Micronutrient deficiencies and inadequacies constitute a global health issue, particularly among countries in the Middle East. The objective of this review is to identify micronutrient deficits in the Middle East and to consider current and new approaches to address this problem. Based on the availability of more recent data, this review is primarily focused on countries that are in advanced nutrition transition. Prominent deficits in folate, iron, and vitamin D are noted among children/adolescents, women of childbearing age, pregnant women, and the elderly. Reports indicate that food fortification in the region is sporadic and ineffective, and the use of dietary supplements is low. Nutrition monitoring in the region is limited, and gaps in relevant information present challenges for implementing new policies and approaches to address the problem. Government-sponsored initiatives are necessary to assess current dietary intakes/patterns, support nutrition education, and to reduce food insecurity, especially among vulnerable population groups. Public–private partnerships should be considered in targeting micronutrient fortification programs and supplementation recommendations as approaches to help alleviate the burden of micronutrient deficiencies and inadequacies in the Middle East.

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Middle East respiratory syndrome coronavirus (MERS-CoV) originated in bats and spread to humans via zoonotic transmission from camels. We analyzed the evolution of the spike (S) gene in betacoronaviruses (betaCoVs) isolated from different mammals, in bat coronavirus populations, as well as in MERS-CoV strains from the current outbreak. Results indicated several positively selected sites located in the region comprising the two heptad repeats (HR1 and HR2) and their linker. Two sites (R652 and V1060) were positively selected in the betaCoVs phylogeny and correspond to mutations associated with expanded host range in other coronaviruses. During the most recent evolution of MERS-CoV, adaptive mutations in the HR1 (Q/R/H1020) arose in camels or in a previous host and spread to humans. We determined that different residues at position 1020 establish distinct inter- and intra-helical interactions and affect the stability of the six-helix bundle formed by the HRs. A similar effect on stability was observed for a nearby mutation (T1015N) that increases MERS-CoV infection efficiency in vitro. Data herein indicate that the heptad repeat region was a major target of adaptive evolution in MERS-CoV-related viruses; these results are relevant for the design of fusion inhibitor peptides with antiviral function.

A post-prandial increase in saturated fatty acids (SFAs) and glucose (Glc) activates an inflammatory response, which may be prolonged following restoration of physiological SFAs and Glc levels — a finding referred to as ‘metabolic memory'.This study examined chronic and oscillating SFAs and Glc on the inflammatory signalling pathway in human adipose tissue (AT) and adipocytes (Ads) and determined whether Ads are subject to “metabolic memory.”Abdominal (Abd) subcutaneous (Sc) explants and Ads were treated with chronic low glucose (L-Glc): 5.6 mM and high glucose (H-Glc): 17.5 mM, with low (0.2 mM) and high (2 mM) SFA for 48 h. Abd Sc explants and Ads were also exposed to the aforementioned treatment regimen for 12-h periods, with alternating rest periods of 12 h in L-Glc.Chronic treatment with L-Glc and high SFAs, H-Glc and high SFAs up-regulated key factors of the nuclear factor-κB (NFκB) pathway in Abd Sc AT and Ads (TLR4, NFκB; P<.05), whilst down-regulating MyD88. Oscillating Glc and SFA concentrations increased TLR4, NFκB, IKKβ (P<.05) in explants and Ads and up-regulated MyD88 expression (P<.05). Both tumor necrosis factor α and interleukin 6 (P<.05) secretion were markedly increased in chronically treated Abd Sc explants and Ads whilst, with oscillating treatments, a sustained inflammatory effect was noted in absence of treatment.Therefore, SFAs may act as key instigators of the inflammatory response in human AT via NFκB activation, which suggests that short-term exposure of cells to uncontrolled levels of SFAs and Glc leads to a longer-term inflammatory insult within the Ad, which may have important implications for patients with obesity and Type 2 diabetes.

Our results report for the first time a positive association of the E23K variant with T2D in an Arab population. Confirmation by a larger study is indicated.

