Department of Internal Medicine III, University of Giessen, 35390 Giessen, Germany.
Department of Gastroenterology, University of Giessen, 35390 Giessen, Germany.
Int J Mol Sci. 2021 Feb 7;22(4):1670. doi: 10.3390/ijms22041670.
CTRP-3 (C1q/TNF-related protein-3) is an adipokine with endocrine and immunological function. The impact of adipocyte CTRP-3 production on systemic CTRP-3 concentrations and on adipocyte biology is unknown. A murine model of adipocyte CTRP-3 knockout (KO) was established (via the system). Serum adipokine levels were quantified by ELISA and adipose tissue (AT) gene expression by real-time PCR. Preadipocytes were isolated from AT and differentiated into adipocytes. Comparative transcriptome analysis was applied in adipocytes and liver tissue. Body weight and AT mass were reduced in CTRP-3 KO mice together with decreased serum leptin. In primary cells from visceral AT of KO mice, expression of adiponectin, progranulin, and resistin was induced, while peroxisome proliferator activated receptor γ () was decreased. M1/M2 macrophage polarization markers were shifted to a more anti-inflammatory phenotype. CTRP-3 expression in AT did not contribute to serum concentrations. AT and liver morphology remained unaffected by CTRP-3 KO. Myelin transcription factor 1-like () was identified as a highly upregulated gene. In conclusion, adipocyte CTRP-3 has a role in adipogenesis and AT weight gain whereas adipocyte differentiation is not impaired by CTRP-3 deficiency. Since no effects on circulating CTRP-3 levels were observed, the impact of adipocyte CTRP-3 KO is limited to adipose tissue. Modified AT gene expression indicates a rather anti-inflammatory phenotype.
CTRP-3（C1q/TNF 相关蛋白-3）是一种具有内分泌和免疫功能的脂肪因子。脂肪细胞 CTRP-3 产生对全身 CTRP-3 浓度和脂肪细胞生物学的影响尚不清楚。建立了脂肪细胞 CTRP-3 敲除（KO）的小鼠模型（通过 系统）。通过 ELISA 定量测定血清脂肪因子水平，通过实时 PCR 测定脂肪组织（AT）基因表达。从 AT 分离前体脂肪细胞并分化为脂肪细胞。应用于脂肪细胞和肝组织的比较转录组分析。与血清瘦素降低一起，CTRP-3 KO 小鼠的体重和 AT 质量降低。在 KO 小鼠内脏 AT 的原代细胞中，脂联素、颗粒蛋白前体和抵抗素的表达被诱导，而过氧化物酶体增殖物激活受体 γ（）则降低。M1/M2 巨噬细胞极化标志物向更抗炎表型转变。AT 中的 CTRP-3 表达不影响血清浓度。AT 和肝形态不受 CTRP-3 KO 的影响。髓鞘转录因子 1 样（）被鉴定为高度上调的基因。总之，脂肪细胞 CTRP-3 在脂肪生成和 AT 体重增加中起作用，而脂肪细胞分化不受 CTRP-3 缺乏的影响。由于未观察到对循环 CTRP-3 水平的影响，脂肪细胞 CTRP-3 KO 的影响仅限于脂肪组织。改变的 AT 基因表达表明一种相当抗炎的表型。
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