Association of lipid profile and waist circumference as cardiovascular risk factors for overweight and obesity among school children in Qatar

Background: Childhood obesity is a national as well as worldwide problem. The aim of this study was to evaluate the association of overweight and obesity among Qatari children with lipid profile and waist circumference as adverse cardiovascular risk factors in children aged 6-11 years. International Obesity Task Force reference values were used to screen for overweight and obesity. Methods: A cross-sectional study in a randomly selected sample was conducted in 315 Qatari primary school students aged 6-11 years. Anthropometric measurements, including body weight, height, waist circumference, and body mass index were calculated for 151 girls and 164 boys. Weight categories were based on International Obesity Task Force reference values. Fasting blood glucose, total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides were measured, and atherogenic index was calculated. Results: In total, 31.71% of boys and 32.78% of girls were overweight or obese. Overweight and obese children screened against International Obesity Task Force reference values had a significantly increased risk of high waist circumference (P < 0.0001), hypertriglyceridemia (P = 0.002), low HDL-C (P = 0.017), and atherogenic index (P = 0.021) compared with children who were not overweight or obese. The partial correlation coefficient for the cardiovascular risk marker of waist circumference indicated a positive significant association with total cholesterol (r = 0.465, P = 0.003), triglycerides (r = 0.563, P < 0.001), and LDL-C (r = 0.267, P = 0.003), and a significant negative association with HDL-C (r = -0.361, P = 0.004). Overweight and obesity significantly increase the odds ratios (ORs) and 95% confidence interval (CIs) of cardiovascular risk factors as follows: Hypertriglyceridemia (OR 6.34, CI 2.49-13.44, P < 0.0001); LDL-C (OR 3.18, CI 1.0419.75, P = 0.043); hypercholesterolemia (OR 1.88, CI 1.10-3.19, P = 0.020); and increased waist circumference (OR 1.40, CI 1.29-1.55, P = 0.022). Overweight and obesity significantly increased the risk of atherosclerosis (assessed by atherogenic index) by about two-fold (OR 1.83, 95% CI 1.06-3.15, P = 0.025). Conclusion: Overweight and obese children screened by International Obesity Task Force reference values are at increased risk of cardiovascular disease in adulthood

The Relationship Between Leptin and PCOS

Background: The ob gene produces a leptin hormone that works as a satiety signal to the hypothalamus. Leptin may have a role in polycystic ovary syndrome (PCOS) via its role on obesity and insulin resistance. Materials and Methods: A prospective, retrospectives cross- sectional study included 78 females student aged 17-25 years. The retrospective data included clinical, anthropometric and hormonal profile of each subject. Leptin concentration was measured by enzyme absorbent by BioVendor Human Leptin ELISA. Statistical analysis was performed by IBM SPSS Statistics 21.0 for Windows XP (IBM, USA). Results: leptin found to be significantly higher in those women with PCOS than in women without PCOS (p-value 0.037). Also, Overweight/Obese subjects had higher leptin level (22.85 ng/ml) than non-overweight/non-obese subjects (8.82 ng/ml) with (p-value <0.05). OW/Ob group showed higher frequency of family history of PCOS and diabetes, irregular menstrual cycle (IP) and high Ferriman-Gallwey score. Leptin is significantly correlated with insulin, testosterone, BMI, DHEAS, progesterone, FAI and PCOS. Conclusion: PCOS, overweight and obese subjects exhibit high leptin level

Elevated serum leptin levels in patients with acute myocardial infarction; correlation with coronary angiographic and echocardiographic findings

