Liver and kidney metabolism during prolonged starvation.
Level 4 - case-series / case-control
Uncontrolled physiological case series in a small cohort without a control group.
PubMed 5773093 · doi:10.1172/JCI106016
What was done
Circulating concentrations of insulin, growth hormone, glucose, free fatty acids, glycerol, beta-hydroxybutyrate, acetoacetate, and alpha-amino nitrogen were measured in 11 obese subjects during prolonged starvation. In 5 of these subjects, the sites and estimated rates of gluconeogenesis and ketogenesis were quantified across the liver and kidneys after 5 to 6 weeks of fasting using organ substrate balances.
What was found
Blood glucose and insulin concentrations fell acutely during the first 3 days of fasting, and alpha-amino nitrogen fell after 17 days. Free fatty acids, beta-hydroxybutyrate, and acetoacetate did not reach a plateau until after 17 days. Estimated total glucose production at 5 to 6 weeks of starvation decreased to approximately 86 g/24 hr, with the liver contributing about one-half and the kidneys contributing the remainder. Nearly all lactate, pyruvate, glycerol, and amino acid carbons extracted by the liver and kidneys were converted to glucose.
Why it matters
This study established that the kidneys become an equal partner to the liver in endogenous gluconeogenesis during prolonged starvation.
Limits
The sample size was very small (n = 11 overall, n = 5 for renal and hepatic catheterization), restricted exclusively to obese subjects undergoing therapeutic fasting, and lacked a non-obese control group. The abstract does not report variance metrics or exact baseline vs final numerical concentrations for circulating hormones and substrates.
Cited by
- supports In 40-day water-only fasting experiments conducted at Harvard, blood ketone levels rose to 5-7 mM and glucose stabilized at 3-4 mM (60-70 mg/dL) within approximately 7 days and remained there for the duration.