Glucose and insulin modulate inflammation and glycolipid metabolism genes in goose muscle via IGFBP2 during fatty liver development

Muscle, the largest tissue in geese, is crucial for developing goose fatty liver. Investigating the influence of Insulin-like Growth Factor Binding Protein 2 (IGFBP2) on muscle during fatty liver development is crucial for understanding its regulatory mechanisms. In this study, twenty-four 70-day-old male Landes geese were divided into two groups: an overfeeding group and a control group (n = 12 each). Pectoral muscle samples were collected at 82 and 94 days of age. Additionally, twenty-four 10-day-old geese were divided into a glucose injection group and a saline control group (n = 12 each), with pectoral muscle samples collected 2 hours post-injection at 17 days of age. Goose primary myocytes were treated with glucose (0, 25, 50, and 100 mmol/L) or insulin (0, 5, 10, and 20 nmol/L) and transfected with an IGFBP2 overexpression vector or an empty vector. Results demonstrated that overfeeding, glucose injection, 50 and 200 mmol/L glucose treatment, and 10 and 20 nmol/L insulin treatment significantly inhibited the expression of IGFBP2 in both muscle and cell samples (P < 0.05). Overexpression of IGFBP2 increased the expression of LOC106030908, FGB, and LOC106040417, while inhibiting PLPP4, PTGS2, IL6, and LOC106041919 (P < 0.05). Notably, gene expression showed an inverse pattern in the muscles of overfed geese. Additionally, glucose and insulin upregulated LOC106041919 and LOC106040417 while downregulating LOC106030908 in goose myocytes (P < 0.05). These results suggest that glucose and insulin modulate inflammation and glycolipid metabolism genes in goose muscle via IGFBP2 during fatty liver development, providing new molecular insights.