Metabolic syndrome (MetS) describes a combination of risk factors that increase the risk of developing chronic diseases. The prevalences of MetS and its risk factors are increasing, especially in the Arab region. A cross-sectional study was carried out to assess the prevalences of MetS and its associated risk factors among adolescents in the United Arab Emirates (UAE). A total of 596 students (308 boys and 288 girls) aged 10 to 15.9 years old were recruited from 14 public secondary schools in Dubai, UAE. Anthropometric and biochemical data were measured. According to the International Diabetes Federation (IDF) criteria, the prevalence of MetS was 3.7%, and it was more common among boys than girls (12 boys versus 10 girls). MetS was also more likely to be found in students who were obese or overweight than those with normal weight. The most prevalent and significant MetS risk factor was low high-density lipoprotein (HDL) cholesterol levels. This study indicates the importance of carrying out further investigations about the constituents of HDL and their atherogenic effects. Additionally, these results strongly recommend setting a consensus for HDL measurement, since small variations in methodologies may lead to substantial deviations in results.

2,3-Diphosphoglycerate (2,3-DPG), found primarily in red blood cells, plays a key role in regulating hemoglobin’s (Hb) affinity for oxygen. Increased 2,3-DPG levels shift the oxygen dissociation curve to the right, reducing Hb’s oxygen affinity and enhancing oxygen delivery to tissues—particularly important in conditions like anemia and high-altitude adaptation. Despite its physiological significance, research on 2,3-DPG is outdated and limited. This review aims to summarize current knowledge and identify research gaps. Measuring 2,3-DPG is challenging due to its instability and the need for careful sample handling. Chromatography and enzymatic methods are commonly used. Several factors influence 2,3-DPG levels, including diet, physiological state, and disease. Dietary phosphorus, for example, can acutely affect 2,3-DPG levels, though the impact of different meal compositions remains unexplored. Age, pregnancy, and physical activity also modulate 2,3-DPG, yet little is known about its role in infants and children. While changes in 2,3-DPG levels under various pathological conditions have been described, the molecular mechanisms behind these alterations remain poorly understood and warrant further investigation.

Introduction: Urinary excretion of calcium (Ca), magnesium (Mg), phosphorus (P), iodine and fluoride is used to assess their statuses and/or the existence of metabolic abnormalities. In the United Arab Emirates (UAE), the urinary concentration of these minerals among children have not been documented.Materials and methods: A cross-sectional study, including 593 subjects (232 boys and 361 girls), was conducted among healthy 6 to 11-year-old Emirati children living in Dubai. Non-fasting morning urine samples and anthropometrical measurements were collected and analyzed. Results were expressed as per mg of creatinine (Cr).Results: On average, estimated Cr excretion was 17.88±3.12 mg/kg/d. Mean urinary Ca/Cr, Mg/Cr and P/Cr excretions were 0.08±0.07 mg/mg, 0.09±0.04 mg/mg, and 0.57±0.26 mg/mg respectively. Urinary excretion of Ca, Mg and P were found to decrease as age increased. Urinary excretion and predicted intake of fluoride were lower than 0.05 mg/kg body weight per day. Surprisingly, more than 50% of the children were found to have urinary iodine excretion level above adequate.Conclusion: The Emirati schoolchildren had comparable levels of urinary Ca, Mg and P excretion to other countries. The 95% percentile allows the use of the current data as a reference value for the detection of mineral abnormalities. Fluoride excretion implies that Emirati children are at low risk of fluorosis. The level of urinary iodine excretion is slightly higher than recommended and requires close monitoring of the process of salt iodization to avoid the harmful impact of iodine overconsumption.

Sodium chloride (NaCl) activates Th17 and dendritic cells in hypertension by stimulating serum/glucocorticoid kinase 1 (SGK1), a sodium sensor. Memory T cells also play a role in hypertension by infiltrating target organs and releasing proinflammatory cytokines. We tested the hypothesis that the role of T cell SGK1 extends to memory T cells. We employed mice with a T cell deletion of SGK1, SGK1^fl/fl × tgCD4^cre mice, and used SGK1^fl/fl mice as controls. We treated the mice with L-NAME (0.5 mg/mL) for 2 weeks and allowed a 2-week washout interval, followed by a 3-week high-salt (HS) diet (4% NaCl). L-NAME/HS significantly increased blood pressure and memory T cell accumulation in the kidneys and bone marrow of SGK1^fl/fl mice compared to knockout mice on L-NAME/HS or groups on a normal diet (ND). SGK1^fl/fl mice exhibited increased albuminuria, renal fibrosis, and interferon-γ levels after L-NAME/HS treatment. Myography demonstrated endothelial dysfunction in the mesenteric arterioles of SGK1^fl/fl mice. Bone marrow memory T cells were adoptively transferred from either mouse strain after L-NAME/HS administration to recipient CD45.1 mice fed the HS diet for 3 weeks. Only the mice that received cells from SGK1^fl/fl donors exhibited increased blood pressure and renal memory T cell infiltration. Our data suggest a new therapeutic target for decreasing hypertension-specific memory T cells and protecting against hypertension.

The relationship between non-communicable diseases and eating behaviour has long been attributed to a surplus of food and energy. However, the increase in the prevalence of non-communicable disease and their underlying low-grade inflammatory milieu among people of low socio-economic status has highlighted the existence of a confounding factor. In this work, we aim to study the effect of lysine deficiency on some inflammatory markers in the absence or presence of an inflammatory insult (lipopolysaccharide (LPS)). For this purpose, thirty-two 5-week-old male Sprague Dawley rats were randomly distributed into four groups: (1) control diet, (2) control diet+LPS, (3) lysine-deficient diet and (4) lysine-deficient diet + LPS. Groups were only allowed their experimental diets for 4 weeks, during which LPS (50 µg/kg) or saline injections were administered intraperitoneally three times per week. The study showed that lysine deficiency blunted growth and body compartments development, decreased albumin production and elevated liver C-reactive protein (CRP) expression, independently of IL-6 and IL-1β, the main precursors of CRP. Also, the insufficient levels of lysine in the diet increased hyperactivity and triggered an anxiety-like behaviour, exacerbated with LPS. This work presents evidence that various physiological changes are associated with the absence of a sufficient amount of lysine in the diet and can potentially increase the risk factor for diseases. Thus, the increment in non-communicable disease among the low socio-economic status populations, who heavily rely on cereals as a main source of protein, can be, at least partially, blamed on low lysine availability in diets.