Next Article in Journal
Reported Energy Intake Accuracy Compared to Doubly Labeled Water and Usability of the Mobile Food Record among Community Dwelling Adults
Previous Article in Journal
Dietary Protein and Amino Acid Supplementation in Inflammatory Bowel Disease Course: What Impact on the Colonic Mucosa?
Previous Article in Special Issue
The Impact of Shiftwork on Skeletal Muscle Health
Article Menu
Issue 3 (March) cover image

Export Article

Open AccessArticle
Nutrients 2017, 9(3), 311; doi:10.3390/nu9030311

Serum Amyloid A Production Is Triggered by Sleep Deprivation in Mice and Humans: Is That the Link between Sleep Loss and Associated Comorbidities?

1
Departamento de Análises Clínicas e Toxicológicas, Universidade de São Paulo, Av. Prof. Lineu Prestes, 580, São Paulo SP 05509-000, Brazil
2
Departamento de Psicobiologia, Universidade Federal de São Paulo, Rua Napoleão de Barros, 925, São Paulo SP 04024-002, Brazil
*
Author to whom correspondence should be addressed.
Received: 29 November 2016 / Revised: 7 March 2017 / Accepted: 16 March 2017 / Published: 21 March 2017
View Full-Text   |   Download PDF [1095 KB, uploaded 21 March 2017]   |  

Abstract

Serum amyloid A (SAA) was recently associated with metabolic endotoxemia, obesity and insulin resistance. Concurrently, insufficient sleep adversely affects metabolic health and is an independent predisposing factor for obesity and insulin resistance. In this study we investigated whether sleep loss modulates SAA production. The serum SAA concentration increased in C57BL/6 mice subjected to sleep restriction (SR) for 15 days or to paradoxical sleep deprivation (PSD) for 72 h. Sleep restriction also induced the upregulation of Saa1.1/Saa2.1 mRNA levels in the liver and Saa3 mRNA levels in adipose tissue. SAA levels returned to the basal range after 24 h in paradoxical sleep rebound (PSR). Metabolic endotoxemia was also a finding in SR. Increased plasma levels of SAA were also observed in healthy human volunteers subjected to two nights of total sleep deprivation (Total SD), returning to basal levels after one night of recovery. The observed increase in SAA levels may be part of the initial biochemical alterations caused by sleep deprivation, with potential to drive deleterious conditions such as metabolic endotoxemia and weight gain. View Full-Text
Keywords: sleep curtailment; sleep loss; obesity; type 2 diabetes; SAA sleep curtailment; sleep loss; obesity; type 2 diabetes; SAA
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

de Oliveira, E.M.; Visniauskas, B.; Tufik, S.; Andersen, M.L.; Chagas, J.R.; Campa, A. Serum Amyloid A Production Is Triggered by Sleep Deprivation in Mice and Humans: Is That the Link between Sleep Loss and Associated Comorbidities? Nutrients 2017, 9, 311.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Nutrients EISSN 2072-6643 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top