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<p>Lipocalin-2 (LCN-2) is an adipocytokine secreted mainly by adipose tissue. Increasing evidences suggest that LCN-2 is an inflammatory factor associated with insulin resistance, obesity, and its complications. The precise mechanism of the development of obesity-related disorders induced by LCN-2 is not very clear. This study evaluated the expression of LCN-2 in pig tissues and its molecular mechanism of regulating preadipocyte differentiation in porcine intramuscular preadipocytes. LCN-2 expression in tissues of Tongcheng pigs, intramuscular adipose tissue of Tongcheng pigs (fat type) and Landrace pigs (lean type) in embryonic stage and growth stage, and adipocyte differentiation–induced porcine intramuscular preadipocytes was detected using reverse transcription polymerase chain reaction (qRT-PCR). After LCN-2 treatment, cell viability was measured by the methyl thiazolyl tetrazolium (MTT) method, mRNA expression of CCAAT/enhancer binding protein-ɑ (C/EBPɑ), adipocyte determination and differentiation factor-1 (ADD1), fatty acid desaturase (FAD), fatty acid synthase (FAS), and glucose transporter (GLUT) 1,4 was determined by qRT-PCR, protein expression of LCN-2 and peroxisome proliferator–activated receptor-γ (PPARγ) was analyzed by Western blot. Results of qRT-PCR indicated that LCN-2 showed significantly higher expression in high-intramuscular fat (IMF) pigs compared to low-IMF pigs (<i>P</i> &lt; 0.05). LCN-2 expression in porcine intramuscular preadipocytes was significantly upregulated after adipocytic differentiation induction (<i>P</i> &lt; 0.05). Silencing of LCN-2 with LCN-2 siRNA (siLCN-2) inhibited cell viability, lipid droplets, protein expression of PPARγ, and mRNA expression of C/EBPa, ADD1, FAD, FAS, and GLUT 1,4. siLCN-2 treated cells also showed a lower content of triglyceride and release of glucose. Moreover, LCN-2-induced downregulation of cell viability, adipocytic differentiation, adipogenesis, and glycometabolism of porcine intramuscular preadipocytes was partially blocked by the PPARγ inhibitor (GW9662). It is indicated that LCN-2 silencing suppresses cell viability, adipocytic differentiation and adipogenesis, glycometabolism, and fat deposition of porcine intramuscular preadipocytes through suppression of the PPARγ signaling pathway.</p>

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The differential expression of lipocalin-2 in pig tissues and its molecular mechanism of regulating cell viability, differentiation, adipogenesis, and glycometabolism in porcine intramuscular preadipocytes

  • 期刊论文

  • 发表日期：

    2026年3月17日

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  • Xiaoying Dong,
  • Yanfei Chen,
  • Liubing Tang,
  • Qinen Wu,
  • Tingjun Li,
  • Qiuxia Wei,
  • Shengqiu Tang

摘要

Lipocalin-2 (LCN-2) is an adipocytokine secreted mainly by adipose tissue. Increasing evidences suggest that LCN-2 is an inflammatory factor associated with insulin resistance, obesity, and its complications. The precise mechanism of the development of obesity-related disorders induced by LCN-2 is not very clear. This study evaluated the expression of LCN-2 in pig tissues and its molecular mechanism of regulating preadipocyte differentiation in porcine intramuscular preadipocytes. LCN-2 expression in tissues of Tongcheng pigs, intramuscular adipose tissue of Tongcheng pigs (fat type) and Landrace pigs (lean type) in embryonic stage and growth stage, and adipocyte differentiation–induced porcine intramuscular preadipocytes was detected using reverse transcription polymerase chain reaction (qRT-PCR). After LCN-2 treatment, cell viability was measured by the methyl thiazolyl tetrazolium (MTT) method, mRNA expression of CCAAT/enhancer binding protein-ɑ (C/EBPɑ), adipocyte determination and differentiation factor-1 (ADD1), fatty acid desaturase (FAD), fatty acid synthase (FAS), and glucose transporter (GLUT) 1,4 was determined by qRT-PCR, protein expression of LCN-2 and peroxisome proliferator–activated receptor-γ (PPARγ) was analyzed by Western blot. Results of qRT-PCR indicated that LCN-2 showed significantly higher expression in high-intramuscular fat (IMF) pigs compared to low-IMF pigs (P < 0.05). LCN-2 expression in porcine intramuscular preadipocytes was significantly upregulated after adipocytic differentiation induction (P < 0.05). Silencing of LCN-2 with LCN-2 siRNA (siLCN-2) inhibited cell viability, lipid droplets, protein expression of PPARγ, and mRNA expression of C/EBPa, ADD1, FAD, FAS, and GLUT 1,4. siLCN-2 treated cells also showed a lower content of triglyceride and release of glucose. Moreover, LCN-2-induced downregulation of cell viability, adipocytic differentiation, adipogenesis, and glycometabolism of porcine intramuscular preadipocytes was partially blocked by the PPARγ inhibitor (GW9662). It is indicated that LCN-2 silencing suppresses cell viability, adipocytic differentiation and adipogenesis, glycometabolism, and fat deposition of porcine intramuscular preadipocytes through suppression of the PPARγ signaling pathway.