BACKGROUND: To assess the relationship between serial serum leptin levels in patients with acute myocardial infarction (AMI) who received thrombolysis and the degree of coronary atherosclerosis, coronary reperfusion, echocardiographic findings, and clinical outcome. 51 consecutive patients presenting with AMI were studied. Clinical characteristics including age, sex, body mass index (BMI) and cardiovascular risk factors were recorded. Serial serum leptin levels at the time of admission and subsequently at 0, 6, 12, 24, 36, 60 hours afterwards were obtained. Coronary angiography was performed in 34 patients; the relation between serum leptin levels and evidence of coronary reperfusion as well as the extent of coronary atherosclerosis according to the coronary artery surgery study classification (CASS) were evaluated. Echocardiographic evaluation was performed in all patients. 36 matched patients were enrolled as control group who had serum leptin level 9.4 ± 6.5 ng/ml. RESULTS: The patients mean age was 50.5 ± 10.6 years. There were 47 males and 3 females. 37.1% were diabetics, 23.5% were hypertensive, 21.6% were dyslipidemic and 22.7% were obese (BMI ≥ 30). Leptin concentrations (ng/ml) increased and peaked at the 4th sample (36 hrs) after admission (mean ± SD) sample (1) =9.55 ± 7.4, sample (2) =12.9 ± 8.4, sample (3) =13.8 ± 10.4, sample (4) =18.9 ± 18.1, sample (5) =11.4 ± 6.5, sample (6) =10.8 ± 8.9 ng/ml. There was a significant correlation between serum leptin and BMI (r = 0.342; p = 0.03). Leptin levels correlated significantly to creatine kinase level on the second day (r = 0.43, p ≤ 0.01). Significant correlation of mean serum leptin with the ejection fraction (P < 0.05) was found. No difference in timing of peak serum leptin between patients who achieved coronary reperfusion vs. those who did not (p = 0.8). There was a trend for an increase in the mean serum leptin levels with increasing number of diseased vessels. There was no correlation between serum leptin levels and outcome neither during the hospitalization nor at 9 months follow up. CONCLUSION: Serum leptin levels increase after myocardial infarction. Serum leptin level may be a predictor of the left ventricular ejection fraction and the degree of atherosclerosis but not of coronary reperfusion

The Role of Systemic Filtrating Organs in Aging and Their Potential in Rejuvenation Strategies

Advances in aging studies brought about by heterochronic parabiosis suggest that aging might be a reversable process that is affected by changes in the systemic milieu of organs and cells. Given the broadness of such a systemic approach, research to date has mainly questioned the involvement of “shared organs” versus “circulating factors”. However, in the absence of a clear understanding of the chronological development of aging and a unified platform to evaluate the successes claimed by specific rejuvenation methods, current literature on this topic remains scattered. Herein, aging is assessed from an engineering standpoint to isolate possible aging potentiators via a juxtaposition between biological and mechanical systems. Such a simplification provides a general framework for future research in the field and examines the involvement of various factors in aging. Based on this simplified overview, the kidney as a filtration organ is clearly implicated, for the first time, with the aging phenomenon, necessitating a re-evaluation of current rejuvenation studies to untangle the extent of its involvement and its possible role as a potentiator in aging. Based on these findings, the review concludes with potential translatable and long-term therapeutics for aging while offering a critical view of rejuvenation methods proposed to date

Association between Insulin and Nitric Oxide in Human Retinal Microvascular Endothelial Cells in vitro

