Tag Archives: high fat diet
Effect of long-term ethanol consumption and a high-fat diet on mitochondrial respiration in rat pancreatic acinar cells and hepatocytes
O. O. Bilonoha*, H. M. Mazur, B. O. Manko,
O. R. Kulachkovsky, V. V. Manko
Ivan Franko National University of Lviv, Lviv, Ukraine;
*e-mail: olha.bilonoha@lnu.edu.ua
Received: 26 March 2024; Revised: 09 May 2024;
Accepted: 25 July 2024; Available on-line: 04 September b2024
Chronic alcohol consumption may cause pancreatitis and alcohol-related liver diseases. Both adaptation and damage of liver mitochondria in animals on chronic ethanol and high-fat diets were demonstrated. It is currently not clear if ethanol or its metabolites such as fatty acid ethyl esters can cause mitochondrial damage to the pancreas. The present study aimed to evaluate the effect of chronic ethanol administration in combination with a high-fat diet on mitochondrial respiration in both pancreatic acinar cells and hepatocytes of rats. Wistar male rats on a high-fat diet (35% calories) were administered ethanol (6 g/kg body weight) by oral gavage for 14 days. Pancreatic acini cells and hepatocytes were isolated with collagenase digestion. The respiration of isolated cells was studied with a Clark electrode. Ethanol administration to rats kept on a high-fat diet was followed by a rapid loss of animal weight during the first 5 days of the experiment and diminished secretory response of pancreatic acini to acetylcholine, however, no changes in acinar cells ultrastructure, basal, oligomycin-insensitive or FCCP-uncoupled respiration were found. Meanwhile ethanol caused a significant (~40%) increase in basal and maximal FCCP-uncoupled respiration rate of isolated hepatocytes. In conclusion, chronic ethanol administration to rats on a high-fat diet does not cause mitochondrial damage in the pancreas, while mitochondria of the liver adapt to ethanol by increasing respiration rate.
Neutrophil activation at high-fat high-cholesterol and high-fructose diets induces low-grade inflammation in mice
G. Bila1, O. Vishchur2, V. Vovk3, S. Vari4, R. Bilyy1*
1Department of Histology, Cytology and Embryology,
Danylo Halytsky Lviv National Medical University, Lviv, Ukraine;
2Institute of Animal Biology NAAS, Lviv, Ukraine;
3Department of Pathological Anatomy and Forensic Medicine,
Danylo Halytsky Lviv National Medical University, Lviv, Ukraine;
4International Research and Innovation in Medicine Program,
Cedars-Sinai Medical Center, Los Angeles, California, USA;
*e-mail: r.bilyy@gmail.com
Received: 05 February 2024; Revised: 17 March 2024;
Accepted: 17 March 2024; Available on-line: 30 April 2024
Nonalcoholic fatty liver disease (NAFLD), which can progress to nonalcoholic steatohepatitis (NASH), is a significant health concern affecting a substantial portion of the population. This study investigates the role of neutrophil extracellular traps (NETs) in liver inflammation induced by high-fat high-cholesterol diet (HFHCD) and high-fructose diet (HFD). The chronic nature of NAFLD involves low-grade inflammation with cytokine elevation. The research aims to visualize neutrophil elastase (NE) activity during HFHCD and HFD representing conditions of low-grade activation and assess neutrophil functional status. The study employs a mouse model subjecting animals to HFHCD, HFD or a standard diet (SD) for six weeks. Various analyses were used including histological evaluations, in vivo imaging of NE activity using a fluorescent probe, fluorescent microscopy, flow cytometry and assessment of neutrophil function through reactive oxygen species (ROS) levels. Mice on HFHCD and HFD display liver damage consistent with NASH, which was validated pathohistologically. NE activity in blood significantly increases after six weeks indicating systemic NETs involvement. In vivo imaging confirms NE activity in multiple organs. Cellular localization reveals NETs persistence even after neutrophil destruction in splenocytes indicating systemic involvement. Neutrophils under HFHCD exhibit a functional phenotype associated with low-grade inflammation, higher basal ROS levels and reduced activation potential. This study establishes the systemic impact of NETs in HFHCD- and HFD-induced liver inflammation, providing insights into the functional state of neutrophils. The findings contribute to understanding the mechanisms underlying chronic liver conditions and may inform future therapeutic strategies.