The transcriptional corepressor CtBP2 serves as a metabolite sensor orchestrating hepatic glucose and lipid homeostasis

Biological systems to sense and respond to metabolic perturbations are critical for the maintenance of cellular homeostasis. Here we describe a hepatic system in this context orchestrated by the transcriptional corepressor C-terminal binding protein 2 (CtBP2) that harbors metabolite-sensing capabili...

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Published inNature communications Vol. 12; no. 1; pp. 6315 - 19
Main Authors Sekiya, Motohiro, Kainoh, Kenta, Sugasawa, Takehito, Yoshino, Ryunosuke, Hirokawa, Takatsugu, Tokiwa, Hiroaki, Nakano, Shogo, Nagatoishi, Satoru, Tsumoto, Kouhei, Takeuchi, Yoshinori, Miyamoto, Takafumi, Matsuzaka, Takashi, Shimano, Hitoshi
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 02.11.2021
Nature Publishing Group
Nature Portfolio
Subjects
119/118
38/39
45/15
45/41
45/91
631/337/572
631/443/319/1642
64/60
692/699/317
96/106
96/35
Alcohol Oxidoreductases - genetics
Alcohol Oxidoreductases - metabolism
Animals
Cell Line
Co-Repressor Proteins - genetics
Co-Repressor Proteins - metabolism
Diabetes mellitus
Disease Models, Animal
Fatty liver
Fatty Liver - etiology
Fatty Liver - metabolism
Fatty Liver - pathology
Forkhead protein
FOXO1 protein
Gluconeogenesis
Glucose
Glucose - metabolism
Homeostasis
Humanities and Social Sciences
Humans
Lipid metabolism
Lipids
Lipids - physiology
Lipogenesis
Liver
Liver - metabolism
Liver - pathology
Metabolism
Metabolites
Mice
Mice, Knockout
Mice, Obese
multidisciplinary
NADH
Nicotinamide adenine dinucleotide
Nutrient status
Obesity
Perturbation
Primary Cell Culture
Proteins
Science
Science (multidisciplinary)
Steatosis
Sterol regulatory element-binding protein
Structure-function relationships
Transcription
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Abstract Biological systems to sense and respond to metabolic perturbations are critical for the maintenance of cellular homeostasis. Here we describe a hepatic system in this context orchestrated by the transcriptional corepressor C-terminal binding protein 2 (CtBP2) that harbors metabolite-sensing capabilities. The repressor activity of CtBP2 is reciprocally regulated by NADH and acyl-CoAs. CtBP2 represses Forkhead box O1 (FoxO1)-mediated hepatic gluconeogenesis directly as well as Sterol Regulatory Element-Binding Protein 1 (SREBP1)-mediated lipogenesis indirectly. The activity of CtBP2 is markedly defective in obese liver reflecting the metabolic perturbations. Thus, liver-specific CtBP2 deletion promotes hepatic gluconeogenesis and accelerates the progression of steatohepatitis. Conversely, activation of CtBP2 ameliorates diabetes and hepatic steatosis in obesity. The structure-function relationships revealed in this study identify a critical structural domain called Rossmann fold, a metabolite-sensing pocket, that is susceptible to metabolic liabilities and potentially targetable for developing therapeutic approaches. Sensing of nutrient status coordinates the regulation of liver glucose and lipid metabolism, and is important for metabolic homeostasis. Here the authors report that transcriptional the corepressor CtBP2 can sense nutrient status and coordinate repression of liver glucose and lipid metabolism via Fox01 and SREBP1, respectively.
AbstractList Biological systems to sense and respond to metabolic perturbations are critical for the maintenance of cellular homeostasis. Here we describe a hepatic system in this context orchestrated by the transcriptional corepressor C-terminal binding protein 2 (CtBP2) that harbors metabolite-sensing capabilities. The repressor activity of CtBP2 is reciprocally regulated by NADH and acyl-CoAs. CtBP2 represses Forkhead box O1 (FoxO1)-mediated hepatic gluconeogenesis directly as well as Sterol Regulatory Element-Binding Protein 1 (SREBP1)-mediated lipogenesis indirectly. The activity of CtBP2 is markedly defective in obese liver reflecting the metabolic perturbations. Thus, liver-specific CtBP2 deletion promotes hepatic gluconeogenesis and accelerates the progression of steatohepatitis. Conversely, activation of CtBP2 ameliorates diabetes and hepatic steatosis in obesity. The structure-function relationships revealed in this study identify a critical structural domain called Rossmann fold, a metabolite-sensing pocket, that is susceptible to metabolic liabilities and potentially targetable for developing therapeutic approaches.
