Tag Archives: pancreatic acinar cells
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.
Bioenergetic functions of mitochondria in liver, pancreatic acinar cells, and sperm cells of rats fed short-term high-fat or high-fat high-sugar diets
B. V. Manko1*, N. M. Kozopas1,2, H. M. Mazur1,
A. М. Voityk1, B. O. Manko1, V. V. Manko1
1Ivan Franko National University of Lviv,
Department of Human and Animal Physiology, Lviv, Ukraine;
2Danylo Halytsky Lviv National Medical University,
Department of Clinical Laboratory Diagnostics, Lviv, Ukraine;
*e-mail: bohdan.manko.ablb@lnu.edu.ua
Received: 26 September 2023; Revised: 23 October 2023;
Accepted: 27 October 2023; Available on-line: 06 November 2023
An unhealthy diet often is a cause of obesity, chronic inflammation, and metabolic disruption in multiple organs. However, the direct influence of elevated lipid or sugar consumption on liver, pancreatic, and sperm mitochondria is not well understood. The aim of the study was to investigate the functional activity of mitochondria of liver, pancreatic acinar cells, and sperm cells in rats on a short-term (7 weeks) diet with high fat or high fat and high sugar content. Male Wistar rats were on a basic, high-fat or high-fat high-sugar diet for 7 weeks. At the end of the experiment, visceral fat mass, blood glucose and lipids were measured. Mitochondrial functional activity was evaluated with oxygen consumption assay. In isolated pancreatic acinar cells, NAD(P)H autofluorescence and mitochondrial membrane potential were also studied. No difference in body mass was observed between the 3 groups at the end of the experiment. Visceral fat mass was slightly but significantly elevated in rats on a high-fat high-sugar diet. Both diets did not affect plasma glucose or triglyceride levels but caused a modest elevation of total plasma cholesterol. Respiration and oxidative phosphorylation of isolated liver mitochondria were not affected by any experimental diet. In pancreatic acinar cells, a high-fat diet caused a significant decrease of basal respiration by ~15%, but no effects were observed on the maximal rate of uncoupled respiration, mitochondrial membrane potential, or NAD(P)H autofluorescence. In these cells, a ketone body 3-hydroxybutyrate caused elevation of uncoupled respiration and NAD(P)H level irrespectively of the diet. Diets did not cause any change in sperm concentration, viability or motility. Surprisingly, in animals on a high-fat high-sugar diet, a significant increase in both basal and maximal respiration of sperm cells was observed. Collectively, these data show that while the elevated fat and sugar content in the diet does not cause significant obesity, no detrimental effects on mitochondria of the liver, pancreas, and sperm cells are observed.