Hepatic ZBTB22 promotes hyperglycaemia and insulin resistance via PEPCK1-driven gluconeogenesis

ABSTRACT: Excessive gluconeogenesis can lead to hyperglycaemia 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 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 benef

SUBMITTER: Dr. Naihua Liu 

PROVIDER: S-SCDT-10_15252-EMBR_202256390 | biostudies-other |

REPOSITORIES: biostudies-other