Mice with low levels of Shc proteins display reduced glycolytic and increased gluconeogenic activities in liver.

Biochem Biophys Rep

VM Molecular Biosciences, School of Veterinary Medicine, University of California, Davis 1089 Veterinary Medicine Dr, VM3B, Davis, CA 95616, USA.

Published: September 2016

AI Article Synopsis

  • Shc proteins are involved in energy metabolism by interacting with the insulin receptor, which affects liver glycolysis and gluconeogenesis in different nutritional states.
  • In experiments comparing Shc knockout (ShcKO) and wild-type (WT) mice, ShcKO mice showed decreased glycolytic activity and increased gluconeogenic enzyme activity, along with altered levels of key metabolic regulators.
  • The findings suggest that Shc proteins help regulate metabolic shifts from glucose breakdown to gluconeogenesis and lipid metabolism, highlighting their potential role in healthy aging and energy selection in the body.

Article Abstract

Shc proteins play a role in energy metabolism through interaction with the insulin receptor. The aim of this study was to determine whether Shc proteins influence liver glycolysis and gluconeogenesis under both fed and fasted states. Decreased glycolytic and increased gluconeogenic and transamination enzyme activities were observed in ShcKO versus WT mice. Levels of key regulatory metabolites, such as fructose-2,6-bisphosphate, matched the activity of metabolic pathways. Protein levels of glycolytic and gluconeogenic enzymes were not different. pAMPK protein levels increased with fasting and were higher in ShcKO versus WT mice. Therefore, Shc proteins play a role in shifting the metabolism from glucose oxidation to gluconeogenesis and lipid catabolism and should be considered as regulators of fuel selection. Fuel selection and utilization could play a critical role in healthy aging. Characterization of metabolic events in ShcKO mice would help to elucidate how metabolism is influenced by these proteins.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5267479PMC
http://dx.doi.org/10.1016/j.bbrep.2016.06.021DOI Listing

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