Adenovirus-mediated overexpression of Tcfe3 ameliorates hyperglycaemia in a mouse model of diabetes by upregulating glucokinase in the liver

Kim, M. Y.; Jo, Seong Ho; Park, J. M.; Kim, T. H.; Im, Seung‐Soon; Ahn, Young Soo

doi:10.1007/s00125-012-2807-7

Cited by 12 publications

(7 citation statements)

References 31 publications

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“…Previous studies using TFE3 transgenic mice showed that TFE3 is capable of activating genes involved in energy metabolism processes including glycolysis and insulin signalling (Nakagawa et al , ; Fujimoto et al , ; Kim et al , ; Xiong et al , ). However, as these studies were limited to overexpression, the physiological role of TFE3 has remained elusive.…”

Section: Discussionmentioning

confidence: 99%

TFE 3 regulates whole‐body energy metabolism in cooperation with TFEB

et al. 2017

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TFE3 and TFEB are members of the MiT family of HLH–leucine zipper transcription factors. Recent studies demonstrated that they bind overlapping sets of promoters and are post‐transcriptionally regulated through a similar mechanism. However, while Tcfeb knockout (KO) mice die during early embryonic development, no apparent phenotype was reported in Tfe3 KO mice. Thus raising the need to characterize the physiological role of TFE3 and elucidate its relationship with TFEB. TFE3 deficiency resulted in altered mitochondrial morphology and function both in vitro and in vivo due to compromised mitochondrial dynamics. In addition, Tfe3 KO mice showed significant abnormalities in energy balance and alterations in systemic glucose and lipid metabolism, resulting in enhanced diet‐induced obesity and diabetes. Conversely, viral‐mediated TFE3 overexpression improved the metabolic abnormalities induced by high‐fat diet (HFD). Both TFEB overexpression in Tfe3 KO mice and TFE3 overexpression in Tcfeb liver‐specific KO mice (Tcfeb LiKO) rescued HFD‐induced obesity, indicating that TFEB can compensate for TFE3 deficiency and vice versa. Analysis of Tcfeb LiKO/Tfe3 double KO mice demonstrated that depletion of both TFE3 and TFEB results in additive effects with an exacerbation of the hepatic phenotype. These data indicate that TFE3 and TFEB play a cooperative, rather than redundant, role in the control of the adaptive response of whole‐body metabolism to environmental cues such as diet and physical exercise.

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Section: Discussionmentioning

confidence: 99%

TFE 3 regulates whole‐body energy metabolism in cooperation with TFEB

et al. 2017

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“…Promoter analysis revealed the overexpression of TFE3 could also enhance the expression of hexokinase 2 (HKII) and liver-type glucokinase in hepatocytes. Simultaneously, some studies revealed that these two genes were downstream targets of TFE3 [18,25]. The nuclear receptor, REV-ERBα, is involved in lipid, bile acid, and glucose metabolism in the liver.…”

Section: Tfe3 Can Regulate the Daily Metabolism Of Hepatocytes By Reg...mentioning

confidence: 97%

Emerging roles of TFE3 in metabolic regulation

Chen

Gong

et al. 2023

Cell Death Discov.

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TFE3 is a member of the MiT family of the bHLH-leucine zipper transcription factor. We previously focused on the role of TFE3 in autophagy and cancer. Recently, an increasing number of studies have revealed that TFE3 plays an important role in metabolic regulation. TFE3 participates in the metabolism of energy in the body by regulating pathways such as glucose and lipid metabolism, mitochondrial metabolism, and autophagy. This review summarizes and discusses the specific regulatory mechanisms of TFE3 in metabolism. We determined both the direct regulation of TFE3 on metabolically active cells, such as hepatocytes and skeletal muscle cells, and the indirect regulation of TFE3 through mitochondrial quality control and the autophagy–lysosome pathway. The role of TFE3 in tumor cell metabolism is also summarized in this review. Understanding the diverse roles of TFE3 in metabolic processes can provide new avenues for the treatment of some metabolism-related disorders.

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“…Subsequent to this study, we hypothesized that transcription factor E3 (TFE3) could be able to up-regulate Gck because TFE3 was shown to up-regulate genes of insulin signaling pathway [15]. Using adenoviral transduction of TFE3, we demonstrated the presence of TFE3 binding site (E-box) in the Gck and TFE3 up-regulates Gck with amelioration of hyperglycemia in the db/db and ob/ob mice [16]. Fig.…”

Section: Srebp-1c and Glucose Metabolismmentioning

confidence: 99%

A Journey to Understand Glucose Homeostasis: Starting from Rat Glucose Transporter Type 2 Promoter Cloning to Hyperglycemia

Ahn

2018

Diabetes Metab J

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My professional journey to understand the glucose homeostasis began in the 1990s, starting from cloning of the promoter region of glucose transporter type 2 (GLUT2) gene that led us to establish research foundation of my group. When I was a graduate student, I simply thought that hyperglycemia, a typical clinical manifestation of type 2 diabetes mellitus (T2DM), could be caused by a defect in the glucose transport system in the body. Thus, if a molecular mechanism controlling glucose transport system could be understood, treatment of T2DM could be possible. In the early 70s, hyperglycemia was thought to develop primarily due to a defect in the muscle and adipose tissue; thus, muscle/adipose tissue type glucose transporter (GLUT4) became a major research interest in the diabetology. However, glucose utilization occurs not only in muscle/adipose tissue but also in liver and brain. Thus, I was interested in the hepatic glucose transport system, where glucose storage and release are the most actively occurring.

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Adenovirus-mediated overexpression of Tcfe3 ameliorates hyperglycaemia in a mouse model of diabetes by upregulating glucokinase in the liver

Cited by 12 publications

References 31 publications

TFE 3 regulates whole‐body energy metabolism in cooperation with TFEB

TFE 3 regulates whole‐body energy metabolism in cooperation with TFEB

Emerging roles of TFE3 in metabolic regulation

A Journey to Understand Glucose Homeostasis: Starting from Rat Glucose Transporter Type 2 Promoter Cloning to Hyperglycemia

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