Search

Introduction: Glucagon-like peptide -1 (GLP-1) is released by intestinal cells to stimulate glucose-dependent insulin release from the pancreas. GLP-1 has been linked to ameliorating obesity and/or diabetic complications as well as controlling reproductive function. Liraglutide is a GLP-1 receptor agonist (GLP-1RA) with 97% homology with GLP-1. The main objective of this study was to investigate the ameliorative role of liraglutide in diabetic-induced reproductive dysfunction in male rats. Methods: Rats were randomly allocated into 3 groups; a control group, a diabetic group, and a liraglutide-treated diabetic group. Results: In the diabetic group, a significant increase in BMI, FBG, HbA1c, HOMA-IR, TC, TAG, LDL, IL6, TNFα, and MDA, as well as decreased serum insulin, HDL, GSH, total testosterone, LH, and FSH, were shown compared to the control group. Furthermore, A significant downregulation in relative hypothalamic gene expression of GLP-1R, PPAR-α, PGC-1α, kiss, kiss1R, leptin, leptin R, GnRH GLP-1R, testicular PGC-1α, PPARα, kiss1, kiss1R, STAR, CYP17A1, HSD17B3, CYP19A, CYP11A1, and Smad7, as well as upregulation in hypothalamic GnIH and testicular TGF- β and Smad2 expression, were noticed compared to the control group. Liraglutide treatment significantly improved such functional and structural reproductive disturbance in diabetic rats. Conclusion: GLP-1RAs ameliorated the deleterious effects of diabetes on reproductive function by targeting GLP-1/leptin/kiss1/GnRH, steroidogenesis, and TGF-ß/Smad pathways. [ABSTRACT FROM AUTHOR]

Introduction and Aim: Increased hepatic iron deposition participate in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Hepcidin is a master iron regulator that decrease iron efflux from hepatocytes and its level in NAFLD is still controversial. 1,25-dihydroxyvitamin D3 (vitamin D3) is a potent regulator of hepcidin and its deficiency was linked with increased severity of NAFLD. Therefore, this study aimed to assess the effect of vitamin D3 on hepatic iron deposition and circulating hepcidin levels in NAFLD model induced in adult male albino rats. Materials and Method: Sixty-four adult male rats average age five months weighing 180-200 g were distributed to eight groups. Group (1): ND (normal diet) fed for 4 weeks, Group (2): ND+VD (normal diet with vitamin D3; injected twice weekly with vitamin D3; 5 g/kg BW) fed for 4 weeks, Group (3): HFD (high-fat diet) fed for 4 weeks, Group (4): HFD+VD (high-fat diet with vitamin D3; injected twice weekly with vitamin D3; 5 g/kg BW) fed for 4 weeks. Group (5): ND (normal diet) fed for 12 weeks, Group (6): ND+VD (normal diet with vitamin D3; injected twice weekly with vitamin D3; 5 g/kg BW) fed for 12 weeks, Group (7): HFD (high-fat diet) fed for 12 weeks, Group (8): HFD+VD (high-fat diet with vitamin D3; injected twice weekly with vitamin D3; 5 g/kg BW) fed for 12 weeks. Body mass index (BMI), abdominal circumference (AC), lipid profile, and serum levels of liver enzymes, hepcidin, IL-6, iron and ferritin, hepatic levels of iron and reactive oxygen species (ROS) were measured in all groups. Histology of hepatic tissues was examined using hematoxylin & eosin, Prussian blue, and Masson's trichrome stains. Results: Vitamin D3 induced significant reduction in BMI, AC, lipid profile parameters (except for high-density lipoprotein HDL which was increased), liver enzymes, hepcidin, IL-6, ferritin, hepatic iron and ROS., Whereas, significant increase in serum iron levels in 4 and 12W-HFD groups was noticed compared to their time-matched HFD groups. Additionally, vitamin D3 abolished the pathological changes associated with HFD in 4-week group and markedly attenuated the changes in 12-week group, and significantly diminished hepatic iron deposition and hepatic fibrosis in these groups in comparison to their time-matched HFD groups. Conclusion: Vitamin D3 protects against HFD-induced NAFLD in adult male albino rats by suppression of hepcidin level and subsequent reduction in hepatic iron deposition that decreased oxidative stress-mediated hepatic injury and fibrosis. [ABSTRACT FROM AUTHOR]

