Vitamin D deficiency might contribute to the pathogenesis of metabolic syndrome and could cause immune disturbance. The aim of this study is to analyze the associations between Vitamin D receptor (VDR) gene polymorphism, serum 25-hydroxy vitamin D, metabolic and inflammatory biomarkers in Egyptian obese women. The study included 201 obese women with vitamin D deficiency and 249 obese matched age healthy controls with sufficient vitamin D levels. Their age ranged between 25 and 35 years. Inflammatory biomarkers (interleukin-6 and C-reactive protein) and serum 25(OH) D were measured by enzyme-linked immunosorbent assay. Insulin resistance (IR) was determined by the homeostasis model assessment of insulin resistance (HOMA-IR).Vitamin D receptor (VDR) gene polymorphisms of FokI, ApaI, and TaqI were studied by PCR using the restriction fragment length polymorphism (RFLP) technique. Obese women with vitamin D deficiency had significant higher values of inflammatory and metabolic parameters compared to controls. Multivariable-logistic regression showed associations between 25(OH) D deficiency and metabolic components when comparing cases with controls. Moreover, cases carrying polymorphic alleles showed significant lower levels of serum 25(OH) D and higher HOMA-IR, blood pressure levels and lipid parameters compared to those with the wild type homozygote in obese cases with vitamin D deficiency. Vitamin D deficiency in Egyptian obese women with vitamin D deficiency is associated with abnormal metabolic components and abnormal inflammatory biomarkers. Moreover, VDR polymorphisms play important role in immune and inflammation status.

The MafB transcription factor is expressed in pancreatic α and β cells during development but becomes exclusive to α cells in adult rodents. -null ( ) mice were reported to have reduced α- and β-cell numbers throughout embryonic development. To further analyze the postnatal function of MafB in the pancreas, we generated endocrine cell-specific ( ) and tamoxifen-dependent ( ) knockout mice. mice exhibited reduced populations of insulin-positive (insulin) and glucagon cells at postnatal day 0, but the insulin cell population recovered by 8 weeks of age. In contrast, the Arx glucagon cell fraction and glucagon expression remained decreased even in adulthood. mice, with deleted after pancreas maturation, also demonstrated diminished glucagon cells and glucagon content without affecting β cells. A decreased Arx glucagon cell population in mice was compensated for by an increased Arx pancreatic polypeptide cell population. Furthermore, gene expression analyses from both and islets revealed that MafB is a key regulator of glucagon expression in α cells. Finally, both mutants failed to respond to arginine, likely due to impaired arginine transporter gene expression and glucagon production ability. Taken together, our findings reveal that MafB is critical for the functional maintenance of mouse α cells , including glucagon production and secretion, as well as in development.

Nerium oleander ( N. oleander ) is a well-known poisonous shrub that is frequently grown in gardens and public areas and contains numerous toxic compounds. The major toxic components are the cardiac glycosides oleandrin and neriin. The aim of our study was to evaluate the toxic effects of an ethanolic N. oleander leaf extract on haematological, cardiac, inflammatory, and serum biochemical parameters, as well as histopathological changes in the heart. N. oleander extract was orally administered for 14 and 30 consecutive days at doses of 100 and 200 mg of dried extract/kg of body weight in 0.5 mL of saline. The results showed significant increases in mean corpuscular volume, white blood cell counts, platelet counts, interleukins (IL-1 and IL-6), tumour necrosis factor alpha, C reactive protein, alanine aminotransferase, lactate dehydrogenase, creatine kinase and creatine kinase MB, especially at high doses. Marked pathological changes were perceived in the heart tissue. Thus, it can be concluded that exposure to N. oleander leaf extract adversely affects the heart and liver.

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Metabolic syndrome (MS) is a cluster of metabolic abnormalities. Obesity and MS are always accompanied by elevated oxidative stress which might affect cellular bio-molecules such as DNA. The aim of the present study is to investigate DNA damage profile in obese premenopausal women and its relation to the risk of MS, polycystic ovary syndrome (PCOS) and history of recurrent pre-eclampsia. The study included 90 obese women included cases with MS (n = 30), PCOS (n = 30) and previous history of recurrent preeclampsia (n = 30) and, age-matched healthy non-obese control women (n = 50). The assessment of leukocyte DNA damage was done by comet assay for all cases and controls. Anthropometry and biochemical parameters have been measured. Results showed that mean percent of DNA damage was significantly higher in MS, PCOS as well as in women with the recurrent preeclampsia as compared to healthy controls. The high level of mean DNA damage frequency in obese women was significantly associated with the increased number of metabolic syndrome components. Cases with 2, 3 and 3–5 components showed significantly higher levels of DNA damage than controls. Moreover, cases with 3–5 MS components showed significant higher DNA compared to those with the two components. Regarding PCOS, significant positive association between the mean frequency of DNA damage and waist circumference was observed. The study suggests that metabolic abnormalities, PCOS and recurrent pre-eclampsia might be contributed in development of DNA damage in obese women. DNA damage can serve as an early marker for obesity complications in premenopausal women.