# Effects of Nutritional Disturbances on the Structure and Function of Mitochondria, Oxidative Stress Level, and Fat Deposition in Chicken Liver Cells

## TL;DR

This study explores how nutritional changes affect chicken liver cells' mitochondria, fat storage, and stress levels, revealing differences based on genetic haplogroups.

## Contribution

The study reveals how mitochondrial haplogroups influence liver cell responses to nutritional disturbances, offering new insights into animal health and performance.

## Key findings

- Refeeding after fasting increases fat deposition and mitochondrial membrane potential in chicken liver cells.
- Mitochondrial quantity and ROS levels differ between haplogroups A and E under nutritional disturbances.
- Glucose and oleic acid treatments have distinct effects on mitochondrial function and ROS levels.

## Abstract

Nutrition and energy are critical factors influencing animal growth, development, production performance, and health status; however, the understanding of the underlying mechanism remains limited. In this study, we found that refeeding after fasting promoted fat deposition and increased mitochondrial membrane potential and the number of clustered ribosomes in liver cells. However, mitochondrial quantity and cellular ROS level were influenced by different mitochondrial haplogroups (A and E Haplogroups). Moreover, Haplogroup A chicken liver cells exhibited stronger adaptability to nutritional disturbances than Haplogroup E. In addition, glucose and oleic acid treatments exerted distinct effects on mitochondria membrane potential, ROS level and CYTB protein abundance in liver cells. These findings provide an insight into the mechanism by which nutritional disturbances influence cell physiological functions and, ultimately, animal performance and health.

As mitochondria play an important role in nutritional/energy metabolism, nutritional disturbances may affect animal growth, development and performance through modulating mitochondrial structure and function. This study aimed to elucidate the effects of nutritional disturbances on mitochondrial structure and function, oxidative stress, and fat deposition in the hepatocytes of chickens with A or E mitochondrial haplogroups (referred to as A-group and E-group). For in vivo experiments, white-feathered broiler chickens were fasted for 12 h or refed for 2 h after 10 h fasting. For in vitro experiments, chicken embryonic primary hepatocytes were treated with 50 mmol/L glucose or 0.25 mmol/L oleic acid. Data indicated that compared to fasted chickens, fat content (p < 0.01), the number of aggregated ribosomes (p < 0.05), and mitochondrial membrane potential (p < 0.05) were increased in the refed chickens of both haplogroups. However, the number of mitochondria was reduced (p < 0.01) and ROS level was increased (p < 0.05) in the refed E-group chickens, and the protein levels of MFN2 and SOD2 were reduced (p < 0.05) in the refed A-group chickens. Moreover, compared to the control cells, triglyceride content was increased in the cells of both haplogroups (p < 0.01), ROS level was reduced in the E-group cells (p < 0.01), and mitochondrial membrane potential was reduced (p < 0.05) and CYTB protein content was increased (p < 0.05) in the A-group cells after treatment with oleic acid. In addition, mitochondrial membrane potential was increased in the A-group cells after treatment with glucose (p < 0.01). These results indicate that nutritional disturbances affected fat deposition, mitochondrial membrane potential, the number of aggregated ribosomes, and ROS level in chicken liver cells. Moreover, ROS level, mitochondrial number, mitochondrial membrane potential, and the abundance of certain mitochondrial proteins were different between the A- and E-groups or between glucose and oleic acid treatments. These findings provide references for improving animal physiological functions and production performance by adjusting nutritional levels.