Summary: After just one sleep deprived night, the ability of the liver to produce glucose and insulin is altered, increasing the risk of developing metabolic diseases, such as type 2 diabetes, researchers report.
Losing a single night’s sleep may affect the liver’s ability to produce glucose and process insulin, increasing the risk of metabolic diseases such as hepatic steatosis (fatty liver) and type 2 diabetes. The findings of the mouse study are published ahead of print in the American Journal of Physiology–Endocrinology and Metabolism. The research was chosen as an APSselect article for September.
Sleep deprivation has been associated with eating more, moving less and having a higher risk of developing type 2 diabetes. However, a team of researchers from Toho University Graduate School of Medicine in Japan, explained, “It was not clear whether glucose intolerance was due to the changes in food intake or energy expenditure or to the sleep deprivation itself.”
The researchers studied two groups of mice: One group was kept awake for six hours each night (“sleep deprivation”), while the control group was allowed to sleep as desired. The research team offered unlimited high-fat food and sugar water–mimicking lifestyle-related food choices that people make–to both groups prior to the study. During the sleep/wake period, the animals had limited opportunity for physical activity.
The researchers measured glucose levels and fat content of the liver immediately after the trial period. Blood glucose levels were significantly higher in the sleep deprivation group than controls after one six-hour session of wakefulness. Triglyceride (fat) levels and the production of glucose in the liver also increased in the sleep deprivation group after a single wake period. Elevated liver triglycerides are associated with insulin resistance, or the inability of the body to process insulin properly. In addition, lack of sleep changed the expression of enzymes that regulate metabolism in the liver in the sleep deprivation group. These findings suggest that “intervention studies designed to prevent sleep deprivation-induced hepatic steatosis and insulin resistance should be performed in the future,” the researchers wrote
About this neuroscience research article
Source: Stacy Brooks – APS Publisher: Organized by NeuroscienceNews.com. Image Source: NeuroscienceNews.com image is in the public domain. Original Research:Abstract for “Mechanisms of sleep deprivation-induced hepatic steatosis and insulin resistance in mice” by Fumika Shigiyama, Naoki Kumashiro, Yousuke Tsuneoka, Hiroyuki Igarashi, Fukumi Yoshikawa, Saori Kakehi, Hiromasa Funato, and Takahisa Hirose in American Journal of Physiology: Endocrinology and Metabolism. Published July 10 2018. doi:10.1152/ajpendo.00072.2018
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[cbtabs][cbtab title=”MLA”]APS”Losing Just Six Hours of Sleep Increases Diabetes Risk.” NeuroscienceNews. NeuroscienceNews, 5 September 2018. <https://neurosciencenews.com/sleep-diabetes-9804/>.[/cbtab][cbtab title=”APA”]APS(2018, September 5). Losing Just Six Hours of Sleep Increases Diabetes Risk. NeuroscienceNews. Retrieved September 5 2018 from https://neurosciencenews.com/sleep-diabetes-9804/[/cbtab][cbtab title=”Chicago”]APS”Losing Just Six Hours of Sleep Increases Diabetes Risk.” https://neurosciencenews.com/sleep-diabetes-9804/ (accessed September 5 2018).[/cbtab][/cbtabs]
Mechanisms of sleep deprivation-induced hepatic steatosis and insulin resistance in mice
Sleep deprivation is associated with increased risk for type 2 diabetes mellitus. However, the underlying mechanisms of sleep deprivation-induced glucose intolerance remain elusive. The aim of this study was to investigate the mechanisms of sleep deprivation-induced glucose intolerance in mice with a special focus on the liver. We established a mouse model of sleep deprivation-induced glucose intolerance using C57BL/6J male mice. A single 6-hr sleep deprivation by the gentle handling method under fasting condition induced glucose intolerance. Hepatic glucose production assessed by pyruvate challenge test was significantly increased, as was hepatic triglyceride content (by 67.9%) in the sleep deprivation group, compared with freely sleeping control mice. Metabolome and microarray analyses were used to evaluate hepatic metabolites and gene expression levels and determine the molecular mechanisms of sleep deprivation-induced hepatic steatosis. Hepatic metabolites, such as acetyl CoA, 3β-hydroxybutyric acid, and certain acylcarnitines were significantly increased in the sleep deprivation group, suggesting increased lipid oxidation in the liver. In contrast, fasted sleep-deprived mice showed that hepatic gene expression levels of Elovl3, Lpin1, Plin4, Plin5 and Acot1, which are known to play lipogenic roles, were 2.7, 4.5, 3.7, 2.9, and 2.8 times, respectively, those of the fasted sleeping control group, as assessed by quantitative RT-PCR. Sleep deprivation-induced hepatic steatosis and hepatic insulin resistance seem to be mediated through upregulation of hepatic lipogenic enzymes.