Lowers liver sugar
Hepatic glucose↓
Also searched as Hepatic glucose.
You want it restrained: reining in excess hepatic glucose output steadies fasting glycemia.
In depth
Hepatic gluconeogenesis — the liver's manufacture of new glucose, which sets fasting blood-sugar.
What drives it
Bile acid hormone reduces it.
Potthoff 2011, Cell Metab 13:729 — FGF15/19 represses hepatic gluconeogenesis by inhibiting the CREB–PGC-1α pathway (lowering PEPCK and G6Pase), independent of insulin. Human liver biopsies with a striking threshold: in class-III obese patients undergoing bariatric surgery, those with type 2 diabetes had lower serum FGF19 and higher FGF21; and when FGF19 was below 200 and FGF21 above 500, 91 percent of patients had diabetes. The signaling arm is intact too — FGF19 acts through FGFR4 and beta-klotho in hepatocytes, and CYP7A1, beta-Klotho, FGFR4 and HNF4-alpha expression differed between patients who did and did not remit diabetes after surgery. But the evidence here is cross-sectional and CASE/CONTROL: it establishes that FGF19 is low in diabetes and that the pathway is dysregulated, not that FGF19 directly represses gluconeogenic transcription. That specific step is asserted in the wider literature but is not demonstrated in the source read here. Treat the direction as supported, the mechanism as not yet evidenced at this pathway.
Energy sensing reduces it.
10.3389/fendo.2018.00802 — Foretz 2005, Diabetes 54:1331 — a constitutively active AMPKα2 in liver represses PEPCK and G6Pase, suppressing hepatic gluconeogenesis. Metformin is not an NAD+ booster. doi 10.3389/fendo.2018.00802
What it drives
It increases Blood-sugar support.
Hepatic-glucose review 2017, Nat Rev Endocrinol — dysregulated hepatic gluconeogenesis is a major contributor to fasting and postprandial hyperglycemia; gluconeogenic rate tracks fasting blood glucose, worsening glycemic control. doi:10.1038/nrendo.2017.80. Increased hepatic gluconeogenesis is named as one of the main contributors to the development of type 2 diabetes, and fasting hyperglycemia in T2D specifically reflects the lack of inhibition of gluconeogenesis and glycogenolysis under insulin resistance. The two rate-limiting enzymes, PEPCK and glucose-6-phosphatase, show elevated expression and activity in T2D patients. The first-line drug is the proof: metformin exerts its primary glucose-lowering effect by reducing hepatic gluconeogenesis — the most-prescribed oral agent in the world works on this edge. Why morning glucose is the tell: gluconeogenesis is what holds blood glucose through a prolonged fast, so its dysregulation shows up as fasting glucose before it shows up after meals. doi 10.1038/nrendo.2017.80.
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.