No abstract

No abstract

Background: Obesity induces bone related diseases as a consequence of reduced bone formation and unwarranted bone resorption. Therefore, the possible impact of adipokines on osteogenesis has been considered. Nevertheless, the osteogenic properties of omentin-1 are indistinct and contentious. The objective of the current work was to determine the regulatory effects of omentin-1 on bone turnover, along with exploring the fundamental molecular mechanisms in obese rats. Methods: The present study investigated the effects of intraperitoneal omentin-1 injection (8 μg/kg, once daily, for 14 days) in rats after feeding a high-fat diet for 10 weeks to induce obesity. Metabolic parameters and bone dry and ash weights were measured; serum calcium, phosphorus, alkaline phosphatase, and growth differentiation factor-11 (GDF-11), and femur histopathological changes were analyzed. Additionally, we investigated the effect of omentin-1 treatment on AMP protein-kinase (AMPK), mammalian target rapamycin (mTORC1) and nuclear receptor peroxisome proliferator-activated receptor-γ (PPAR-γ) expression. Results: The results revealed significant improvement in metabolic, bone biochemical parameters and histopathological changes in the omentin-1 treated group with a significant increase in area % of bone. A significant down-regulation of mTORC1 was identified through AMPK/mTORC1/PPAR-γ pathway accompanied by an increase in serum GDF-11.Conclusions: Omentin-1 can significantly promote bone health and viability via down-regulation of the AMPK/mTORC1/PPAR-γ signaling pathway and up-regulation of serum GDF-11, thus it can promote bone formation and prevent osteoporosis.

Sleep deprivation (SD) during pregnancy can impact the delivery procedure, with prolongation of the labor duration. Matrix metalloproteinase-9 (MMP9) and transforming growth factor-β (TGF-β) are regulators of uterine remodeling. Their dysregulation is vital for abnormal placentation and uterine enlargement in complicated pregnancies. Therefore, this study aims to explore the outcome of SD throughout pregnancy on ex vivo uterine contractility, MMP9 and TGF-β, and uterine microscopic structure. A total of 24 pregnant rats were divided into two groups. From the first day of pregnancy, animals were exposed to partial SD/6 h/day. Uterine in vitro contractile responses to oxytocin, acetylcholine, and nifedipine were assessed. Additionally, uterine levels of superoxide dismutase and malondialdehyde and uterine mRNA expression of MMP9, TGF-β, and apoptotic biomarkers were analyzed. The results showed that SD significantly reduced uterine contractile responses to oxytocin and acetylcholine, while it augmented the relaxing effect of nifedipine. In addition, it significantly increased oxidative stress status, MMP9, TGF-β, and apoptotic biomarkers mRNA expression. All were accompanied by degeneration of endometrial glands, vacuolization with apoptotic nuclei, and increased area % of collagen fibers. Finally, increased uterine MMP9 and TGF-β mRNA expression during SD clarified their potential role in modulating uterine contractility and structure.

The Dexamethasone Suppression Test in Depressed Kuwaiti Patients SIR: We read with interest the multicentre WHO collaborative study of the response to the dexameth asone suppression test (DST) (Journal, April 1987, 150, 459-462). The only Arab centre involved in this study was in Casablanca, Morocco (12 patients). In Kuwait, we recently carried out a similar study on 19 Kuwaiti depressed in-patients (I 1 males and 8 females; mean age = 34.3 ± 2.2 years) and 23 healthy controls.