There are no studies evaluating the glucose variability in different periods of Ramadan fasting in patients with type 2 diabetes using continuous glucose monitoring (CGM). This study examined the effect of Ramadan fasting on interstitial glucose (IG) variability in early,- late-, and post-Ramadan compared to pre-Ramadan days in non-insulin-treated type 2 diabetes patients. Participants had a CGM system connected 2 or 3 days before Ramadan start, which was removed on the third or fourth day of Ramadan. CGM performance continued for a total of 6 days. A second CGM performance started on the 27th or 28th day of Ramadan and ended on the 4th or 5th post-Ramadan day. First, CGM recordings were divided into pre-Ramadan and early-Ramadan CGM, and second recordings into late-Ramadan and post-Ramadan. At each visit, blood pressure, body weight, and waist circumference were measured, and fasting blood samples were collected for HbA1c and plasma glucose. All patients received recommended Ramadan education before Ramadan. Thirty-three patients (mean age 55.0 ± 9.8 years, 73% males) were prospectively included. IG variability, estimated as mean amplitude of glycaemic excursions (MAGE), increased significantly in early-Ramadan compared to pre-Ramadan (P = 0.006) but not in late-Ramadan and post-Ramadan recording days. Only patients on >2 anti-diabetic drugs (n = 16, P = 0.019) and those on sulphonylureas (n = 14, P = 0.003) showed significant increase in MAGE in early-Ramadan. No significant changes were seen in coefficient of variation, time in range, time in hyperglycaemia, or time in hypoglycaemia. Except for an initial increase in glucose variability, fasting Ramadan for patients with non-insulin-treated type 2 diabetes did not cause any significant changes in glucose variability or time in hypoglycaemia during CGM recording days compared to non-fasting pre-Ramadan period.

Background: Insulin-resistant individuals are known to have dyslipidemia and are predicted to be at high risk of cardiovascular events. Vitamin D deficiency was shown to be associated with dyslipidemia; however, the type of dyslipidemia associated with vitamin D deficiency in insulin-resistant individuals is not determined. Furthermore, there is evidence linking insulin resistance with low-grade inflammation suggesting levels of pro-inflammatory cytokines to be increased in insulin-resistant states. Objective: This study was performed to evaluate the impact of vitamin D deficiency, defined as serum level of 25(OH)D below 20 ng/mL, on lipid profile and inflammatory markers such as interleukin (IL-6) and IL-8, as well as soluble thrombomodulin (TM) in the serum of insulin-resistant individuals. Methods: A total of 4114 individuals had simultaneous serum 25(OH)D, insulin, and lipid panel testing during 2013 as part of the United Arab Emirates National Diabetes and Lifestyle (UAEDIAB) study. Multivariate logistic regression analysis was used to assess the association between serum level of 25(OH)D and lipid profile in insulin-sensitive versus -resistant individuals. The lipid panel was stratified into high total cholesterol (TC: > 6.2 mmol/L), high low-density lipoprotein-cholesterol (LDL-C: > 2.59 mmol/L), high triglycerides (TG: > 2.3 mmol/L), and low high-density lipoprotein-cholesterol (HDL-C: < 1.55 mmol/L) dyslipidemia. Furthermore, the immunomodulatory and vasculoprotective effects of 25(OH)D were assessed by measuring the levels of IL-6, IL-8, and soluble TM in serum using ELISA. Results: More than half of the 4114 individuals were insulin resistant (n=2760, 67%) and around one-fifth of them were vitamin D-deficient (n=796, 19%). After adjusting for age, gender, body mass index, smoking, ethnicity, and educational level, the only dyslipidemia associated with vitamin D-deficient-insulin-resistant individuals (OR 2.09 [95]; P=0.009) was lower HDL-C. Furthermore, deficient 25(OH)D individuals with low HDL-C levels had higher circulatory IL-6 and IL-8 levels, and higher serum soluble TM compared to individuals with sufficient 25(OH)D and normal lipid profiles (median, IL-6 pg/mL 0.82 vs 1.71, P=0.001; median, IL-8 pg/mL 51.31 vs 145.6, P=0.003; and median, soluble TM ng/mL 5.19 vs 7.38, P< 0.0001; in sufficient vs deficient groups, respectively). Conclusion: The results of our study showed that in insulin-resistant individuals, vitamin D deficiency status is associated with HDL-C dyslipidemia and higher serum inflammatory and endothelial damage markers.

Introduction: Previous studies have suggested the involvement of chronic low‐grade inflammation in the pathogenesis of diabetic neuropathy (DNP). However, none of these studies have examined the levels of monocyte chemoattractant protein-1 (MCP-1) in type 2 diabetes mellitus (T2DM) patients with confirmed diagnosis of neuropathy. Therefore, the present study aims to investigate the levels of MCP-1 along with IL-6, IL-8 and TGF-β in patients with T2DM and confirmed neuropathy and identify correlations, if any, between MCP-1 and other parameters. Methods: A single center cross-sectional clinical study was conducted at University Hospital Sharjah (UHS) and University of Sharjah. One hundred and two patients with T2DM were recruited from diabetes clinics at UHS and were stratified into different groups based on diagnosis of DNP and other parameters. Several analyses were conducted to evaluate and compare the levels of MCP-1, IL-6, IL-8, and TGF-β across these groups of patients and identify correlations, if any, between MCP-1 and other variables. Results: A significant increase was found in the levels of MCP-1 in T2DM patients with DNP compared to the patients without DNP (p=0.002, p-adj=0.007). Further analysis has shown that levels of IL-8 (p=0.008) and TGF-β (p=0.06) were increased and decreased, respectively, in patients with DNP compared to patients without DNP. Moreover, strong correlations were found between MCP-1, IL-8 and TGF-β levels. Conclusion: The key finding of the present study is the significant elevation in levels of MCP-1 in T2DM patients with DNP compared to the patients without DNP and IL-8 and TGF-β were strong predictors of MCP-1 increased levels.

