ACTA ENDOCRINOLOGICA (BUC)

Context. Nesfatin-1 is a novel peptide with both central and peripheral anorexigenic regulatory properties. Besides its effects on food intake, few studies have suggested a possible role for this peptide in the pathogenesis of diabetes mellitus type 2. Objective. To compare serum levels of nesfatin-1 between healthy, normal-weight persons and three groups including healthy underweight, healthy obese and diabetic subjects. Design. Prospective, case-control study, performed between January 2015 and January 2016. Subjects and Methods. Fasting levels in serum nesfatin-1 were measured in 30 healthy, normal-weight individuals (controls), 30 healthy underweight persons, 30 healthy obese persons, and 30 patients with newly diagnosed diabetes type 2 using standard enzyme-linked immunosorbent assay (ELISA) kits. Results. The mean serum nesfatin-1 level was significantly higher in controls (2.61 ng/mL) compared to that in obese (1.13 ng/mL) and diabetic (0.99 ng/mL) patients; and significantly lower than that in the underweight group (3.50 ng/mL). The obese and diabetic groups were comparable in this regard. No significant association was found between serum nesfatin-1 level and age, sex, or body mass index. Conclusions. Serum nesfatin-1 is possibly associated with weight-related abnormalities in otherwise healthy subjects and diabetes type 2. Obesity and diabetes type 2 may share a common pathologic point in this regard.

Aim. The epidemic of metabolic syndrome increases worldwide and correlates with elevation in serum uric acid and marked increase in total fructose intake. Fructose raises uric acid and the latter inhibits nitric oxide bioavailability. We\r\nhypothesized that fructose-induced hyperuricemia may have a pathogenic role in metabolic syndrome and treatment of\r\nhyperuricemia or increased nitric oxide may improve it.\r\nMethods. Two experiments were performed. Male Sprague-Dawley rats were fed a control diet or a high fructose diet to\r\ninduce metabolic syndrome. The latter received either sodium nitrate or allopurinol for 10 weeks starting with the 1st day of fructose to evaluate the preventive role of the drugs or after 4 weeks to evaluate their therapeutic role.\r\nResults. A high-fructose diet was associated with hyperuricemia, hypertension, dyslipidemia, insulin resistance, decreased tissue nitrite and increased adiposity index. Sodium nitrate or allopurinol was able to reverse these features in the preventive study better than the therapeutic study.\r\nConclusion. Fructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid. Either sodium nitrate or allopurinol can\r\nprevent this pathological condition by different mechanisms of action.

Context. The grey mullet, Mugil cephalus, is an edible fish of high economic importance. Breeding biology with reference to hormonal/growth factor regulation of oocyte maturation needs to be known for its commercial production. Objective. The present study was conducted to examine the potency of maturation inducing hormones, chorionic gonadotropin (hCG), bovine-insulin, and insulin like growth factor1 (h-IGF-1) I on ovarian steroidogenesis and oocyte maturation. Design. The role of hormones and growth factors on steroidogenesis and oocyte maturation was investigated using specific inhibitors, Wortmannin for phosphatidylinositol-3 (PI3) kinase, trilostane for 3β-hydroxysteroid dehydrogenase, 1-octanol and 1-heptanol for gap junctions, actinomycin D for transcription and cycloheximide for translation of signal molecules. Methods. Actions of hormonal and growth factors were examined for steroidogenesis, by radioimmunoassay and oocyte maturation by germinal vesicle breakdown (GVBD). Specific inhibitors were used to determine the cell signaling pathways, PI3 kinase. Results. All the inhibitors attenuated the hCGinduced oocyte maturation (GVBD%), steroidogenesis including transcription, translation, gap junctions and PI3 kinase signaling. These inhibitors failed to inhibit h-IGF-I and b-insulin-induced oocyte maturation, steroidogenesis, translation and PI3 kinase signaling. Conclusion. hCG induces oocyte maturation via steroid dependent pathway involving gap junctions, transcription, translation and PI3 kinase signaling, unlike h-IGF-I and b-insulin in the mullet.