FABP4 regulates inflammation and lipid transport via PPARγ signaling pathway in goose primary hepatocytes

Q: What are the key findings of this study?

FABP4 overexpression significantly suppressed the mRNA levels of TNF, IL1, IL6, and ApoB (P<0.05) via the PPARγ signaling pathway in goose primary hepatocytes.

Q: What is the clinical evidence from this study?

Population: Hepatic lipid accumulation / Fatty liver. Intervention: FABP4 overexpression and knockdown. Primary outcome: mRNA levels of TNF, IL1, IL6, and ApoB (p=< 0.05).

Q: What question did this study set out to answer?

This study aims to clarify the role of FABP4 in regulating inflammation and lipid metabolism in goose hepatocytes.

Xu Liu; Zihan Deng; 秦淑清; Huijing Liu; YANG Can; Yuying Deng; Qingyuan Ouyang; Changqing He; XiangYong Qu

doi:10.1016/j.psj.2026.107488

July 1, 2026Poultry ScienceOpen Access

FABP4 regulates inflammation and lipid transport via PPARγ signaling pathway in goose primary hepatocytes

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Key result

FABP4 overexpression suppresses inflammatory cytokines and ApoB via PPARγ signaling in goose hepatocytes.

P<0.05

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Why the study?

Geese fatty liver does not induce inflammation despite severe steatosis, but the role of FABP4 in goose fatty liver formation remains unclear.

Key Points

This study aims to clarify the role of FABP4 in regulating inflammation and lipid metabolism in goose hepatocytes.
Isolated primary hepatocytes from Xupu goose to study FABP4 functions.
Conducted transcriptome sequencing to analyze differentially expressed genes.
Used a specific PPARγ inhibitor to evaluate the dependency of FABP4's effects on PPARγ signaling.
FABP4 overexpression significantly suppressed mRNA levels of TNF, IL1, IL6, and ApoB (P < 0.05).
FABP4 knockdown upregulated expression of IL6, ApoB, CD36, and FABP5 (P < 0.05).
PPARγ inhibition partially reversed the suppression of ApoB, IL1, and IL6 induced by FABP4 overexpression.

Structured PICO

P

Population

Primary hepatocytes isolated from Xupu goose used to investigate the function of FABP4 in fatty liver formation.

I

Intervention

FABP4 overexpression, FABP4 knockdown, and PPARγ inhibitor treatment

C

Comparator

Control hepatocytes

O

Outcome

mRNA expression levels of inflammatory cytokines (TNF, IL1, IL6) and lipid transport genes (ApoB, CD36, FABP5)surrogate

Main Result

p-value: p=< 0.05

Implication

In goose primary hepatocytes, FABP4 suppresses inflammatory cytokines and ApoB expression via the PPARγ signaling pathway, providing insights into the lack of inflammation in goose fatty liver.

Abstract

Unlike human nonalcoholic fatty liver disease, fatty liver in geese do not induce inflammation even under severe steatosis, making it a unique model for studying hepatic lipid accumulation. Fatty acid-binding protein 4 (FABP4) is known to regulate lipid metabolism and inflammation, but its role in goose fatty liver formation remains unclear. In this study, primary hepatocytes were successfully isolated from Xupu goose and used to investigate the function of FABP4. The results showed that FABP4 overexpression significantly suppressed the mRNA levels of TNF, IL1, IL6 , and ApoB ( P < 0.05), while FABP4 knockdown upregulated the expression of IL6, ApoB, CD36 , and FABP5 ( P < 0.05). Transcriptome sequencing analysis revealed that differentially expressed genes mainly enriched in immune response and cytokine-cytokine receptor interaction pathways. Furthermore, treatment with the PPARγ inhibitor partially reversed the suppression of ApoB, IL1, and IL6 induced by FABP4 overexpression, indicating that FABP4 functions downstream of PPARγ. In conclusion, FABP4 selectively suppresses inflammatory cytokines and ApoB expression via the PPARγ signaling pathway in goose primary hepatocytes. This study provides novel evidence in geese for a regulatory relationship between FABP4 and ApoB, offering new insights into the protective mechanisms underlying goose fatty liver formation.

Discussion

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Cite This Study

Liu et al. (2026) studied Hepatic lipid accumulation / Fatty liver. FABP4 overexpression and knockdown was evaluated on mRNA levels of TNF, IL1, IL6, and ApoB (p=< 0.05). FABP4 overexpression significantly suppressed the mRNA levels of TNF, IL1, IL6, and ApoB (P<0.05) via the PPARγ signaling pathway in goose primary hepatocytes.

synapsesocial.com/papers/6a6794fcbb2605d1235fba26 https://doi.org/10.1016/j.psj.2026.107488

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FABP4 regulates inflammation and lipid transport via PPARγ signaling pathway in goose primary hepatocytes

Figures

Key Points

Structured PICO

Main Result

Implication

Abstract

Discussion

Cite This Study

FABP4 regulates inflammation and lipid transport via PPARγ signaling pathway in goose primary hepatocytes

Figures

Key Points

Structured PICO

Main Result

Implication

Abstract

Discussion

Cite This Study

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