The Journal of nutrition · 2026
A high-carbohydrate diet-induced lipid deposition is alleviated by sodium pyruvate via suppression of the cPLA2-arachidonic acid-PPARγ axis.
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Lv Ze-Dong, Zhao Sheng-You, Pan Si-Miao, Wu Chen-Chen, Limbu Samwel Mchele, Qiao Fang, Zhang Mei-Ling, Luo Yuan, Du Zhen-Yu
Аннотация
BACKGROUND: Pyruvate is a critical node linking glycolysis and lipid metabolism. However, its regulatory role and mechanism in fish fed high-carbohydrate diets (HCD) remain obscure.
OBJECTIVES: In this study, we determined the role of sodium pyruvate (SP) in metabolic disorders induced by HCD and elucidated its underlying mechanisms using in vivo and in vitro models.
METHODS: All-male 4-mo-old AB strain zebrafish (Danio rerio) (0.356 ± 0.02 g) were fed a control diet, HCD, or HCD supplemented with 2% or 4% SP for four weeks (3 tanks/treatment, 30 fish/tank). Juvenile all-male 3-mo-old Nile tilapia (Oreochromis niloticus) (4.00 ± 0.19 g) were fed a control diet, HCD, or HCD with 1% or 2% SP for 8 wk (3 tanks/treatment, 30 fish/tank). Zebrafish liver cell line (ZFL) was treated with 10 mM glucose, 25 mM glucose, or 25 mM glucose plus 4 or 8 mM SP for 24 hours (n = 3).
RESULTS: Dietary SP reduced hepatic lipid accumulation in both species. In zebrafish, 4% SP reduced whole-body lipid content by 36.7% and hepatic triglyceride (TG) by 71.5% compared with HCD (P < 0.01). In Nile tilapia, 2% SP lowered liver total lipid by 21.8%, serum TG by 50.7%, and hepatosomatic index by 13.2% (P < 0.05). SP increased hepatic phospholipid content by 52.2% and hepatic superoxide dismutase activity by 21.0% (P < 0.05). In ZFL cells, 8 mM SP reduced intracellular TG by 59.2% compared with high-glucose treatment (P < 0.001). Mechanistically, SP downregulated cytosolic phospholipase A2 (cPLA2) expression, reduced arachidonic acid (AA) (by 24.0%) and 15-deoxy-Δ12,14-prostaglandin J2 (by 24.7%) levels, thereby suppressing peroxisome proliferator-activated receptor γ (PPARγ) signaling (P < 0.05).
CONCLUSION: This study demonstrates that dietary SP alleviates high-glucose-induced metabolic disorders via the cPLA2-AA-PPARγ axis, providing novel insights into optimising HCD utilisation in fish.
OBJECTIVES: In this study, we determined the role of sodium pyruvate (SP) in metabolic disorders induced by HCD and elucidated its underlying mechanisms using in vivo and in vitro models.
METHODS: All-male 4-mo-old AB strain zebrafish (Danio rerio) (0.356 ± 0.02 g) were fed a control diet, HCD, or HCD supplemented with 2% or 4% SP for four weeks (3 tanks/treatment, 30 fish/tank). Juvenile all-male 3-mo-old Nile tilapia (Oreochromis niloticus) (4.00 ± 0.19 g) were fed a control diet, HCD, or HCD with 1% or 2% SP for 8 wk (3 tanks/treatment, 30 fish/tank). Zebrafish liver cell line (ZFL) was treated with 10 mM glucose, 25 mM glucose, or 25 mM glucose plus 4 or 8 mM SP for 24 hours (n = 3).
RESULTS: Dietary SP reduced hepatic lipid accumulation in both species. In zebrafish, 4% SP reduced whole-body lipid content by 36.7% and hepatic triglyceride (TG) by 71.5% compared with HCD (P < 0.01). In Nile tilapia, 2% SP lowered liver total lipid by 21.8%, serum TG by 50.7%, and hepatosomatic index by 13.2% (P < 0.05). SP increased hepatic phospholipid content by 52.2% and hepatic superoxide dismutase activity by 21.0% (P < 0.05). In ZFL cells, 8 mM SP reduced intracellular TG by 59.2% compared with high-glucose treatment (P < 0.001). Mechanistically, SP downregulated cytosolic phospholipase A2 (cPLA2) expression, reduced arachidonic acid (AA) (by 24.0%) and 15-deoxy-Δ12,14-prostaglandin J2 (by 24.7%) levels, thereby suppressing peroxisome proliferator-activated receptor γ (PPARγ) signaling (P < 0.05).
CONCLUSION: This study demonstrates that dietary SP alleviates high-glucose-induced metabolic disorders via the cPLA2-AA-PPARγ axis, providing novel insights into optimising HCD utilisation in fish.