ATF3 expression is induced by low glucose in pancreatic α and  	β cells and regulates glucagon but not insulin gene transcription

Lee, Yong-Soo; Kobayashi, Masaki; Kikuchi, Osamu; Sasaki, Tsutomu; Yokota-Hashimoto, Hiromi; Susanti, Vina Yanti; Kitamura, Yoichi; Kitamura, Tadahiro

doi:10.1507/endocrj.ej13-0383

Cited by 13 publications

(14 citation statements)

References 12 publications

(33 reference statements)

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“…41 Conversely, a study in pancreatic cell lines found that ATF3 increased glucagon transcription, but had no effect on insulin transcription. 42 In support of this finding, Wang et al . 43 discovered an alternatively spliced isoform of ATF3, named ATF3b, which binds to the ATF/CRE site on the proglucagon gene promoter and increases its transcription.…”

Section: Role Of Atf3 In Maintenance Of Normal Glucose Homeostasismentioning

confidence: 77%

Activating transcription factor 3 in immune response and metabolic regulation

Jadhav

Zhang

2017

Liver Research

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Activating transcription factor 3 (ATF3) is a member of the ATF/cAMP-response element binding protein (CREB) family of transcription factors. In response to stress stimuli, ATF3 forms dimers to activate or repress gene expression. Further, ATF3 modulates the immune response, atherogenesis, cell cycle, apoptosis, and glucose homeostasis. Recent studies have shown that ATF3 may also be involved in pathogenesis of other diseases. However, more studies are needed to determine the role of ATF3 in metabolic regulation.

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Section: Role Of Atf3 In Maintenance Of Normal Glucose Homeostasismentioning

confidence: 77%

Activating transcription factor 3 in immune response and metabolic regulation

Jadhav

Zhang

2017

Liver Research

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“…ATF3 expression is upregulated by low glucose and downregulated by high glucose in bothαTC-1.6 and ßTC3 cells. ATF3 increases the transcription of glucagon but not that of insulin (30). Zmuda et al (31) showed that ATF3 KO islets are protected from three stress models, including islet isolation, treatment of inflammatory cytokines, and hypoxia.…”

Section: Role Of Atf3 In Glucose Metabolismmentioning

confidence: 99%

Master Regulator Activating Transcription Factor 3 (ATF3) in Metabolic Homeostasis and Cancer

2020

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Activating transcription factor 3 (ATF3) is a stress-induced transcription factor that plays vital roles in modulating metabolism, immunity, and oncogenesis. ATF3 acts as a hub of the cellular adaptive-response network. Multiple extracellular signals, such as endoplasmic reticulum (ER) stress, cytokines, chemokines, and LPS, are connected to ATF3 induction. The function of ATF3 as a regulator of metabolism and immunity has recently sparked intense attention. In this review, we describe how ATF3 can act as both a transcriptional activator and a repressor. We then focus on the role of ATF3 and ATF3-regulated signals in modulating metabolism, immunity, and oncogenesis. The roles of ATF3 in glucose metabolism and adipose tissue regulation are also explored. Next, we summarize how ATF3 regulates immunity and maintains normal host defense. In addition, we elaborate on the roles of ATF3 as a regulator of prostate, breast, colon, lung, and liver cancers. Further understanding of how ATF3 regulates signaling pathways involved in glucose metabolism, adipocyte metabolism, immuno-responsiveness, and oncogenesis in various cancers, including prostate, breast, colon, lung, and liver cancers, is then provided. Finally, we demonstrate that ATF3 acts as a master regulator of metabolic homeostasis and, therefore, may be an appealing target for the treatment of metabolic dyshomeostasis, immune disorders, and various cancers.

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“…Tissues were sectioned and stained with anti-glucagon (G2654, Sigma, USA) and antiinsulin antibodies (A0564, Dako, USA). We visualized immune complexes with fluorescein isothiocyanate-or Cy3-conjugated secondary antibodies [12].…”

Section: Insr Overexpression In Db/db Mice Does Not Rescue Bone Defecmentioning

confidence: 99%

Overexpression of insulin receptor partially improves obese and diabetic phenotypes in <i>db/db</i> mice

et al. 2015

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THERE are 347 million diabetic patients worldwide and 95 % of them are type 2 diabetes mellitus (T2DM), hallmarks of which are impaired secretion and action of insulin [1,2]. Several treatment options for T2DM are in clinical use, including injecting insulin, promoting insulin secretion by insulin secretagogues (such as sulfonylureas and glinides), and improving insulin sensitivity by insulin sensitizers (such as biguanides and thiazolidinediones). However, increasing the amount of insulin receptor in insulin-target tissues has not been explored.Insulin exerts its physiological effects through insulin receptors by binding to the alpha subunit of insulin receptor and stimulating the intrinsic kinase activity of the beta subunit [3][4][5]. However, chronic exposure of cells to insulin leads to down-regulation of insulin signaling through a net loss of insulin receptor from the plasma membrane [6], which is one of the mechanisms involved in insulin resistance. Therefore, increasing the amount of insulin receptor could alleviate insulin resistance. Leptin is an adipokine crucial for the regulation of energy homeostasis [7]. A homozygous loss-of-function mutation in the leptin receptor (the db mutation) causes hyperphagia and obesity, leading to diabetes in mice [8,9]. Since obesity is a major risk factor for impaired insulin sensitivity and T2DM, db/db mice are used as a genetic model of T2DM.

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ATF3 expression is induced by low glucose in pancreatic α and β cells and regulates glucagon but not insulin gene transcription

Cited by 13 publications

References 12 publications

Activating transcription factor 3 in immune response and metabolic regulation

Activating transcription factor 3 in immune response and metabolic regulation

Master Regulator Activating Transcription Factor 3 (ATF3) in Metabolic Homeostasis and Cancer

Overexpression of insulin receptor partially improves obese and diabetic phenotypes in <i>db/db</i> mice

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