Biological systems to sense and respond to metabolic perturbations are critical for the maintenance of cellular homeostasis. Here we describe a hepatic system in this context orchestrated by the transcriptional corepressor C-terminal binding protein 2 (CtBP2) that harbors metabolite-sensing capabilities. The repressor activity of CtBP2 is reciprocally regulated by NADH and acyl-CoAs. CtBP2 represses Forkhead box O1 (FoxO1)-mediated hepatic gluconeogenesis directly as well as Sterol Regulatory Element-Binding Protein 1 (SREBP1)-mediated lipogenesis indirectly. The activity of CtBP2 is markedly defective in obese liver reflecting the metabolic perturbations. Thus, liver-specific CtBP2 deletion promotes hepatic gluconeogenesis and accelerates the progression of steatohepatitis. Conversely, activation of CtBP2 ameliorates diabetes and hepatic steatosis in obesity. The structure-function relationships revealed in this study identify a critical structural domain called Rossmann fold, a metabolite-sensing pocket, that is susceptible to metabolic liabilities and potentially targetable for developing therapeutic approaches. Sensing of nutrient status coordinates the regulation of liver glucose and lipid metabolism, and is important for metabolic homeostasis. Here the authors report that transcriptional the corepressor CtBP2 can sense nutrient status and coordinate repression of liver glucose and lipid metabolism via Fox01 and SREBP1, respectively.
Biological systems to sense and respond to metabolic perturbations are critical for the maintenance of cellular homeostasis. Here we describe a hepatic system in this context orchestrated by the transcriptional corepressor C-terminal binding protein 2 (CtBP2) that harbors metabolite-sensing capabilities. The repressor activity of CtBP2 is reciprocally regulated by NADH and acyl-CoAs. CtBP2 represses Forkhead box O1 (FoxO1)-mediated hepatic gluconeogenesis directly as well as Sterol Regulatory Element-Binding Protein 1 (SREBP1)-mediated lipogenesis indirectly. The activity of CtBP2 is markedly defective in obese liver reflecting the metabolic perturbations. Thus, liver-specific CtBP2 deletion promotes hepatic gluconeogenesis and accelerates the progression of steatohepatitis. Conversely, activation of CtBP2 ameliorates diabetes and hepatic steatosis in obesity. The structure-function relationships revealed in this study identify a critical structural domain called Rossmann fold, a metabolite-sensing pocket, that is susceptible to metabolic liabilities and potentially targetable for developing therapeutic approaches.Sensing of nutrient status coordinates the regulation of liver glucose and lipid metabolism, and is important for metabolic homeostasis. Here the authors report that transcriptional the corepressor CtBP2 can sense nutrient status and coordinate repression of liver glucose and lipid metabolism via Fox01 and SREBP1, respectively.
Sensing of nutrient status coordinates the regulation of liver glucose and lipid metabolism, and is important for metabolic homeostasis. Here the authors report that transcriptional the corepressor CtBP2 can sense nutrient status and coordinate repression of liver glucose and lipid metabolism via Fox01 and SREBP1, respectively.
