ArticleEMBO reports2023
Hepatic ZBTB22 promotes hyperglycemia and insulin resistance via PEPCK1-driven gluconeogenesis.
Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- The Role of the Major Histocompatibility Complex Region on Chromosome 6 in Skin Atrophy: A Mendelian Randomization Study.Journal of cosmetic dermatology · 2025Article
- A comprehensive analysis of allele-specific expression and transcriptomic profiling in pig limbic and endocrine tissues.Frontiers in molecular neuroscience · 2025Article
- PCK1 as a target for cancer therapy: from metabolic reprogramming to immune microenvironment remodeling.Cell death discovery · 2024Review
- Sinensetin Attenuated Macrophagic NLRP3 Inflammasomes FormationACS omega · 2023Article
- Hepatic Clstn3 Ameliorates Lipid Metabolism Disorders in High Fat Diet-Induced NAFLD through Activation of FXR.ACS omega · 2023Article
- Hepatic ZBTB22 promotes hyperglycemia and insulin resistance via PEPCK1-driven gluconeogenesis.EMBO reports · 2023Article
- Exploring the pathogenesis of colorectal carcinoma complicated with hepatocellular carcinoma via microarray data analysis.Frontiers in pharmacology · 2023Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive gluconeogenesis can lead to hyperglycemia and diabetes through as yet incompletely understood mechanisms. Herein, we show that hepatic ZBTB22 expression is increased in both diabetic clinical samples and mice, being affected by nutritional status and hormones. Hepatic ZBTB22 overexpression increases the expression of gluconeogenic and lipogenic genes, heightening glucose output and lipids accumulation in mouse primary hepatocytes (MPHs), while ZBTB22 knockdown elicits opposite effects. Hepatic ZBTB22 overexpression induces glucose intolerance and insulin resistance, accompanied by moderate hepatosteatosis, while ZBTB22-deficient mice display improved energy expenditure, glucose tolerance, and insulin sensitivity, and reduced hepatic steatosis. Moreover, hepatic ZBTB22 knockout beneficially regulates gluconeogenic and lipogenic genes, thereby alleviating glucose intolerance, insulin resistance, and liver steatosis in db/db mice. ZBTB22 directly binds to the promoter region of PCK1 to enhance its expression and increase gluconeogenesis. PCK1 silencing markedly abolishes the effects of ZBTB22 overexpression on glucose and lipid metabolism in both MPHs and mice, along with the corresponding changes in gene expression. In conclusion, targeting hepatic ZBTB22/PEPCK1 provides a potential therapeutic approach for diabetes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.