Endogenous circadian system and circadian misalignment impact glucose tolerance via separate mechanisms in humans.
Level 2 - randomized trial
Controlled human laboratory intervention trial
PubMed 25870289 · doi:10.1073/pnas.1418955112
What was done
Healthy adults completed two 8-day laboratory protocols designed to separate the independent effects of endogenous circadian phase, behavioral cycles (sleep/wake and fasting/feeding), and circadian disruption (a 12-hour behavioral cycle inversion). The researchers measured postprandial glucose and insulin dynamics, polysomnographic sleep, and 24-hour hormonal profiles.
What was found
Postprandial glucose was 17% higher in the biological evening (8:00 PM) compared to the biological morning (8:00 AM) independent of behavioral cycles, accompanied by 27% lower early-phase insulin. Independently, circadian misalignment (12-hour behavioral cycle inversion) increased postprandial glucose by 6% despite 14% higher late-phase insulin and no change in early-phase insulin.
Why it matters
This study demonstrates that evening glucose intolerance is driven directly by endogenous circadian rhythmicity via reduced beta-cell response, whereas circadian misalignment independently impairs glucose tolerance via reduced insulin sensitivity, providing distinct mechanistic pathways for elevated diabetes risk in shift workers.
Limits
The abstract does not disclose the sample size, participant demographics (such as age or sex distribution), or statistical variance/p-values. Testing occurred under acute, highly controlled inpatient conditions in healthy adults, which may not capture chronic shift-work adaptations or responses in populations with underlying metabolic dysfunction.
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