CTRP4 ameliorates dexamethasone‑induced insulin resistance through the IRS‑1/PI3K/AKT pathway in 3T3‑L1 adipocytes

(HOMA‑IR) were evaluated using Spearman's correlation analysis. Recombinant CTRP4 protein was administered to fully differentiated 3T3‑L1 adipocytes to explore the impact of CTRP4 on lipid accumulation. In addition, the effects of CTRP4 on restoring impaired glucose uptake were examined through the glucose oxidase‑peroxidase method. Molecular marker expression levels in the insulin signaling pathway, in 3T3‑L1 adipocytes with IR induced by 1 µM dexamethasone, were also examined, through western blotting. The expression levels of CTRP4 exhibited a negative association with body mass index (r=‑0.35; P<0.001), HOMA‑IR (r=‑0.24; P=0.048), waist circumference (r=‑0.38; P<0.001) and abdomen circumference (r=‑0.39; P<0.001). Following treatment of cells with recombinant CTRP4, a significant reduction in lipid accumulation was observed in 3T3‑L1 adipocytes, alongside with an increase in the glucose uptake rate in dexamethasone‑induced 3T3‑L1 adipocytes (all, P<0.05). Furthermore, a marked elevation in the expression levels of insulin receptor substrate 1 (IRS‑1), PI3K and AKT phosphorylation and GLUT4 was observed in the IR model of 3T3‑L1 adipocytes. Serum CTRP4 concentration levels were negatively correlated with IR in overweight/obese patients. CTRP4 suppressed lipid accumulation and promoted glucose uptake through the IRS‑1/PI3K/AKT signaling pathway and caused increased GLUT4 expression in 3T3‑L1 adipocytes.8.