Background: The effect of vigorous exercise on testicular function is poorly understood. This work aims to identify the resveratrol influence on the altered reproductive function induced by forced exercise and to screen the relevant possible mechanisms. Methods: The study comprised control, forced exercise (FE), and resveratrol treatment groups carried out on a total of 24 adult male rats. After 8 weeks of the exercise, the pituitary and testicular hormones, corticosterone, tumor necrosis factor (TNF-α), IL-6, epididymal sperm parameters, testicular oxidant-antioxidant markers, testicular ornithine decarboxylase (ODC) activity, polyamines, testicular histopathology, and immunohistochemistry for apoptotic reactions were all measured. Results: The FE group showed significant reductions in the pituitary and testicular hormones, sperm count, and motility, while corticosterone, TNFα, IL-6 serum levels, and aberrant forms of sperms were significantly increased. Testicular tissue displayed abnormal architecture, apoptotic changes with a significantly increased malondialdehyde level, ODC activity and polyamines, and a reduction in superoxide dismutase activity. In comparison to the FE group, administration of resveratrol significantly improved the gonadal hormones, corticosterone, TNF-α, IL-6 levels, sperm parameters, oxidant-antioxidant system, ODC activity, and polyamines with an enhancement of testicular architecture and apoptosis. Conclusion: Resveratrol was effective in attenuating testicular dysfunction caused by forced swimming exercise in rats. [ABSTRACT FROM AUTHOR]

Background: Omentin-1 an adipokine expressed in visceral fat, endothelium and gut. Its level was found lower in obesity and type II diabetes. It is expressed in placenta and was associated with insulin sensitivity during pregnancy. Methods: Rats were divided into 4 groups; group I: control, group II: sham group (normal pregnant), group III: gestational diabetic group and group IV: omentin-1 treated gestational diabetic group. Blood glucose, insulin HOMA-IR, lipid profile, CRP and osteopontin (OPN) levels were measured and gene expression of PI3K, AKT, GSK-3, NF-κB and OPN Results: In group III, a significant increase in insulin resistance, CRP, OPN, increased mRNA expression of GSK-3, NF-κB, and OPN while PI3K and AKT expression decreased. Omentin-1 treatment in group IV attenuated insulin resistance, increased PI3K and AKT expression but decreased OPN, GSK-3, and NF-κB expression. Conclusion: Omentin-1 administration in gestational diabetic rats improved insulin sensitivity and attenuated inflammatory response through PI3K/AKT/GSK-3 pathway. [ABSTRACT FROM AUTHOR]

Background: Neonatal sepsis is a lethal syndrome that necessitates prompt treatment to avoid disease complications. As a result, biomarkers that may either differentiate sepsis early or predict the outcome of sepsis are essential., Aim: The goal of this research was to find out the clinical weight of using miR181b-5p and miR21-5p expression levels as diagnostic and prognostic new genetic markers for neonatal sepsis., Method: A total of 60 neonates with sepsis and 60 healthy neonates were involved in this study. Laboratory tests include complete blood count (CBC), random blood sugar (RBS), arterial blood gases (ABG), and serum C-reactive protein (CRP). Neonates with sepsis were assessed by the Score for Neonatal Acute Physiology II (SNAP II). The serum fold changes of the target miRNAs were determined using qRT-PCR and the 2 -ΔΔCt equation., Results: The relative serum level of miR181b-5p was [ median (IQR) = 0.2509 (0.0009-4.11)] and for miR21-5p was [median (IQR) = 0.07 (0.007-7.16)] which were significantly downregulated in patients with neonatal sepsis compared to controls ( p  < 0.001 each). There was a strong significant positive correlation between miR181b-5p and miR21-5p with r  = 0.718 and p  < 0.001. MiR181b-5p and miR21-5p were significantly negatively correlated with total leucocytic count (TLC), lymphocytic count, and CRP. While they were both positively correlated to the SNAP II score. Obvious association between higher expressions of target genes and higher SNAP II score groups. After a following-up period, twenty-two (36.7%) neonates died, while 38 (63.3%) of the babies became better and were released from the hospital. We reported that miR-181-5p , miR21-5p , SNAP II score and CRP were significantly higher in non-survivors than survivors. Only miR181b-5p , miR21-5p , and SNAP II were predictive factors of septic mortality., Conclusion: MiR181b-5p and miR21-5p are diagnostic and prognostic biomarkers of neonatal sepsis., Competing Interests: The authors declare that they have no competing interests., (© 2022 The Authors.)