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Strategies to increase energy expenditure are an attractive approach to reduce excess fat storage and body weight to improve metabolic health. The aim of the present study was to investigate the effects of endurance training combined with adenosine injection on the gene expression of UCP-1 and MAPK p38 in the subcutaneous adipose tissue of male rats fed a high-fat diet.

Forty rats were randomly divided into 4 groups: 1. normal control, 2. high-fat diet (HFD) control, 3. HFD + adenosine, and 4. HFD + endurance training + adenosine. After 13 weeks of HFD, 12 weeks of endurance training on a moderate-intensity treadmill was performed. UCP-1 and MAPK p38 mRNA levels were measured by RT-PCR.

A significant increase in UCP-1 was observed with in HFD + endurance training + adenosine and HFD + adenosine compared to normal and HFD controls. A significant decrease in MAPK p38 was also observed with HFD + endurance training + adenosine and HFD + adenosine compared to HFD.

Endurance training and adenosine are likely activators of UCP-1 gene expression and can be used as effective lipolytic agents in obesity. The MAPK p38 pathway increases glucose uptake by insulin and also induces oxidative phosphorylation in mitochondria following a healthy diet and aerobic activity.

Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease caused by the accumulation of large amounts of fat in the hepatocytes. Given that atorvastatin is effective for treatment of NAFLD, the present study investigated effects of high-fat/fructose diet (HFFD) with atorvastatin on liver enzymes and lipid profile in a NAFLD rat model.

Thirty-two male Wistar rats were divided into four groups: 1) normal control, 2) HFFD control, 3) HFFD + atorvastatin, and 4) normal + atorvastatin. The groups received HFFD for 15 weeks to induce hepatosteatosis. Atorvastatin was administrated at the dose of 10 mg/kg/day. Lipid profile and liver enzymes were measured after eight weeks of intervention.

Triglyceride, cholesterol, gamma-glutamyl transferase, and aspartate transaminase were significantly reduced in the HFFD + atorvastatin group compared with the HFFD control group. In addition, cholesterol, high-density lipoprotein, alkaline phosphatase, and gamma-glutamyl transferase were significantly increased in the normal + atorvastatin group compared with the normal control group. Low-density lipoprotein increased significantly in the HFFD + atorvastatin group and the normal + atorvastatin group compared with other groups. There was a significant difference in the alanine transaminase levels between the groups taking atorvastatin. In fact, alanine transaminase level was lowest in the normal + atorvastatin group.

Atorvastatin improves the lipid profile and fatty liver and controls liver enzymes. Therefore, it can be used with caution to improve the lipid profile and reduce the complications of NAFLD.

Cerebral ischemia can cause irreversible structural and functional damages to the brain, especially to the hippocampus. Preconditioning with endurance training and endogenous adenosine infusion may reduce ischemia-associated damages.

This study aimed to evaluate the effect of preconditioning with endurance training and endogenous adenosine infusion on cell death in the hippocampal CA1 region following ischemia/reperfusion injuries in a rat model.

Male Wistar rats were divided into five groups: (1) control (n = 8); (2) ischemia (n = 12); (3) endurance training + ischemia (n = 12); (4) adenosine infusion + ischemia (n = 12); and (5) endurance training + adenosine infusion + ischemia (n = 12). The rats in the training groups ran on a treadmill five days per week for eight weeks. In the adenosine infusion groups, the rats were injected 0.1 mg/mL/kg of adenosine intraperitoneally. Also, in the ischemic groups, both common carotid arteries were clamped for 45 minutes. Cresyl violet staining and real-time polymerase chain reaction (PCR) assay were used to evaluate cell death and cytokine gene expression, respectively.

Based on the present results, treatments, including endurance training + ischemia, adenosine infusion + ischemia, and endurance training + adenosine infusion + ischemia reduced the level of interleukin-6 (IL-6) and glutamate gene expression, respectively, compared to the group of ischemia only. In contrast, the expression of nerve growth factor (NGF) and adenosine receptor (A2A) genes increased by seven, four, and two folds in the endurance training + ischemia, adenosine infusion + ischemia, and endurance training + adenosine infusion + ischemia groups, respectively, compared to the group of ischemia only.

Endurance training on a treadmill and exogenous adenosine infusion synergistically diminished cell death and reduced the expression of pro-inflammatory cytokines, while promoting the neurotrophic factor expression. When endurance training and adenosine infusion were used as stimulants before the induction of cerebral ischemia, they significantly reduced cell death.

Accumulation of fat in the liver is one of the causes of non-alcoholic fatty liver disease (NAFLD), which affects about 30% of the world's population. Animal models have been useful tools for investigating the mechanisms involved in the etiology of NAFLD and developing new drugs.

This study aimed to present a new model for the detection of NAFLD in rats.

Forty-eight rats were randomly divided into six experimental groups: (1) control; (2) 45% fructose + 35% olive oil + carbon tetrachloride (FFC1); (3) carbon tetrachloride (1: 4 in olive oil) (C1); (4) carbon tetrachloride (1: 6 in olive oil) (C2); (5) 12.5% fructose + 12.5% olive oil (FF); and (6) 20% fructose + carbon tetrachloride (1: 4 in olive oil) (FC1). Blood samples were taken in three steps, and liver tissue was dissected at the end of the sixth week for histopathological assessments.

After six weeks, the alanine transaminase (131.63 ± 1.51), aspartate transaminase (275 ± 1.0), and gamma-glutamyl transferase (4.30 ± 0.1) levels increased significantly in the C1 group (P < 0.05). The serum lipid profile showed significant changes in all groups compared to the controls (P < 0.01). According to the histological results, all experimental groups, except the C2 group, showed symptoms of NAFLD; nevertheless, a higher NAFLD Activity Score (NAS) was found in the C1 group, followed by the FC1 group, compared to the other groups.

The present results revealed that injection of 0.1 mL/kg of carbon tetrachloride (C1 group), alone or along with a diet containing 20% fructose (FC1 group), provided useful animal models of NAFLD, although carbon tetrachloride injection alone is the most effective model in inducing NAFLD model that can be used as a new strategy in nutritional and pharmacological studies.
Keywords

Changes in diet to high-fat and high-calorie diets along with reduced physical activity increase obesity and UCP-1 plays a preventive role against weight gain, obesity, and type 2 diabetes. The present study aimed to evaluation of the effect of aerobic exercise on the expression of UCP1 and MAPK p38 heat gene in subcutaneous adipose tissue in male Wistar rats fed a high-fat diet.

15 rats were randomly divided into 3 groups: normal control, high-fat diet control (40% fat), and high-fat diet+aerobic exercise. After 13 weeks of consumption of a high-fat diet, the aerobic exercise group performed the exercise protocol on a treadmill for 12 weeks and 5 sessions per week. UCP1 and MAPK p38 levels were measured using RT-PCR. One-way ANOVA analysis of variance and Kruskal-Wallis test were used at the level of P≤0.05.

There was no significant difference in UCP-1 mRNA expression between the normal control (P=0.151) and the high-fat diet group but there was a significant difference between the normal control and the high-fat diet+aerobic exercise group (P=0.008). Also, the expression of MAPK p38 in the high-fat diet control had a significant increase compared to the normal control (P=0.008), and a significant decrease in the expression of MAPK P38 in the high-fat diet+aerobic exercise compared to the high-fat diet control was observed (P=0.008).

Aerobic exercise can be a suitable stimulus in the expression of UCP-1. The complexity of MAPK p38 pathway activity is due to its dependence on the type of stimulus and the cell.