Issue: May 2018
March 23, 2018
1 min read
Save

Dual-hormone clamp mediates effects of sleep restriction on insulin resistance

Issue: May 2018
You've successfully added to your alerts. You will receive an email when new content is published.

Click Here to Manage Email Alerts

We were unable to process your request. Please try again later. If you continue to have this issue please contact customerservice@slackinc.com.

Peter Liu
Peter Y. Liu

CHICAGO — The negative effect of sleep restriction on glucose metabolism was reduced during a dual-hormone clamp intervention of testosterone and cortisol in young men, according to a presenter here.

“Insufficient sleep reduces testosterone and increases cortisol,” Peter Y. Liu, MBBS, PhD, professor of medicine with the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center in Torrance, Calif., told Endocrine Today. “This testosterone-cortisol imbalance leads to an anabolic-catabolic imbalance and the development of insulin resistance.”

Liu and colleagues conducted a dual-hormone clamp intervention on 34 healthy men (mean age, 33.3 years; mean BMI, 25.4 kg/m2) to determine whether testosterone and cortisol affect insulin resistance due to sleep restriction. Researchers conducted 5 nights of sleep studies and controlled what the participants ate and how much they slept. Participants were permitted to sleep 10 hours the first night and were restricted to 4 hours per night for the remaining 4 nights on two separate occasions; during the first occasion, participants underwent a testosterone-cortisol clamp and during the second, matching placebo. After the baseline night and the fourth night of sleep restriction, participants underwent a 3-hour OGTT to calculate insulin resistance.

In both conditions, Matsuda Index revealed greater insulin resistance after sleep restriction; however, the increase was dampened during the clamp condition compared with placebo (P = .029 for interaction). Similar patterns were observed for insulin area under the curve (AUC; P = .012) and insulin/glucose AUC ratio (P = .022).

“Manipulating the specific downstream molecular mediators of the testosterone-cortisol imbalance that cause insulin resistance could lead to novel methods to prevent the metabolic sequalae of insufficient sleep, such as prediabetes or type 2 diabetes, without requiring more sleep,” Liu told Endocrine Today. “[Research moving forward needs to] identify these downstream mediators. Also, although we discovered a hormone mechanism by which insufficient sleep leads to insulin resistance, there are other mechanisms at play. We need to work to work out what these other mechanisms are.” – by Amber Cox

Reference:

Sidebottom DH, et al. OR15-3. Presented at: The Endocrine Society Annual Meeting; March 17-20, 2018; Chicago.

Disclosures: The authors report no relevant financial disclosures.