Okuda Tetsuya
Bio-Design Research Group, Bioproduction Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Central 6, 1-1-1 Higashi, Tsukuba, Ibaraki, 305-8566, Japan.
Data Brief. 2019 Oct 2;27:104604. doi: 10.1016/j.dib.2019.104604. eCollection 2019 Dec.
The data presented herein pertain to a research article entitled "A low-carbohydrate ketogenic diet promotes ganglioside synthesis via the transcriptional regulation of ganglioside metabolism-related genes" [1]. The present article provides additional structural analysis data for the characterization of hepatic glycoproteins in mice fed a low-carbohydrate ketogenic diet (LCKD). Analysis of hepatic glycoproteins by enzyme-linked assay using the lectins UEA-I, ConA, LCA, and WGA showed that the LCKD decreased mature forms of complex-type glycans but increased immature forms of glycans on glycoproteins. An enzyme-linked immunosorbent assay using an anti-α2,6-sialyl LacNAc antibody also supported this result, indicating that dietary carbohydrate restriction results in aberrant glycosylation of tissue glycoproteins. These structural alterations of hepatic glycoproteins were not correlated with the expression levels of glycosyltransferase genes but were correlated with down-regulated expression of the gene, which encodes a rate-limiting enzyme for the synthesis of sugar nucleotide donors for protein glycosylation in the liver. This property differed from glycosphingolipid metabolism in the liver of LCKD-fed mice.
本文所呈现的数据与一篇题为《低碳水化合物生酮饮食通过对神经节苷脂代谢相关基因的转录调控促进神经节苷脂合成》的研究文章相关[1]。本文提供了额外的结构分析数据，用于表征喂食低碳水化合物生酮饮食（LCKD）的小鼠肝脏糖蛋白。使用凝集素UEA-I、ConA、LCA和WGA通过酶联测定法对肝脏糖蛋白进行分析表明，LCKD降低了糖蛋白上复合型聚糖的成熟形式，但增加了聚糖的未成熟形式。使用抗α2,6-唾液酸乳糖胺抗体的酶联免疫吸附测定也支持了这一结果，表明饮食碳水化合物限制导致组织糖蛋白的异常糖基化。肝脏糖蛋白的这些结构改变与糖基转移酶基因的表达水平无关，但与该基因的表达下调相关，该基因编码肝脏中蛋白质糖基化糖核苷酸供体合成的限速酶。这一特性与喂食LCKD的小鼠肝脏中糖鞘脂代谢不同。