(1) Background: Vitamin D deficiency is a common public health problem in the United Arab Emirates (UAE) and globally, and interestingly, improvements in diabetic neuropathy after taking Vitamin D supplementation for a short time have been reported. Despite living in a country that is sunny all year round, hypovitaminosis D, indicated by an obvious low serum vitamin D level, has been recurrently noted in the UAE, as well as in the surrounding Arabian Gulf countries. This problem is receiving much attention and attracting clinical and academic interest. Therefore, the main objective of the present study is to identify the association, if any, between vitamin D deficiency and the development of diabetic neuropathy in the UAE population with T2DM. (2) Methods: a total of 600 Emirati patients (male and female) with T2DM, aged between 20 and 80, were recruited from University Hospital Sharjah (UHS). The medical records of the patients were reviewed and analyzed. (3) Results: The results of the present study showed that among the 600 patients, 50% were affected with diabetic neuropathy. Vitamin D level in patients with neuropathy were estimated to be around 20 ng/mL (IQR 14–25), and vitamin D levels were significantly higher (33 ng/mL (IQR 20–42)) among patients without neuropathy, with p < 0.001. Another important finding was that patients without neuropathy had a better vitamin D status, with only 19% being deficient and 18% having insufficient vitamin D levels, compared to patients with neuropathy, where 39% were deficient (vitamin D < 20 ng/mL) and 44% had insufficient vitamin D levels (20–30 ng/mL). (4) Conclusion: The findings of the present study show that the prevalence of vitamin D deficiency (low serum 25-hydroxy vitamin D 25-OHD level) is significantly high in diabetic neuropathy in Emirati patients with T2DM.

Background: Breast cancer is the most frequently reported cancer among women in the Middle East and North Africa (MENA) region. However, the available data about women breast cancer from the MENA and particularly from the Northern Emirates region of the United Arab Emirates (UAE) are scarce and inconsistent. Therefore, this study estimated the incidence, patient-specific factors including 25(OH)D levels, and clinicopathological features of breast cancer in women from the Northern Emirates. Methods: We conducted this retrospective case–control study on 1,048 women who were referred to the Sharjah Breast Care Centre at University Hospital Sharjah between March 2016 and July 2018. Multivariate logistic regression was used for the statistical analysis of clinical data. Results: Out of 1048 women with breast-related conditions referred to our canter, 94 (10%) were diagnosed with breast cancer (1 in 11), and approximately 1 in 5 of these women was younger than 40 years. After adjusting for age, body mass index and menopause status, women with serum 25-hydroxyvitamin D [25(OH)D] levels lower than 20 ng/mL were found to be at higher risk of breast cancer (odd ratio, 4.63; 95% CI, 2.61– 8.23). The majority of breast cancer cases had invasive-ductal carcinoma with hormone-positive receptor molecular subtype (78 cases out of 94, 83%). HER2 overexpressing tumor (3+ by immunohistochemistry (IHC) or by fluorescence in situ hybridization (FISH)) was seen more in women younger than 40 years as compared to older women (7 cases out of 19 HER2 expressed tumors, p= 0.007). Conclusion: Our study cohort showed a mean age of diagnosis of breast cancer in women a decade earlier than in the developed countries. Furthermore, women with breast cancer tend to be serum 25(OH)D deficient at diagnosis and to have luminal A tumors.

Background: There is growing evidence that stress and sleep deprivation are involved in development of type 2 diabetes (T2DM). The latter is one of the most challenging health problems in the UAE. Therefore, the present study aimed to investigate the effects of personalized intervention on glycemic and weight control in Emirati patients with T2DM. The intervention involved assessment and modification of stress levels and sleep patterns. Methods: This was a randomized controlled study conducted on 51 Emirati patients with T2DM (age 18–60 years, body-mass index (BMI) ≥25 kg/m²): those in the intervention group who completed the trial numbered 18 and those in the control group who completed the trial numbered 17. Heart-rate variability was used for real-life and long-term assessments of stress, sleep, and recovery. Body weight, BMI, HbA_1c and lipid profile were included in the investigation. The National Clinical Trial identifier number is NCT03644134. Results: Percentage change in body weight was significantly greater (P<0.05) in the intervention group (–3.2±2.9) than the control group (–0.02). Percentage change in the BMI of the intervention group was –4.50±5.9, while the control group exhibited less change in BMI (–0.0003±3.3, P<0.05). In addition, a significant reduction in HbA_1c was observed in the intervention group (–5.3±15.7) and an increase of 9.9±13.1 was observed in the control group (P<0.01). Conclusion: The findings of the present study show that personalized approaches that reduce stress levels, increase recovery levels, and promote healthy sleep habits play an important role in weight management and glycemic control in T2DM.