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组织转谷氨酰胺酶敲除前体脂肪细胞和附睾脂肪来源的米色细胞,其线粒体功能下降,无法满足产热的需求。

Tissue Transglutaminase Knock-Out Preadipocytes and Beige Cells of Epididymal Fat Origin Possess Decreased Mitochondrial Functions Required for Thermogenesis.

机构信息

Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Egyetem ter 1., H-4032 Debrecen, Hungary.

Doctoral School of Molecular Cell and Immune Biology, University of Debrecen, Egyetem ter 1., H-4032 Debrecen, Hungary.

出版信息

Int J Mol Sci. 2022 May 5;23(9):5175. doi: 10.3390/ijms23095175.

Abstract

Beige adipocytes with thermogenic function are activated during cold exposure in white adipose tissue through the process of browning. These cells, similar to brown adipocytes, dissipate stored chemical energy in the form of heat with the help of uncoupling protein 1 (UCP1). Recently, we have shown that tissue transglutaminase (TG2) knock-out mice have decreased cold tolerance in parallel with lower utilization of their epididymal adipose tissue and reduced browning. To learn more about the thermogenic function of this fat depot, we isolated preadipocytes from the epididymal adipose tissue of wild-type and TG2 knock-out mice and differentiated them in the beige direction. Although differentiation of TG2 knock-out preadipocytes is phenotypically similar to the wild-type cells, the mitochondria of the knock-out beige cells have multiple impairments including an altered electron transport system generating lower electrochemical potential difference, reduced oxygen consumption, lower UCP1 protein content, and a higher portion of fragmented mitochondria. Most of these differences are present in preadipocytes as well, and the differentiation process cannot overcome the functional disadvantages completely. TG2 knock-out beige adipocytes produce more iodothyronine deiodinase 3 (DIO3) which may inactivate thyroid hormones required for the establishment of optimal mitochondrial function. The TG2 knock-out preadipocytes and beige cells are both hypometabolic as compared with the wild-type controls which may also be explained by the lower expression of solute carrier proteins SLC25A45, SLC25A47, and SLC25A42 which transport acylcarnitine, Co-A, and amino acids into the mitochondrial matrix. As a consequence, the mitochondria in TG2 knock-out beige adipocytes probably cannot reach the energy-producing threshold required for normal thermogenic functions, which may contribute to the decreased cold tolerance of TG2 knock-out mice.

摘要

米色脂肪细胞具有产热功能,在寒冷环境中通过棕色化过程在白色脂肪组织中被激活。这些细胞与棕色脂肪细胞类似,在解偶联蛋白 1(UCP1)的帮助下,以热量的形式消耗储存的化学能。最近,我们发现组织转谷氨酰胺酶(TG2)敲除小鼠对寒冷的耐受性降低,同时其附睾脂肪组织的利用率降低,棕色化减少。为了更深入地了解这个脂肪组织的产热功能,我们从野生型和 TG2 敲除小鼠的附睾脂肪组织中分离出前体脂肪细胞,并将其向米色方向分化。尽管 TG2 敲除前体脂肪细胞的分化表型与野生型细胞相似,但敲除米色细胞的线粒体存在多种损伤,包括改变的电子传递系统导致电化学势能差降低、耗氧量降低、UCP1 蛋白含量降低以及更多的线粒体碎片化。这些差异大多数在前体脂肪细胞中也存在,而且分化过程并不能完全克服功能缺陷。TG2 敲除米色脂肪细胞产生更多的甲状腺素脱碘酶 3(DIO3),可能会使建立最佳线粒体功能所需的甲状腺激素失活。与野生型对照相比,TG2 敲除前体脂肪细胞和米色细胞的代谢都较低,这也可能是由于转运酰基辅酶 A、Co-A 和氨基酸进入线粒体基质的溶质载体蛋白 SLC25A45、SLC25A47 和 SLC25A42 的表达较低所致。因此,TG2 敲除米色脂肪细胞中的线粒体可能无法达到正常产热功能所需的能量产生阈值,这可能导致 TG2 敲除小鼠对寒冷的耐受性降低。

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