Sphingosine Kinase 2 Knockout Mice Resist HFD-Induced Obesity Through Increasing Energy Expenditure.

IF 2.1 Q3 ENDOCRINOLOGY & METABOLISM

International Journal of Endocrinology and Metabolism Pub Date : 2023-07-30 eCollection Date: 2023-07-01 DOI:10.5812/ijem-136539

Jiawei Zhao, Menq-Jer Lee

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引用次数: 0

Abstract

Background: It has been reported that sphingosine kinase (SK) 2 plays a role in maintaining metabolism and glucose homeostasis. However, the mechanism remains uncertain.

Objectives: The present research aimed to further investigate the effect of SK2 knockout on high-fat diet (HFD)-induced obesity and metabolic regulation.

Methods: Male SK2-/- and wild-type (WT) control mice were challenged with HFD for 8 weeks. Then, body composition, inguinal white adipose tissue (IWAT) histology, intraperitoneal glucose tolerance tests (IPGTT), and metabolic parameters were examined, and expression levels of uncoupling protein 1 (UCP1), a key molecular marker of thermogenesis, in IWAT were determined.

Results: After 8 weeks of HFD challenge, compared with WT mice, SK2-/- mice displayed decreased whole body, epididymal white adipose tissue (EWAT) and IWAT weights, reduced fat/lean body mass ratios and inguinal adipocytes size; also, SK2-/- mice exhibited improved intraperitoneal glucose tolerance. Next, elevated energy expenditure was observed in SK2-/- mice compared with WT mice; however, neither food intake nor physical activity showed obvious difference between SK2-/- and WT mice. Furthermore, we found that the expressions of UCP1 was markedly increased in IWAT from SK2-/- mice.

Conclusions: SK2-/- mice may resist HFD-induced obesity through increasing energy expenditure by promoting thermogenesis in the beige adipose tissue.

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鞘氨醇激酶2敲除小鼠通过增加能量消耗抵抗hfd诱导的肥胖

背景：据报道，鞘氨醇激酶（SK）2在维持代谢和葡萄糖稳态中发挥作用，但其机制尚不确定。目的：本研究旨在进一步研究SK2基因敲除对高脂饮食（HFD）诱导的肥胖和代谢调节的影响。方法：雄性SK2−/−和野生型（WT）对照小鼠用HFD攻击8周，然后检查身体组成、腹股沟白色脂肪组织（IWAT）组织学、腹膜内葡萄糖耐量试验（IPGTT）和代谢参数，并测定产热关键分子标记物解偶联蛋白1（UCP1）在IWAT中的表达水平。结果：在HFD攻击8周后，与WT小鼠相比，SK2−/-小鼠表现出全身、附睾白色脂肪组织（EWAT）和IWAT重量减少，脂肪/瘦体质量比和腹股沟脂肪细胞大小减少；此外，SK2-/-小鼠表现出改善的腹膜内葡萄糖耐受性。其次，与WT小鼠相比，SK2--/-小鼠的能量消耗增加；然而，在SK2-/-和WT小鼠之间，无论是食物摄入还是体力活动都没有显示出明显的差异。此外，我们发现，在SK2//-小鼠的IWAT中，UCP1的表达显著增加。结论：SK2-/-小鼠可以通过促进米色脂肪组织的产热来增加能量消耗，从而抵抗HFD诱导的肥胖。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

International Journal of Endocrinology and Metabolism ENDOCRINOLOGY & METABOLISM-

CiteScore

3.10

自引率

4.80%

发文量

期刊介绍： The aim of the International Journal of Endocrinology and Metabolism (IJEM) is to increase knowledge, stimulate research in the field of endocrinology, and promote better management of patients with endocrinological disorders. To achieve this goal, the journal publishes original research papers on human, animal and cell culture studies relevant to endocrinology.