body mass index (BMI), waist circumference (WC) or waist–hip ratio (WHR) were created adjusted for age, year of survey, smoking status and alcohol consumption. Results: For both genders, BMI-defined obesity (greater than or equal to30 kg m−2) was not associated with either an increased risk of all-cause mortality or CHD mortality. However, there was an increased risk of incident CHD among the obese men (hazard ratio (HR)=1.78; 95% confidence interval=1.37–2.31) and obese women (HR=1.93; 95% confidence interval=1.44–2.59). There was a similar pattern for WC with regard to the three outcomes; for incident CHD, the HR=1.70 (1.35–2.14) for men and 1.71 (1.28–2.29) for women in the highest WC category (men greater than or equal to102 cm, women greater than or equal to88 cm), synonymous with abdominal obesity. For men, the highest category of WHR (greater than or equal to1.0) was associated with an increased risk of all-cause mortality (1.29; 1.04–1.60) and incident CHD (1.55; 1.19–2.01). Among women with a high WHR (greater than or equal to0.85) there was an increased risk of all outcomes: all-cause mortality (1.56; 1.26–1.94), CHD mortality (2.49; 1.36–4.56) and incident CHD (1.76; 1.31–2.38). Conclusions: In this study excess adiposity was associated with an increased risk of incident CHD but not necessarily death. One possibility is that modern medical intervention has contributed to improved survival of first CHD events. The future health burden of increased obesity levels may manifest as an increase in the prevalence of individuals living with CHD and its consequences

Impact of cigarette smoking on the relationship between body mass index and coronary heart disease: a pooled analysis of 3264 stroke and 2706 CHD events in 378579 individuals in the Asia Pacific region

BACKGROUND: Elevated levels of body mass index (BMI) and smoking are well established lifestyle risk factors for coronary heart disease (CHD) and stroke. If these two risk factors have a synergistic relationship, rigorous lifestyle modification may contribute to greater reduction in cardiovascular burden than previously expected. METHODS: A pooled analysis of individual participant data from 38 cohorts, involving 378,579 participants. Hazards ratios (HRs) and 95% confidence intervals (CIs) for BMI by cigarette smoking status were estimated using Cox proportional hazard models. RESULTS: During a mean follow-up of 3.8 years, 2706 CHD and 3264 strokes were recorded. There was a log-linear, positive relationship of BMI with CHD and stroke in both smokers and non-smokers with evidence of a synergistic effect of smoking on the association between BMI and CHD only: HRs (95% CIs) associated with a 2 kg/m2 higher BMI were 1.13 (1.10-1.17) in current smokers and 1.09 (1.06-1.11) in non-smokers (p-value for interaction=0.04). CONCLUSION: Smoking amplifies the positive association between BMI and CHD but not stroke. If confirmed, these results suggest that effective strategies that target smoking cessation and weight loss are likely to have a greater impact than anticipated on reducing the burden of CHD.published_or_final_versio

Obesity and the Microvasculature: A Systematic Review and Meta-Analysis

10.1371/journal.pone.0052708PLoS ONE82