Upregulation of aspartoacylase activity in the duodenum of obesity induced diabetes mouse

Implications on diabetic neuropathy

Sankar Surendran, Reuben Matalon, Stephen K. Tyring

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Aspartoacylase (ASPA) hydrolyzes N-acetylaspartic acid (NAA) into aspartate and acetate. Normal hydrolysis of NAA is important to maintain healthy neurons. Since enteric neuropathy is one of the events seen in diabetes, whether ASPA activity is affected in diabetic condition is not known. In order to investigate the possibility, ASPA activity was examined in the duodenum and brain of obesity induced diabetes model mouse. Aspartoacylase activity was high in the diabetic mouse duodenum compared to control duodenum. The same result was also observed by immunostaining of the mouse duodenum. The activity of ASPA was found to be elevated in the brain of diabetic mouse compared to the control brain. These data suggest that normal hydrolysis of NAA is affected by ASPA activity seen in the type 2 diabetes model mouse and this change is likely to contribute to neuropathy seen in diabetes, if documented also in patients with type 2 diabetes.

Original languageEnglish (US)
Pages (from-to)973-975
Number of pages3
JournalBiochemical and Biophysical Research Communications
Volume345
Issue number3
DOIs
StatePublished - Jul 7 2006

Fingerprint

Diabetic Neuropathies
Medical problems
Duodenum
Up-Regulation
Obesity
Brain
Type 2 Diabetes Mellitus
Hydrolysis
Intestinal Pseudo-Obstruction
Aspartic Acid
Neurons
aspartoacylase
Acetates
N-acetylaspartate

Keywords

  • Aspartoacylase
  • Duodenum
  • Neuropathy
  • Obesity induced diabetes
  • Type 2 diabetes

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Upregulation of aspartoacylase activity in the duodenum of obesity induced diabetes mouse : Implications on diabetic neuropathy. / Surendran, Sankar; Matalon, Reuben; Tyring, Stephen K.

In: Biochemical and Biophysical Research Communications, Vol. 345, No. 3, 07.07.2006, p. 973-975.

Research output: Contribution to journalArticle

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