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Objective: We aimed to study Endothelial dysfunction and Arterial Stiffness in Diabetes mellitus. Methods: 29 women with type 2 diabetes and 8 non-diabetic controls were included. Vascular function was studied with pOpmetre® (Axelife SAS-France) to assess the foot to toe Pulse Wave Velocity; and EndoPAT2000® (ITAMAR-Israel) to measure endothelial vasodilatation dependent by measurement of reactive hyperhemic index (RHI). Results: Diabetics were 56 ± 6 years vs 47 ± 9 years. Mean diabetes duration was 9.07 ± 6.15 years. RHI was normal in all controls (1.94 ± 0.68) and abnormal in 51.72% of diabetics (1.83 ± 0.12). An abnormal ftPWV was found in 38% of diabetic subjects (11.6 ± 7.7 m/s) vs 12% of controls (7.7 ± 2.3 m/s, normal

Background: Hydro-electrolyte balance is necessary to maintain body homeostasis and blood pressure values within narrow limits. This is accomplished, in part, by renal responses. We conducted this study to determine the effects of Combretum micranthum on hydro-electrolyte metabolism, renal function and arterial blood pressure. Subjects and methods: We conducted a pilot study including 40 subjects: 10 control subjects, 10 subjects under Combretum micranthum G. Don (400 mg/day), 10 subjects under furosemide (120 mg/day), and 10 subjects under spironolactone (50 mg/day).Anthropobiometric, cardiovascular parameters and the body composition were collected from each subject. Blood and 24-hour urine samples were collected for biological tests. Results: At baseline, clinical and biological parameters were comparable for all groups. Consumers of combretum micranthum had a significant decrease in global body fat percentage (−1.63 %; p = 0.045). In the group of combretum micranthum consumers, the body water mass (BWM) is significantly evolved in the direction of an increase (4.37; p = 0.023) and similar to what was observed in the group of subjects treated with spironolactone (0.67; p = 0.042). Consumption of combretum micranthum showed a marked reduction in hypertension indices (systolic blood pressure, diastolic blood pressure and heart rate) identical to that induced by consumption of furosemide or spironolactone. The consumption of combretum micranthum resulted in a significant reduction in kaliemia (−1.07; p

Abstract Background Obesity and related metabolic disorders are associated with genetic and epigenetic alterations. In this study, we have examined the association between polymorphisms and hypermethylation of the CD36 gene promoter with obesity in Senegalese females with or without type 2 diabetes mellitus to identify novel molecular markers of these pathologies (obesity and type 2 diabetes mellitus). Materials and methods The study was conducted in Senegal with healthy lean control, obese, and obese diabetic (age; 49.98 years ± 7.52 vs 50.50 years ± 8.76 vs 51.06 ± 5.78, and body mass index (BMI); 24.19 kg/m2 ± 2.74 vs 34.30 kg/m2 ± 4.41 vs 33.09 kg/m2 ± 4.30). We determined three genetic polymorphisms of CD36 i.e., rs1761667, rs1527483, and rs3211867 by real-time polymerase chain reaction, and methylation of CPG islands of CD36 was assessed by methylation-specific polymerase chain reaction (MS-PCR) in DNA isolated from peripheral blood of each participant. Plasma sCD36 levels and DNA methyltransferase 3a (DNMT3a) levels were determined by enzyme-linked immunosorbent assay (ELISA). According to the standard laboratory protocol, all biochemical parameters were analyzed from fasting serum or plasma. Results For rs1761667, obese and obese diabetic subjects had statistically significant different parameters depending on the genotypic distribution. These were waist size for obese and HDL cholesterol for obese diabetic, they were significantly higher in subjects harboring GG genotype of rs1761667 (respectively p = 0.04 and p = 0.04). For rs3211867, obese subjects harboring the AA/AC genotype had significantly higher BMI (p = 0.02) and total cholesterol (p = 0.03) than obese subjects harboring the CC genotype. At the same time, the obese diabetic subjects harboring the AA/AC genotype had total cholesterol levels significantly higher than the obese diabetic subjects harboring the CC genotype (p = 0.03). For rs1527483, only the control subjects had statistically significant different parameters depending on the genotypic distribution. The control subjects harboring the GG genotype had a significantly higher BMI than the control subjects harboring the AA/AG genotype (p = 0.003). The CD36 gene methylation was significantly 1.36 times more frequent in obese and obese diabetic compared to lean control (RR = 1.36; p = 0.04). DNMT3a levels were higher in subjects with CD36 gene methylation than in subjects without CD36 gene methylation in each group. Obese diabetic subjects with CD36 gene methylation had significantly fewer plasmas sCD36 (p = 0.03) and more LDL-cholesterol (p = 0.01) than obese diabetic subjects without CD36 gene methylation. In the control group, an increase in sCD36 levels would be associated with a decrease in total cholesterol and triglyceride levels (coef = -7647.56 p = 0.01 and coef = -2528.50 p = 0.048, respectively) would be associated with an increase in LDL cholesterol levels. For the obese group, an increase in sCD36 levels would be associated with an increase in fasting insulin levels (coef = 490.99 p = 0.02) and a decrease in glycated hemoglobin levels (coef = -1196.26 p = 0.03). An increase in the sCD36 levels would be associated with an increase in the triglyceride levels in the obese diabetic group (coef = 9937.41 p = 0.02). The AA/AC genotype of SNP rs3211867 polymorphism was significantly associated with CD36 gene methylation in the control and obese diabetic groups (respectively p = 0.05, p = 0.002; 95% CI). Conclusion These observations suggest that polymorphisms and epigenetic changes in CD36 gene promoters may be implicated in the onset of obesity and its related complication type 2 diabetes mellitus.

