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Abstract: SA-PO781

Sleep Deprivation Induces Metabolic Reprogramming in Kidney

Session Information

  • CKD: Mechanisms - III
    November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2103 CKD (Non-Dialysis): Mechanisms

Authors

  • Mao, Xiaoming, Nanjing Medical University, Nanjing, China
  • Jiang, Lei, Nanjing Medical University, Nanjing, China
  • Luo, Jing, Nanjing Medical University, Nanjing, China
  • Yang, Junwei, Nanjing Medical University, Nanjing, China
Background

Sleep is critical to human being. Sleep deficiency, or sleep deprivation, is an increasingly important global issue of human health, and has been linked to obesity, diabetes, and cardiovascular disease. Many findings published has addressed the interaction between sleep and metabolism, and metabolic health relies strongly on sleep. Sleep deprivation is known to promote the development of chronic kidney disease . Individuals with shorter time of sleep were more likely to have proteinuria, and faster decline of glomerular filtration rate, yet little is known about the mechanism by which sleep deprivation deteriorate renal function.

Methods

Wild-type male C57BL/6J mice were housed in a 12:12 hr light/dark cycle (light on 8:00 A.M. to 8:00 P.M) at a constant temperature (22±1°C) with free access to food and water. For sleep deprivation, mice were placed in a chamber with a sweep bar moving along the bottom of the cage every 1 min for 20 hours (ZT0-8, ZT12-24) and shut-off for 4 hours. Control mice received no disruption during sleep were living with stationary sweep bars. Mice were sacrificed after the procedure of sleep deprivation lasts for 4 weeks at ZT0 and ZT12.

Results

Though body weight and food/water intake did not differ from SD group to control group, biochemical analysis revealed statistical differences in serum albumin, AST, SOD, STB, phosphorus (p<0.05) between SD mice and control. Oil Red O staining indicated larger lipid droplets in SD kidney. No difference in urinary albumin excretion was observed between the two groups, while a tendency towards higher urine albumin-creatinine ratio was seen in SD group. Transcription analysis identified altered gene expression most significantly involved in lipid metabolism and biosynthesis, insulin signaling pathway, and circadian rhythm. Protein expression confirmed by Western blot (CPT1α, ACADL, FASN, ADFP, CD36, PDK4, PDH) indicated depressed fatty acid oxidation, increased lipid accumulation and glycolysis.

Conclusion

Sufficient sleep is associated with kidney metabolic homeostasis. More lipid utilization might be occurred in kidney during sleep than waking state. Metabolism disorder caused by chronic sleep deprivation may be concerned in the progression renal function decline or proteinuria.

Funding

  • Government Support - Non-U.S.