Deficiency of C1q/TNF-related protein 3 (CTRP3) decreases adipose tissue weight in diet-induced obesity mice
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SHORT COMMUNICATION
Deficiency of C1q/TNF‑related protein 3 (CTRP3) decreases adipose tissue weight in diet‑induced obesity mice Takashi Maeda1 · Satoshi Wakisaka1 Received: 21 July 2020 / Accepted: 7 October 2020 © Springer Nature B.V. 2020
Abstract Adipokines are important regulators of lipid and glucose metabolism. A family of adiponectin paralogs is known as C1q and tumor necrosis factor (TNF)-related proteins (CTRPs). One line of Ctrp3-deficient mice shows reduced liver size in response to obesity. We generated and characterized another line of Ctrp3 knockout (KO) mice to reveal novel physiological functions of CTRP3. Interestingly, high fat diet (HFD)-fed Ctrp3 KO mice displayed a decrease in the epididymal white adipose tissue (WAT) weight to total body weight ratio. Histologically, adipocyte size was significantly smaller in the epididymal WAT of HFD-fed Ctrp3 KO mice than wild-type (WT) controls. The expression of several genes involved in lipogenesis, lipolysis and adipogenesis in the epididymal WAT of Ctrp3 KO mice fed a HFD was decreased. The present findings provide new insight into the role of CTRP3 as adipokine in the regulation of adipose tissue in obesity. Keywords Adipokine · CTRP3 · Obesity · Adipose tissue
Introduction Adipose tissue stores lipids as an energy reservoir in the form of triglycerides (TGs). When dietary energy intake is excessive, adipose tissue synthesizes TGs by esterification of fatty acids to glycerol. Conversely, during starvation, the hydrolysis of TGs into free fatty acids and glycerol occurs in adipose tissue [1]. Adipose tissue also secretes numerous peptide hormones as an endocrine organ. These hormones, called adipokines, regulate lipid and glucose metabolism [2]. A family of adiponectin paralogs, known as C1q and tumor necrosis factor (TNF)-related proteins (CTRPs), has been discovered. The CTRP family comprises 15 members, and they show a similar structure, with four distinct domains [3, 4]. Several CTRP family members have lipid and glucose metabolic functions like adiponectin [5, 6]. CTRP3, a chondrocyte-derived secretory protein [7], also has similar Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11033-020-05905-6) contains supplementary material, which is available to authorized users. * Takashi Maeda [email protected]‑u.ac.jp 1
Department of Anatomy and Cell Biology, Graduate School of Dentistry, Osaka University, 1‑8 Yamadaoka, Suita, Osaka 565‑0871, Japan
metabolic functions [8]. Administration of CTRP3 lowers blood glucose levels and decreases hepatic gluconeogenic gene expression in mice [9]. Transgenic Ctrp3 mice resisted against high-fat diet (HFD)-induced hepatic steatosis, and CTRP3 administration reduced hepatic TG levels in dietinduced obese (DIO) mice [10]. Ctrp3 transgenic mice were also protected against alcohol-induced hepatic TG accumulation in a chronic model of alcohol consumption [11]. In addition, the liver sizes were reduced in Ctrp3-deficient mice fed a HFD [12]. In humans, circul
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