Twenty-eight-day bed rest with hypercortisolemia induces peripheral insulin resistance and increases intramuscular triglycerides.
Level 4 - case-series / case-control
Uncontrolled pre-post experimental study in a single small human cohort.
PubMed 19919871 · doi:10.1016/j.metabol.2009.09.014
What was done
Six young, healthy volunteers were subjected to 28 days of bed rest with oral hydrocortisone administration to maintain hypercortisolemia (20-24 mg/dL). On days 1 and 28, leg insulin sensitivity was evaluated using a local two-stage hyperinsulinemic-euglycemic clamp via femoral arterial insulin infusion (stage 1: 35 microU/min per mL of leg; stage 2: 70 microU/min per mL of leg). Intramuscular lipid content was measured using magnetic resonance spectroscopy.
What was found
Leg glucose uptake during hyperinsulinemia decreased from 9.1 ± 1.3 to 5.2 ± 0.7 mg/kg of leg per minute (mean ± SEM, P = .015). Intramuscular triglyceride signal area ratio increased from 0.077 ± 0.011 to 0.136 ± 0.018 (P = .009). Intramuscular lipid content inversely correlated with glucose uptake at day 28 (R = -0.85, P = .035).
Why it matters
The findings demonstrate that concurrent inactivity and elevated cortisol directly promote peripheral insulin resistance and intramuscular lipid accumulation in healthy human muscle.
Limits
The sample size is very small (n = 6). There were no comparator groups (such as bed rest alone or hypercortisolemia alone) to separate the independent effects of inactivity and cortisol. Participant sex and long-term recovery were not reported.
Cited by
- supports Hypercortisolemia impairs insulin sensitivity and glucose disposal.