Hepatic Glucocorticoid Receptor Action and Glucose Homeostasis.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic, in vitro, and animal research with no new human data.
PubMed 40892984 · doi:10.1210/endrev/bnaf030
What was done
This is a narrative review summarizing the molecular and cellular mechanisms of hepatic glucocorticoid receptor (GR) signaling in glucose homeostasis. The authors reviewed literature on GR-mediated transcription of glucose-regulating genes, primary hepatic target genes, transcriptional coregulators, signaling pathways activated by chronic glucocorticoid exposure, metabolic findings from liver-specific GR knockout mouse models, and determinants of individual glucocorticoid sensitivity.
What was found
The abstract reports no quantitative empirical data. It describes the transcriptional mechanisms by which hepatic GR regulates glucose metabolism, how chronic glucocorticoid exposure induces hyperglycemia and insulin resistance, and the metabolic alterations observed in liver-specific GR knockout models alongside inter-individual variation in glucocorticoid response.
Why it matters
Understanding the transcriptional pathways of hepatic GR signaling clarifies how glucocorticoid therapy produces adverse metabolic effects like hyperglycemia and insulin resistance, informing efforts to develop targeted therapies with reduced metabolic side effects.
Limits
This is a narrative review containing no primary data, quantitative synthesis, or systematic search protocol. Much of the reviewed evidence is derived from preclinical animal models and molecular assays, which may not translate directly to human clinical outcomes.
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