Splanchnic regulation of glucose production.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing physiological mechanisms without primary empirical data or systematic review methodology
PubMed 17465853 · doi:10.1146/annurev.nutr.27.061406.093806
What was done
This paper is a narrative review describing the physiological and pathophysiological mechanisms governing splanchnic and hepatic glucose production in healthy states (fasting, postprandial, exercise) and in diabetes.
What was found
The abstract reports physiological principles without primary statistical comparisons or effect sizes. In overnight fasting, glycogenolysis and gluconeogenesis contribute roughly equally to hepatic glucose production. Hepatic glycogen is depleted after 36 to 48 hours of fasting, after which gluconeogenesis sustains output. Short-term intense exercise utilizes hepatic glycogenolysis, whereas prolonged exercise relies progressively on gluconeogenesis in response to falling insulin and rising glucagon. Both type 1 and type 2 diabetes feature enhanced hepatic gluconeogenesis and increased hepatic glucose production.
Why it matters
It provides a consolidated conceptual framework for how the liver balances glycogen breakdown and de novo glucose synthesis under varied metabolic demands and in diabetic hyperglycemia.
Limits
As a narrative review, it presents no primary clinical data, quantitative statistical estimates, sample sizes, or systematic review methodology.
Cited by
- context It takes approximately 10 to 12 hours of fasting for the liver to deplete glycogen stores and initiate the metabolic switch to ketosis.