Hyperadrenocorticism of calorie restriction contributes to its anti-inflammatory action in mice.
Level 5 - mechanism / opinion, no new human data
Animal research
PubMed 30938024 · doi:10.1111/acel.12944
What was done
Researchers tested whether the moderate hyperadrenocorticism associated with calorie restriction (CR; 60% of ad libitum [AL] intake) mediates its anti-inflammatory effects. Using glucocorticoid-deficient corticotropin-releasing-hormone knockout (CRHKO) mice and wild-type (WT) littermates, they evaluated four control groups (WT and CRHKO mice fed AL or CR diets) and three experimental groups: AL-fed CRHKO mice supplemented with corticosterone (CORT) titrated to match 24-hr plasma levels of AL-fed WT mice, CR-fed CRHKO mice given CORT matching AL-fed WT levels, and CR-fed CRHKO mice given CORT matching CR-fed WT levels. Inflammation was assessed volumetrically via carrageenan-induced footpad edema.
What was found
The abstract reports directions of effect without numerical values or variance statistics. CR attenuated carrageenan-induced footpad edema in WT mice. This attenuation was significantly blocked in CORT-deficient CR-fed CRHKO mice. Restoring CORT in CR-fed CRHKO mice to the elevated levels seen in CR-fed WT mice restored the anti-inflammatory effect of CR, whereas CORT titrated to AL-fed WT levels did not.
Why it matters
This study identifies elevated glucocorticoids as an essential endocrine mediator linking calorie restriction to reduced peripheral inflammation in mice.
Limits
Findings are limited to an acute local chemical injury model (carrageenan edema) in rodents and may not translate to chronic inflammatory states or human physiology. Total animal counts (n), sample sizes per group, and exact numerical measurements are not provided in the abstract.
Cited by
- supports Animals placed on calorie restriction or intermittent fasting have elevated cortisol/corticosterone levels despite living longer.