ABSTRACT
This study aimed to investigate the effect of cerium oxide nanoparticles (CeO2-NPs) on non-alcoholic fatty liver disease in postmenopausal obesity and the underlying mechanisms.64 adult female rats were allocated into Sham, ovariectomized (OVX), high-fat high-fructose dietfed- OVX (HFHF-OVX), and HFHF-OVX-CeO2-NPs-treated (CeO2-HFHF-OVX) groups. OVX and HFHF-OVX rats presented a significant increase in overall and visceral obesity, dyslipidemia, liver enzymes, serum malondialdehyde, liver TNF-α, TGF-ß1 and free fatty acids, liver X receptor (LXR) expression associated with decreased serum total antioxidant capacity and liver short heterodimer partner (SHP) expression vs. Sham group. Also, histomorphometric studies displayed a significant higher scores of liver steatosis, inflammation and fibrosis. All these parameters were significantly improved by CeO2-NPs treatment in CeO2-HFHF-OVX vs. HFHF-OVX rats. Thus, CeO2-NPs treatment ameliorates liver steatosis, steatohepatitis, and fibrosis in postmenopausal obese rats via alleviation of obesity, dyslipidemia, modulating liver genes involved in lipid metabolism (LXR and SHP), decreasing liver lipogenesis besides its antioxidant and anti-inflammatory effects.
Subject(s)
Dyslipidemias , Nanoparticles , Non-alcoholic Fatty Liver Disease , Animals , Female , Humans , Rats , Anti-Inflammatory Agents , Antioxidants/metabolism , Cerium , Dyslipidemias/complications , Dyslipidemias/metabolism , Dyslipidemias/pathology , Fatty Acids, Nonesterified/metabolism , Fibrosis , Fructose/metabolism , Liver/metabolism , Liver X Receptors/metabolism , Malondialdehyde/metabolism , Non-alcoholic Fatty Liver Disease/complications , Non-alcoholic Fatty Liver Disease/drug therapy , Non-alcoholic Fatty Liver Disease/metabolism , Obesity/complications , Obesity/drug therapy , Obesity/metabolism , Ovariectomy , Postmenopause , Transforming Growth Factor beta1/metabolism , Tumor Necrosis Factor-alpha/metabolismABSTRACT
This study was conducted to evaluate gastric acid secretion in acute renal failure, highlighting the roles of renal mass and gastrin hormone. Acute uremic rats were divided into bilateral nephrectomized and bilateral ureteric obstruction groups. Gastric juice was collected for 2 h and analyzed for volume, free acidity, total acidity, and total acid output. Plasma levels of creatinine, urea, and gastrin were also determined. Bilateral nephrectomized and bilateral ureteric obstruction groups showed a significant increase in levels of free acidity, total acidity, and plasma gastrin. Compared with the ureteric obstruction group, nephrectomized rats showed a significant increase in gastric juice volume, total acid output, and plasma gastrin levels. Following pentagastrin stimulation, gastric juice volume, total acid output, free acidity, and total acidity were increased in the bilateral nephrectomy and ureteric obstruction groups compared with the respective control groups. The free and total acidity and total acid output also increased compared with the respective non-stimulated groups. Plasma creatinine and urea levels were significantly positively correlated with plasma gastrin, free acidity, and total acidity. Creatinine was positively correlated with total acid output, and gastrin was positively correlated with total acidity. In conclusion, acute renal failure promotes gastric acid hypersecretion that could potentially be attributed to high levels of gastrin hormone and uremic state per se.
