Dietary Myo-Inositol Improves Growth Performance and Glycolipid Metabolism in Yellow River Carp (Cyprinus carpio haematopterus) Fed High-Carbohydrate-High-Fat Diets: Involvement of PI3K/Akt and FXR/SHP Pathways.
- 1Aquatic Animal Nutrition and Feed Research Team College of Fisheries Henan Normal University Xinxiang 453007 Henan Province China henannu.edu.cn.
- 2College of Life Sciences Henan Normal University Xinxiang 453007 Henan Province China henannu.edu.cn.
- 3College of Fisheries Xinyang Agriculture and Forestry University Xinyang 464000 Henan Province China xyafu.edu.cn.
Abstract
High-carbohydrate-high-fat (HCHF) diets often induce glycolipid metabolism disorders, Hepatosomatic fat deposition, and compromised growth in fish. Myo-inositol (MI) is a known metabolic regulator, yet its specific mechanism in mitigating HCHF-induced metabolic stress in Yellow River carp remains unclear. This study investigated the effects of dietary MI on growth, glycolipid metabolism, and bile acid signaling in fish fed HCHF diets. Six experimental diets were formulated: a control diet, an HCHF diet, and the HCHF diet supplemented with graded levels of MI (125, 250, 500, and 1000 mg·kg⁻¹). After a 9-week feeding trial, results showed that MI supplementation dose-dependently improved growth performance (FBW, WGR, and SGR) and feed utilization (FCR), while significantly reducing the hepatosomatic index (HSI). Physiologically, MI reduced serum glucose and triglycerides (TGs), as well as hepatopancreatic total cholesterol (T-CHO) and TG levels, while elevating high-density lipoprotein cholesterol (HDL-C), suggesting enhanced lipid transport capacity. Regarding glycolipid metabolism, MI promoted glycolysis by increasing hk and pfk mRNA expression, while suppressing gluconeogenesis (pepck) and lipogenesis (fas, pparγ). These metabolic changes were accompanied by alleviated hepatocyte vacuolation and morphological abnormalities, with reduced hepatocellular vacuolation and lipid deposition in HCHF-fed fish. Mechanistically, bile acid metabolism and phosphatidylinositol 3-kinase (PI3K)/Akt (protein kinase B) signaling pathways participated extensively and served important roles in the action of MI. Based on comprehensive analysis of growth and physiological indicators, the optimal MI supplementation level in the HCHF diet is recommended as 230-475 mg·kg⁻¹. In conclusion, MI alleviates HCHF diet-induced metabolic disorders and hepatopancreatic morphological abnormalities in Yellow River carp, and this effect is associated with the PI3K/Akt and farnesoid X receptor (FXR)/SHP (small heterodimer partner) pathways, providing a theoretical basis for functional feed development for fish.
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BibTeX
@article{yan2026dietary,
title = {{Dietary Myo-Inositol Improves Growth Performance and Glycolipid Metabolism in Yellow River Carp (Cyprinus carpio haematopterus) Fed High-Carbohydrate-High-Fat Diets: Involvement of PI3K/Akt and FXR/SHP Pathways.}},
author = {Xiao Yan and Xin Long and Rumeng Qiao and Peng Pang and Junli Wang and Shaoyang Zhi and Jiali Mi and Mingming Niu and Chaobin Qin and Liping Yang and Guoxing Nie},
journal = {Aquaculture nutrition},
year = {2026},
month = oct,
doi = {10.1155/anu/4324808},
url = {https://europepmc.org/article/MED/42928767},
note = {CC BY},
}
RIS
TY - JOUR
TI - Dietary Myo-Inositol Improves Growth Performance and Glycolipid Metabolism in Yellow River Carp (Cyprinus carpio haematopterus) Fed High-Carbohydrate-High-Fat Diets: Involvement of PI3K/Akt and FXR/SHP Pathways.
AU - Xiao Yan
AU - Xin Long
AU - Rumeng Qiao
AU - Peng Pang
AU - Junli Wang
AU - Shaoyang Zhi
AU - Jiali Mi
AU - Mingming Niu
AU - Chaobin Qin
AU - Liping Yang
AU - Guoxing Nie
PY - 2026
DA - 2026/10/25
JO - Aquaculture nutrition
DO - 10.1155/anu/4324808
UR - https://europepmc.org/article/MED/42928767
AB - High-carbohydrate-high-fat (HCHF) diets often induce glycolipid metabolism disorders, Hepatosomatic fat deposition, and compromised growth in fish. Myo-inositol (MI) is a known metabolic regulator, yet its specific mechanism in mitigating HCHF-induced metabolic stress in Yellow River carp remains unclear. This study investigated the effects of dietary MI on growth, glycolipid metabolism, and bile acid signaling in fish fed HCHF diets. Six experimental diets were formulated: a control diet, an HCHF diet, and the HCHF diet supplemented with graded levels of MI (125, 250, 500, and 1000 mg·kg⁻¹). After a 9-week feeding trial, results showed that MI supplementation dose-dependently improved growth performance (FBW, WGR, and SGR) and feed utilization (FCR), while significantly reducing the hepatosomatic index (HSI). Physiologically, MI reduced serum glucose and triglycerides (TGs), as well as hepatopancreatic total cholesterol (T-CHO) and TG levels, while elevating high-density lipoprotein cholesterol (HDL-C), suggesting enhanced lipid transport capacity. Regarding glycolipid metabolism, MI promoted glycolysis by increasing hk and pfk mRNA expression, while suppressing gluconeogenesis (pepck) and lipogenesis (fas, pparγ). These metabolic changes were accompanied by alleviated hepatocyte vacuolation and morphological abnormalities, with reduced hepatocellular vacuolation and lipid deposition in HCHF-fed fish. Mechanistically, bile acid metabolism and phosphatidylinositol 3-kinase (PI3K)/Akt (protein kinase B) signaling pathways participated extensively and served important roles in the action of MI. Based on comprehensive analysis of growth and physiological indicators, the optimal MI supplementation level in the HCHF diet is recommended as 230-475 mg·kg⁻¹. In conclusion, MI alleviates HCHF diet-induced metabolic disorders and hepatopancreatic morphological abnormalities in Yellow River carp, and this effect is associated with the PI3K/Akt and farnesoid X receptor (FXR)/SHP (small heterodimer partner) pathways, providing a theoretical basis for functional feed development for fish.
SN - 1353-5773
SN - 1365-2095
ER -