Obesity and type 2 diabetes is characterized by insulin resistance which has been reported as the major risk factors associated with the development of the endothelial dysfunction and vascular complications such as atherosclerosis. Induction of the vascular dysfunction is obviously a proved metabolic consequence of insulin resistance. Diabetes leads to altered retinal microvascular function and ultimately diabetic retinopathy. Insulin signaling may play a role in this process, and animal studies indicated a role of the insulin in the pathogenesis of retinal neovascularization through its effect on endothelial cells. Endothelial dysfunction impairs ocular hemodynamics by reducing the bioavailability of NO and increasing the production of reactive oxygen species (ROS) and may be responsible for the pathogenesis of vascular dysfunction in retinopathy. Diabetic retinopathy (DR) a major consequence of diabetes is considered the leading cause of vision loss and blindness worldwide among working adults. Endothelial dysfunction expediting imbalance in vascular homeostasis, is one of the primary manifestation leading to the pathogenesis of DR. NO a major vasodilator involved in the regulation of vascular homeostasis is reported to be released by insulin dependent PI3K/Akt signaling pathway. Endothelial dysfunction impairs ocular hemodynamics by reducing the bioavailability of NO and increasing the production of reactive oxygen species (ROS) and may be responsible for the pathogenesis of vascular dysfunction in retinopathy. Insulin stimulated NO productions are reported to be well established in cardiovascular and macrovascular endothelium and its association with PI3K/Akt pathway. Contrary to this insulin signaling in retinal endothelium have minimal reports with some studies suggesting it to be an important physiology player in hyperglycemia or insulin resistance induced DR. This prompted us to investigate the association between hyperglycemia and insulin mediated PI3K/Akt pathway eNOS directed NO production and associated multivariate effect on HRMECs survival, proliferation, angiogenesis, adhesion, apoptotic and inflammatory markers. The aim of this study is to examine the examine the effect of insulin on NO production in human retinal microvascular endothelial cells cultured in hyperglcemic conditions. In the current study in order to examine the effect of insulin on NO production, HRECs cells were cultured and grown in high glucose (30 mM) and normal (5 mM) glucose for 24 hours. Subsequently, the cells were treated with 100 nM insulin for 10 minutes, 1, 2, and 4 hours. The various parameters of PI3K/Akt signaling pathway were analyzed. IRS-1, IRS-2, PI3K, Akt, eNOS, VEFGA, NFkB were analyzed for gene expression. Adhesion molecules such as P-selectin and ICAM-1 were assessed by flow cytometry. ROS and NO production were measured by immunofluorescence and fluorometry respectively. The cell viability, cell cycle, apoptosis and total oxidative stress were evaluated by imaging flowcytometery. This study demonstrated that hyperglycemia causes an increase in ROS/oxidative stress and apoptosis, while insulin promotes a significant decrease in ROS and apoptosis. eNOS mediated NO production increases with hyperglycemia but remarkably decreases with insulin treatment after 1 hour, 2 hours and 4 hours. This dissimilarity of the results to previously reported studies could be due to different endothelial cell types used or varied duration of experimental hyperglycemia. The most significant reason for the variation may be due to different method of NO measurement where, most previous studies measured NO production by isolated NO meters. However, in the current study fluorometry a more sensititve method to measure oxidized product of NO, nitrite an indicator direct NO production was utilized and confirmed by the immunoflouresence technique using the dye DAF-FM Diacetate. The assessment of PI3K/Akt pathway gene expression revealed that this study demonstrates a slight increase but insignificant elevation of IRS-1 and IRS-2 genes expression in hyperglycemic condition compared to the basal control condition, while gene expression of PI3K, Akt and eNOS were significantly upregulated in the presence of high glucose. Insulin treatment caused an up regulation of IRS-1 and IRS-2 genes after 1 hour however, PI3K, Akt and eNOS were significantly reduced. The analysis of angiogenic and proapoptotic markers VEGFA and NFkB by RT-PCR showed no significant change in the expression of NFkB in hyperglycemic alone, hyperglycemic and normoglycemic cells with insulin treatment at all-time points. However, hyperglycemia significantly increased the expression of VEGF. Though compared to basal control group insulin treatment significantly increased the expression of VEGFA in both hyperglycemic and normoglycemic cells yet the expression was low compared to HG state. Consistent with the VEGFA gene expression HG significantly increased the increase the cell migration and angiogenesis while insulin treatment significantly improves barrier function. Hyperglycemia significantly increased adhesion protein P-selectin with significant reduction at 4hrs insulin treatment in the current study. This study demonstrated a significant reduction in P-selectin after insulin suggesting that insulin could participate in preventing leukocyte adhesion thereby attenuating the progression of DR. This study could not demonstrate significance change in the ICAM-1 protein. This could be due to difference in the endothelial cells used, the duration and the type of insulin treatment used. This study reported that short acting insulin commonly used in the treatment of DR could control the metabolic fluxes thereby leading to improvement in oxidative stress and apoptosis. This could prevent early changes in vasodilator, adhesion and angiogenic markers such as NO, VEGFA, P-selectin involved in the angiogenesis, inflammation and neovascularization involved in retinal vascular functioning. The study shows the potent effect of short-acting insulin treatment to counteract these biomarkers and factors involved in the pathogenesis of DR and conserving microvascular function in HRMECs exposed to hyperglycemia (30 mM) and were reported to be improved. Thus, the diabetic interventions using insulin as a key therapy with others may have the potential to be utilized as a readily available, safe and inexpensive medicine to protect against microvascular complications of DR and delay its onset. In conclusion, this study demonstrated that Hyperglycemia causes an increase in ROS/oxidative stress and apoptosis, while insulin promotes a significant decrease in ROS and apoptosis, eNOS mediated NO production increases with hyperglycemia but remarkably decreases with insulin treatment after 1 hour, 2 hours and 4 hours, insulin could counteract the hyperglycemic effect on AKT/pI3 kinase which mediates NO production and VEGF-A, decreased adhesion molecules p-selectin involved in barrier disorder of retinal endothelial cells. Thus it could be proposed that insulin could be considered as regulators of angiogenesis.qscienc