Skip to main content
eScholarship
Open Access Publications from the University of California

UC Santa Cruz

UC Santa Cruz Previously Published Works bannerUC Santa Cruz

Metabolic and transcriptomic analysis of Huntington's disease model reveal changes in intracellular glucose levels and related genes.

  • Author(s): Chaves, Gepoliano
  • Özel, Rıfat Emrah
  • Rao, Namrata V
  • Hadiprodjo, Hana
  • Costa, Yvonne Da
  • Tokuno, Zachary
  • Pourmand, Nader
  • et al.
Abstract

Huntington's Disease (HD) is a neurodegenerative disorder caused by an expansion in a CAG-tri-nucleotide repeat that introduces a poly-glutamine stretch into the huntingtin protein (mHTT). Mutant huntingtin (mHTT) has been associated with several phenotypes including mood disorders and depression. Additionally, HD patients are known to be more susceptible to type II diabetes mellitus (T2DM), and HD mice model develops diabetes. However, the mechanism and pathways that link Huntington's disease and diabetes have not been well established. Understanding the underlying mechanisms can reveal potential targets for drug development in HD. In this study, we investigated the transcriptome of mHTT cell populations alongside intracellular glucose measurements using a functionalized nanopipette. Several genes related to glucose uptake and glucose homeostasis are affected. We observed changes in intracellular glucose concentrations and identified altered transcript levels of certain genes including Sorcs1, Hh-II and Vldlr. Our data suggest that these can be used as markers for HD progression. Sorcs1 may not only have a role in glucose metabolism and trafficking but also in glutamatergic pathways affecting trafficking of synaptic components.

Many UC-authored scholarly publications are freely available on this site because of the UC's open access policies. Let us know how this access is important for you.

Main Content
Current View