Original citation: J Clin Invest. 2017;127(11):4059–4074. https://doi.org/10.1172/JCI94585

Citation for this corrigendum: J Clin Invest. 2018;128(3):1199. https://doi.org/10.1172/JCI99009

Following publication of this article, the authors became aware that reference 22 was not accurately described in Results. The corrected paragraph that pertains to this reference appears below.

ChREBP has many overlapping functions with SREBP1c, as both have been reported to increase expression of lipogenic genes, such as Fasn and Acaca (20). ChREBP has also been shown to induce fibroblast growth factor 21 (Fgf21), which can regulate fatty acid oxidation (21). In the current study, we observed increased expression of fatty acid oxidation genes in animals fed HFD+Gluc compared with HFD+Fruct in concert with increased expression of total ChREBP (Figures 3D and 4D). However, ChREBP has actually been shown to decrease expression of the key fatty acid oxidation gene CPT1a (22), and our study did not include measures of direct transcriptional activation. Thus, the general increase in fatty acid oxidation genes observed with feeding of HFD+Gluc, including increases in carnitine palmitoyltransferase 2 (Cpt2), family member 12, medium, long, and very long chain acyl–coenzyme A dehydrogenase (Acad12, Acadm, Acadl, Acadvl), acetyl–coenzyme A acyltransferase 2 (Acaa2), and the α and β subunits of hydroxyacyl–coenzyme A dehydrogenase (Hadha and Hadhb), cannot be ascribed to ChREBP. Further studies will be required to fully understand the relevant regulatory networks mediating increased expression of enzymes regulating fatty acid oxidation in mice on HFD+Gluc. However, what is clear is that glucose as compared to fructose supplementation of HFD induces very different programs of metabolic regulation in liver, reflecting both complex transcriptional and posttranscriptional regulation.

During the preparation of the manuscript, Figure 2D was inadvertently mislabeled by the journal. The corrected figure part is below.

The authors regret the error.

Footnotes

See the related article at Divergent effects of glucose and fructose on hepatic lipogenesis and insulin signaling.

原始引文：J Clin Invest。2017; 127（11）：4059–4074。https://doi.org/10.1172/JCI94585

该勘误的引文：J Clin Invest。2018; 128（3）：1199。https://doi.org/10.1172/JCI99009

在本文发表后，作者意识到参考文献22在“结果”中的描述不正确。与该参考文献相关的更正段落如下所示。

ChREBP基因与SREBP1c许多重叠的功能，因为这两个已经被报道提高脂肪生成基因，如表达FASN和ACACA（20）。ChREBP还显示出可诱导成纤维细胞生长因子21（Fgf21），该因子可调节脂肪酸氧化（21）。在当前的研究中，我们观察到与HFD + Fruct相比，喂食HFD + Gluc的动物中脂肪酸氧化基因的表达增加，同时总ChREBP的表达增加（图3D和4D）。但是，实际上已显示ChREBP会降低关键脂肪酸氧化基因CPT1a的表达（22），并且我们的研究未包括直接转录激活的量度。因此，在脂肪酸氧化基因的普遍增加与HFD + GLUC的馈送，包括增加在肉碱棕榈2（观察CPT2），家庭成员12，中，长和非常长链酰基辅酶A脱氢酶（Acad12，ACADM，Acadl，Acadvl），乙酰辅酶A酰基转移酶2（Acaa2）以及羟酰基辅酶A脱氢酶的α和β亚基（Hadha和Hadhb），不能归因于ChREBP。需要进一步研究以充分了解相关的调节网络，其介导在HFD + Gluc上的小鼠中调节脂肪酸氧化的酶的表达增加。然而，很清楚的是，与补充果糖相比，葡萄糖对人体健康的影响很大，肝脏代谢调节的程序不同，反映了复杂的转录和转录后调节。

在手稿的准备过程中，图2D被日记误贴了标签。更正的图形部分如下。

作者对这个错误感到遗憾。

脚注

请参阅有关葡萄糖和果糖对肝脏脂肪生成和胰岛素信号传导的发散作用的相关文章。