Aging leads to increased levels of protein O-linked N-acetylglucosamine in heart, aorta, brain and skeletal muscle in Brown-Norway rats

Biogerontology. 2008 Jun;9(3):139. doi: 10.1007/s10522-007-9123-5. Epub 2008 Jan 10.

Abstract

Changes in the levels of O-linked N-acetyl-glucosamine (O-GlcNAc) on nucleocytoplasmic protein have been associated with a number of age-related diseases such as Alzheimer's and diabetes; however, there is relatively little information regarding the impact of age on tissue O-GlcNAc levels. Therefore, the goal of this study was to determine whether senescence was associated with alterations in O-GlcNAc in heart, aorta, brain and skeletal muscle and if so whether there were also changes in the expression of enzymes critical in regulating O-GlcNAc levels, namely, O-GlcNAc transferase (OGT), O-GlcNAcase and glutamine:fructose-6-phosphate amidotransferase (GFAT). Tissues were harvested from 5- and 24-month old Brown-Norway rats; UDP-GlcNAc, a precursor of O-GlcNAc was assessed by HPLC, O-GlcNAc and OGT levels were assessed by immunoblot analysis and GFAT1/2, OGT, O-GlcNAcase mRNA levels were determined by RT-PCR. In the 24-month old animals serum insulin and triglyceride levels were significantly increased compared to the 5-month old group; however, glucose levels were unchanged. Protein O-GlcNAc levels were significantly increased with age (30-107%) in all tissues examined; however, paradoxically the expression of OGT, which catalyzes O-GlcNAc formation, was decreased by approximately 30% in the heart, aorta and brain. In the heart increased O-GlcNAc was associated with increased UDP-GlcNAc levels and elevated GFAT mRNA while in other tissues we found no difference in UDP-GlcNAc or GFAT mRNA levels. These results demonstrate that senescence is associated with increased O-GlcNAc levels in multiple tissues and support the notion that dysregulation of pathways leading to O-GlcNAc formation may play an important role in the development of age-related diseases.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Acetylglucosamine / genetics
  • Acetylglucosamine / metabolism*
  • Aging / metabolism*
  • Animals
  • Aorta / metabolism*
  • Base Sequence
  • Brain / metabolism*
  • Chromatography, High Pressure Liquid
  • DNA Primers
  • Male
  • Muscle, Skeletal / metabolism*
  • Myocardium / metabolism*
  • Proteins / metabolism*
  • RNA, Messenger / genetics
  • Rats
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • DNA Primers
  • Proteins
  • RNA, Messenger
  • Acetylglucosamine