Abstract Background Several predisposing factors for diabetes mellitus have been identified, including cluster determinant 36 (CD36) receptor expression. We aimed to determine the effects of CD36 gene polymorphisms and hypermethylation on the plasma CD36 protein levels in type 2 diabetes. Materials and methods We conducted a cross-sectional study involving 100 females (lean healthy control subjects and subjects with type 2 diabetes). This study was conducted at the Human Physiology Laboratory at the Dakar Faculty of Medicine in Senegal. Circulating sCD36 levels and DNA methyltransferase 3a levels were determined by enzyme-linked immunosorbent assay. The other biological parameters were evaluated in a biochemical laboratory. CD36 gene polymorphisms and methylation were explored by real-time polymerase chain reaction and methylation-specific polymerase chain reaction, respectively. Results sCD36 was negatively correlated with HDL-cholesterol levels (r = − 0.52 p = 0.0001) and triglyceride levels (r = − 0.36 p = 0.01) in control subjects. However, in the type 2 diabetes group, sCD36 levels were positively correlated with total cholesterol levels (r = 0.28 p = 0.04). For rs3211867, control subjects harboring the CC genotypes had significantly higher sCD36 levels than control subjects harboring the AA/AC genotype (p = 0.02); in the type 2 diabetes group, the sCD36 level was not significantly lower in subjects harboring the AA/AC genotype than in subjects harboring the CC genotype (p = 0.27). CD36 gene methylation reduced the sCD36 level in the control subjects compared to control subjects without CD36 gene methylation (p = 0.03). This difference was not significant in the type 2 diabetes group comparing subjects with diabetes with CD36 gene methylation to subjects with diabetes without CD36 gene methylation (p = 0.09). We noted a nonsignificant increase in sCD36 levels in subjects with diabetes with CD36 gene methylation compared to control subjects with CD36 gene methylation (p = 0.27). A combination of the CD36 polymorphism effect and the CD36 methylation effect did not significantly reduce sCD36 levels in subjects with type 2 diabetes. Conclusion CD36 gene polymorphisms and CD36 gene methylation separately reduce sCD36 levels. Their impacts are compensated for in subjects with type 2 diabetes by an increase in sCD36 levels, the mechanism of which needs to be elucidated.

Rosai-Dorfmann disease manifests on the skin commonly as papules, nodules or rarely as infiltrated plaques. Authors report the case of a 27 year-old-man, presenting diffuse, budding and pediculated tumoral skin lesions associated with superficial and deep lymphadenaopathies and fever. The histopathological examination showed caracteristic features of emperipolesis. The Rosaï-Dorfman disease is remarkable in our case by its tumoral and profus presentation, as well as its pseudo-xanthomatous aspect. RÉSUMÉ Les lésions cutanées de la maladie de Rosai-Dorfman sont le plus souvent à type de papules, nodules ou plus rarement de plaques infiltrées. Les auteurs rapportent l’observation d’un homme de 27 ans, présentant des lésions tumorales cutanées bourgeonnantes, pédiculées, diffuses, associées à des polyadénopathies superficielles et profondes fébriles, avec des images caractéristiques d’empéripolèse à l’histologie. La maladie de Rosaï-Dorfman est remarquable dans notre observation par sa présentation cutanée tumorale et profuse, ainsi que l’aspect pseudo-xanthomateux.

Background: The purpose of this study was to assess the arterial stiffness (AS) in black africans patients with systemic scleroderma. Patients and Methodology: A prospective cross-sectional hospital survey has been performed over a 6-month period, including 55 black african individuals, aged over 16 years and consenting, consisting of 29 patients with systemic scleroderma and 26 hospitalized controls. The finger-toe pulse wave velocity (ft-PWV) was recorded by popmetre® and comparaison between the 2 groups has been performed with statistical analysis. Results: The mean ft-PWV was 9,56 m/s ± 3,09 in the patient group and 7,71 m/s ± 2,63 in control group. The ft-PWV was significantly higher in patients with scleroderma compared to controls (p