Browsing by Subject "NAFLD"

Now showing 1 - 3 of 3
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    Effect of diet/atorvastatin on atherosclerotic lesions associated to nonalcoholic fatty liver disease in chickens
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2015) Sánchez-Polo, Maria T.; García Pérez, Bartolomé; Martín, Antonia; Adánez Martínez, María de Gracia; Ayala de la Peña, Ignacio; Castells Mora, María Teresa
    Comparative histological examination of both liver and the supra-aortic arteries have not previously examined the consequences of atherosclerosis and nonalcoholic fatty liver disease (NAFLD), and their response to diet and atorvastatin therapy. This study evaluates the effects of diet alone or in combination with atorvastatin therapy on the progression/regression of atherosclerosis and its correlation with NAFLD. This research was performed on a cohort of chickens on standard (SD) or hyperlipidemic diets (HD), either with or without atorvastatin therapy. The development of atherosclerotic lesions was assessed by histology, immunohistochemistry and quantitative image analysis and correlated with liver histology. The lowest levels of atherosclerotic lesions were found in animals on the HD for 3 months, followed by 3 months of SD in combination with oral atorvastatin. There was a strong association between the histologic findings of atherosclerosis and those of NAFLD. These studies show that standard diet and atorvastatin therapy can positively affect both arterial and hepatic lesions, influencing the regression of the changes. These results support the hypothesis that NAFLD and atherosclerosis may be actually two aspects of a shared disease and suggest the possibility of regression of both disorders with dietary and pharmacologic manipulations.
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    Intermittent fasting-induced autophagy normalization confers hepatic protection in metabolic dysfunction-associated fatty liver disease: Mechanistic insights and implications
    (2026) Gehan El-Akabawy; MoezAlIslam E. Faris; Manoj B. Menon; Mohamed Abdel Wahab; Farida Hussan; Mohd Hazim Bin Zulkaflee; Nabil Eid; Payal Bhatnagar; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e Histiologia
    Metabolic dysfunction-associated fatty liver disease (MAFLD) is a chronic liver condition that can progress to steatohepatitis, cirrhosis, and even liver cancer. Macroautophagy (hereinafter referred to as autophagy) is a pro-survival mechanism that facilitates the lysosomal clearance of damaged organelles, abnormal proteins, and excess lipids. A growing body of evidence indicates that autophagy dysfunction and reduced autophagic flux play critical roles in the pathogenesis of MAFLD. Therefore, restoring autophagy in MAFLD may help reduce steatosis and prevent disease progression. Intermittent fasting (IF), involving periods of restricted to no food intake alternating with periods of regulated/free eating, has been demonstrated to have beneficial effects on body composition, glucose regulation, lipid profiles, and liver function in studies involving both animal models of MAFLD and human subjects. Studies involving individuals with obesity and MAFLD have shown that Ramadan intermittent fasting (RIF), an Islamic religious practice that involves abstaining from food and water intake from sunrise to sunset over approximately 30 consecutive days, significantly reduces body weight, BMI, fat mass, and inflammatory markers while improving liver function and steatosis. The hepatoprotective effects of RIF are associated with the enhanced expression of autophagy-related genes and the restoration of autophagic flux. This upregulation of autophagy as a result of RIF makes it a potentially promising therapeutic strategy for MAFLD. This review summarizes various forms of IF, the mechanisms of autophagy, and evidence of autophagy dysfunction in MAFLD. It also explores how IF, specifically RIF, may normalize autophagy, reduce hepatic steatosis, and improve liver function in human subjects.
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    Pinocembrin ameliorates non-alcoholic fatty liver disease by activating Nrf2/HO-1 and inhibiting the NF-κB signaling pathway
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Chen Weina; Xue Diming; Feng Xia; Zhong Yinhang; Li Quanqing; Zhang Weihang; Jiang Guojun; Biología Celular e Histología
    Objectives. The high intake of high-fat diets and changes in sedentary lifestyles have led to an increase in non-alcoholic fatty liver disease (NAFLD). This study aimed to investigate the effect and mechanism of Pinocembrin (Pin) on NAFLD in vivo and in vitro. Methods. The pharmacodynamics of Pin alone or in combination with ML385 was assessed in high-fat diet (HFD)-mediated NAFLD mice. HepG2 cells were treated with palmitic acid (PA)/oleic acid (OA) (1:2) as an in vitro model to study the effect of Pin on lipid deposition and oxidative stress. The roles of Pin in glucose and lipid metabolism, inflammation, oxidative stress, and the Nrf2/HO-1/NF-κB pathway were measured. Results. Pin alleviated lipid deposition, inflam-matory response, and oxidative stress in HFD-induced NAFLD mice and PA/OA-induced HepG2 cells. Moreover, ML385 partly attenuated the protection of Pin on inflammatory response and oxidative stress in vivo and in vitro. More importantly, feeding with an HFD significantly decreased the expression of Nrf2 and HO-1, but treatment with Pin increased their expression, accompanied by an increased nuclear transposition of Nrf2. Conclusion. Taken together, these results indicated that Pin alleviated glucose and lipid metabolism disorders, inflammation, and oxidative stress in NAFLD by activating the Nrf2/HO-1 signaling pathway and restraining the NF-κB pathway