Abstract. We studied the association between RBP4 and various markers related to insulin resistance and diabetic complications as well as inflammatory markers in Saudi population suffering from type 2 diabetes and coronary heart disease. Patients with type 2 diabetes were divided into 3 groups according to the type of treatment and involvement of coronary artery disease. Serum RBP4, TNF-α, insulin, CRP, resistin, leptin and adiponectin were analysed in all samples. RBP4 levels increased significantly in the group of diabetic subjects treated with oral hypoglycemic agents and diabetic patients with coronary heart disease (30.2 ± 11.8; 33.4 ± 13.6 respectively), while there was no significant change in the other group for diabetic subjects on low-carbohydrate diet (25.1 ± 10.9) compared to control group (22.6 ± 9.5). RPB4 levels were positively correlated with TNF-α in the group of diabetic subjects on oral hypoglycemic agents and diabetic patients with coronary heart disease (r = 0.52, P < 0.05; r = 0.58, P < 0.05 respectively). No correlations were found between RBP4 levels and insulin resistance in all studied groups. Our findings suggest that serum RBP4 levels is associated with pro-inflammatory cytokine (TNF-α) and is not associated with insulin resistance among patients with type 2 diabetes and coronary heart disease.

Eur J Clin Invest 2012; 42 (11): 1221–1226 Abstract Background  The hallmark of vascular inflammation is the recruitment of circulating leucocytes, primarily monocytes, macrophages and T lymphocytes, into the vascular wall; however, the link between monocyte/macrophage activation and hypertension has not been established as yet. In this study, we determined how sCD163, a monocyte/macrophage soluble scavenger receptor and immunomodulator, relates to arterial blood pressure (BP) in hypertensive Saudi individuals. Materials and methods  A total of 90 (30 non‐hypertensive obese, 30 hypertensive obese and 30 lean normotensive controls) adult Saudi subjects, aged 40–60 years, participated in this cross‐sectional study. Serum fasting blood glucose, triglycerides, total cholesterol, HDL‐cholesterol (HDL‐C), LDL‐cholesterol (LDL‐C), leptin, adiponectin, resistin, insulin, tumour necrosis factor‐alpha (TNF‐α), PAI‐1, angiotensin II, high‐sensitivity C‐reactive protein (hsCRP) and sCD163 were measured in all subjects studied. Results  sCD163 concentrations were significantly increased in obese hypertensive patients compared to controls (P = 0·016). Positive correlations between sCD163 and body mass index (BMI) (r = 0·27, P = 0·01), systolic BP (r = 0·25, P = 0·01), diastolic BP (r = 0·33, P = 0·001), LDL‐C (r = 0·21, P = 0·04), TNF‐α (r = 0·23, P = 0·02) and hsCRP (r = 0·33, P = 0·008) were observed. Positive correlations between sCD163 and diastolic BP (r = 0·23, P = 0·04) and LDL‐C (r = 0·22, P = 0·03) remained significant after controlling for BMI. Conclusions  Taken together, these data demonstrate that the monocyte/macrophage activation‐related sCD163 is positively associated with BMI and increased arterial BP with the elevation in diastolic BP being independent of the BMI.

Vitamin D is a key component for optimal growth and for calcium–phosphate homeostasis. Skin photosynthesis is the main source of vitamin D. Limited sun exposure and insufficient dietary vitamin D supply justify vitamin D supplementation in certain age groups. In older adults, recommended doses for vitamin D supplementation vary between 200 and 2000 IU/day, to achieve a goal of circulating 25-hydroxyvitamin D (calcifediol) of at least 50 nmol/L. The target level depends on the population being supplemented, the assessed system, and the outcome. Several recent large randomized trials with oral vitamin D regimens varying between 2000 and 100,000 IU/month and mostly conducted in vitamin D-replete and healthy individuals have failed to detect any efficacy of these approaches for the prevention of fracture and falls. Considering the well-recognized major musculoskeletal disorders associated with severe vitamin D deficiency and taking into account a possible biphasic effects of vitamin D on fracture and fall risks, an European Society for Clinical and Economic Aspects of Osteoporosis, Osteoarthritis and Musculoskeletal Diseases (ESCEO) working group convened, carefully reviewed, and analyzed the meta-analyses of randomized controlled trials on the effects of vitamin D on fracture risk, falls or osteoarthritis, and came to the conclusion that 1000 IU daily should be recommended in patients at increased risk of vitamin D deficiency. The group also addressed the identification of patients possibly benefitting from a vitamin D loading dose to achieve early 25-hydroxyvitamin D therapeutic level or from calcifediol administration.