Biological systems to sense and respond to metabolic perturbations are critical for the maintenance of cellular homeostasis. Here we describe a hepatic system in this context orchestrated by the transcriptional corepressor C-terminal binding protein 2 (CtBP2) that harbors metabolite-sensing capabilities. The repressor activity of CtBP2 is reciprocally regulated by NADH and acyl-CoAs. CtBP2 represses Forkhead box O1 (FoxO1)-mediated hepatic gluconeogenesis directly as well as Sterol Regulatory Element-Binding Protein 1 (SREBP1)-mediated lipogenesis indirectly. The activity of CtBP2 is markedly defective in obese liver reflecting the metabolic perturbations. Thus, liver-specific CtBP2 deletion promotes hepatic gluconeogenesis and accelerates the progression of steatohepatitis. Conversely, activation of CtBP2 ameliorates diabetes and hepatic steatosis in obesity. The structure-function relationships revealed in this study identify a critical structural domain called Rossmann fold, a metabolite-sensing pocket, that is susceptible to metabolic liabilities and potentially targetable for developing therapeutic approaches.Biological systems to sense and respond to metabolic perturbations are critical for the maintenance of cellular homeostasis. Here we describe a hepatic system in this context orchestrated by the transcriptional corepressor C-terminal binding protein 2 (CtBP2) that harbors metabolite-sensing capabilities. The repressor activity of CtBP2 is reciprocally regulated by NADH and acyl-CoAs. CtBP2 represses Forkhead box O1 (FoxO1)-mediated hepatic gluconeogenesis directly as well as Sterol Regulatory Element-Binding Protein 1 (SREBP1)-mediated lipogenesis indirectly. The activity of CtBP2 is markedly defective in obese liver reflecting the metabolic perturbations. Thus, liver-specific CtBP2 deletion promotes hepatic gluconeogenesis and accelerates the progression of steatohepatitis. Conversely, activation of CtBP2 ameliorates diabetes and hepatic steatosis in obesity. The structure-function relationships revealed in this study identify a critical structural domain called Rossmann fold, a metabolite-sensing pocket, that is susceptible to metabolic liabilities and potentially targetable for developing therapeutic approaches.
ArticleNumber 6315
Author Sekiya, Motohiro
Sugasawa, Takehito
Nakano, Shogo
Takeuchi, Yoshinori
Matsuzaka, Takashi
Kainoh, Kenta
Nagatoishi, Satoru
Tsumoto, Kouhei
Miyamoto, Takafumi
Yoshino, Ryunosuke
Shimano, Hitoshi
Hirokawa, Takatsugu
Tokiwa, Hiroaki
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  organization: Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba
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  surname: Matsuzaka
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  organization: Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Transborder Medical Research Center, University of Tsukuba
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  orcidid: 0000-0002-5562-5572
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/34728642$$D View this record in MEDLINE/PubMed
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SSID ssj0000391844
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Snippet Biological systems to sense and respond to metabolic perturbations are critical for the maintenance of cellular homeostasis. Here we describe a hepatic system...
Sensing of nutrient status coordinates the regulation of liver glucose and lipid metabolism, and is important for metabolic homeostasis. Here the authors...
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SourceType Open Website
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Publisher
StartPage 6315
SubjectTerms 119/118
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631/337/572
631/443/319/1642
64/60
692/699/317
96/106
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Alcohol Oxidoreductases - genetics
Alcohol Oxidoreductases - metabolism
Animals
Cell Line
Co-Repressor Proteins - genetics
Co-Repressor Proteins - metabolism
Diabetes mellitus
Disease Models, Animal
Fatty liver
Fatty Liver - etiology
Fatty Liver - metabolism
Fatty Liver - pathology
Forkhead protein
FOXO1 protein
Gluconeogenesis
Glucose
Glucose - metabolism
Homeostasis
Humanities and Social Sciences
Humans
Lipid metabolism
Lipids
Lipids - physiology
Lipogenesis
Liver
Liver - metabolism
Liver - pathology
Metabolism
Metabolites
Mice
Mice, Knockout
Mice, Obese
multidisciplinary
NADH
Nicotinamide adenine dinucleotide
Nutrient status
Obesity
Perturbation
Primary Cell Culture
Proteins
Science
Science (multidisciplinary)
Steatosis
Sterol regulatory element-binding protein
Structure-function relationships
Transcription
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Title The transcriptional corepressor CtBP2 serves as a metabolite sensor orchestrating hepatic glucose and lipid homeostasis
URI https://link.springer.com/article/10.1038/s41467-021-26638-5
https://www.ncbi.nlm.nih.gov/pubmed/34728642
https://www.proquest.com/docview/2591866933
https://www.proquest.com/docview/2593027634
https://pubmed.ncbi.nlm.nih.gov/PMC8563733
https://doaj.org/article/996f1a434a0445a0ba8691377b30fab1
Volume 12
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