Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake.
Level 5 - mechanism / opinion, no new human data
Animal research (preclinical mouse model)
PubMed 12724520 · doi:10.1073/pnas.1035720100
What was done
C57BL6 mice were maintained on an intermittent fasting (alternate-day fasting) regimen to evaluate its effects on overall food intake, body weight, glucose metabolism, and neuronal vulnerability. Serum glucose and insulin levels were assessed, along with brain neuronal resistance to excitotoxic stress.
What was found
The abstract reports no numerical values, sample sizes, or effect sizes. Qualitatively, intermittent fasting did not decrease overall food intake and maintained body weight. Intermittent fasting resulted in reduced serum glucose and insulin levels and increased resistance of brain neurons to excitotoxic stress, matching or exceeding effects typically attributed to caloric restriction.
Why it matters
This study demonstrates in a mouse model that the metabolic and neuroprotective benefits of dietary restriction can occur through meal timing and fasting intervals independently of net calorie reduction.
Limits
The study was conducted entirely in mice, preventing direct clinical extrapolation to humans. The abstract omits sample sizes, experimental durations, and exact numerical measurements for glucose, insulin, or neuronal survival.
Cited by
- supports In mice on every-other-day fasting that maintain normal body weight and calorie intake by eating double on feeding days, intermittent fasting independently protects hippocampal neurons against epileptic seizures.