Cerium oxide nanoparticles modulate liver X receptor and short heterodimer partner, and attenuate liver steatosis and steatohepatitis in a rat model of postmenopausal obesity.

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.

Cardioprotective effect of vitamin D2 on isoproterenol-induced myocardial infarction in diabetic rats.

OBJECTIVES: To assess the effect of vitamin D2 and to elucidate the underlying mechanisms on acute myocardial injury induced by isoproterenol (ISO) in diabetic rats. METHODS: Rats were divided into control rats, diabetic rats (DM), diabetic rats received ISO (DM-ISO), and diabetic rats pretreated with vitamin D2 and received ISO (DM-D2-ISO). RESULTS: Vitamin D2 pretreatment significantly decreased fasting glucose and myocardial malondialdehyde, associated with increased insulin, myocardial glutathione and superoxide dismutase in DM-D2-ISO versus DM-ISO. The serum triglycerides, total cholesterol, and LDL were significantly decreased, along with increased HDL and adiponectin. Poly-ADP ribose polymerase, cyclooxygenase-2, tumour necrosis factor alpha, interleukin-6, caspase-3, BAX, and p53 were significantly downregulated in myocardium of DM-D2-ISO versus DM-ISO. Histological studies showed diminished inflammatory cells infiltration in myocardium of DM-D2-ISO versus DM-ISO. CONCLUSION: Vitamin D2 ameliorates hyperglycaemia, dyslipidaemia, redox imbalance, inflammatory and apoptotic processes, protecting the myocardium of diabetic rats against acute myocardial infarction.

Triiodothyronine improves age-induced glucose intolerance and increases the expression of sirtuin-1 and glucose transporter-4 in skeletal muscle of aged rats.

To evaluate the potential beneficial impact and to clarify the underlying mechanisms of triiodothyronine (T3) on glucose intolerance in aged rats. Rats were divided into adult group, aged group, and T3-treated aged group (T3-aged). T3 was administered at a dose of 8 µg/kg body weight for 2 weeks. In comparison to adult group, aged rats presented significant higher levels of fasting insulin and homeostatic model assessment of insulin resistance (HOMA-IR). Glucose area under the curve (AUC), and peak glycemia, estimated from oral glucose tolerance curve, were significantly increased along with decreased mRNA expression of skeletal muscle sirtuin-1, glucose transporter-4 (GLUT-4) and uncoupling protein-3 (UCP-3) in aged versus adult group. T3 administration significantly decreased the serum levels of fasting insulin, HOMA-IR, glucose AUC, and peak glycemia in T3-aged versus aged rats. Skeletal muscle mRNA expression of sirtuin-1 and GLUT-4 were increased, whereas UCP-3 was not changed by T3 administration. T3 administration improved glucose intolerance, and decreased insulin resistance in aged rats. This was associated with upregulation of skeletal muscle sirtuin-1 and GLUT-4 which could mediate such beneficial effect.

Triiodothyronine attenuates the progression of renal injury in a rat model of chronic kidney disease.

This study was designed to investigate whether and how triiodothyronine (T3) affects renal function in an experimental model of chronic kidney disease. Twenty-four female rats were divided into the following groups: sham-operated control group (n = 8), 5/6 nephrectomized group (Nx, n = 8), and 5/6 nephrectomized group treated with T3 for 2 weeks (T3-Nx, n = 8). T3 administration significantly decreased serum levels of urea, creatinine, tumour necrosis factorα, and interleukin-6 compared with serum levels in the Nx group. The levels of malondialdehyde, transforming growth factor ß, fibronectin, and collagen IV, as well as the expression of inducible nitric oxide synthase, nuclear factor κB, poly(ADP-ribose) polymerase, caspase-3, and Bax were all significantly decreased, though not normalized, in the remnant kidney of rats in the T3-Nx group compared with Nx rats. Glutathione, heme oxygenase-1 levels, as well as endothelial nitric oxide synthase expression were increased in the remnant kidney of the T3-Nx group. Histological studies revealed focal necrosis of renal tubules associated with inflammatory cell infiltration and fibrosis in the Nx group. These changes were alleviated in T3-Nx rats. This study showed that T3 administration attenuated the clinical and histological signs of renal injury in 5/6 nephrectomized rats by mitigating renal oxidative stress, inflammation, apoptosis, and fibrosis.

Heart rate variability analysis during immediate recovery from exercise in overweight/obese healthy young adult females.

BACKGROUND: Data on heart rate variability (HRV) changes during immediate recovery period after exercise in overweight/obese healthy young adult females are still inconclusive. The aim of this study was to evaluate the heart rate variability (HRV), heart rate recovery (HRR), and arterial blood pressure immediately after cessation of exercise in overweight/obese healthy young adult females. METHODS: This study was carried out in the laboratory of the Physiology Department, Faculty of Medicine, King Abdulaziz University. Fifty-five female students were classified into normal weight group and overweight/obese group. HRV, HRR, and systolic and diastolic blood pressures (SBP, DBP) were estimated at resting condition and immediately after cessation of exercise. RESULTS: During recovery, heart rate was significantly increased in overweight/obese group along with significant decrease in rMSSD (square root of the mean of the sum of the squares of differences between adjacent NN intervals) and HF (high-frequency power) compared with normal group. The recovery of heart rate, normalized HF, and normalized sympathovagal balance to their baseline values were significantly lowered in overweight/obese group. Both SBP and DBP were significantly lowered from their baseline values during recovery in normal group but unchanged in overweight/obese group. CONCLUSIONS: This study provides evidence that overweight/obesity are associated with decreased HRR and delayed vagal reactivation, in addition to impaired postexercise hypotension early in the recovery period after exercise in healthy young adult females.