Adipocyte abundances of CES1, CRYAB, ENO1 and GANAB are modified in-vitro by glucose restriction and are associated with cellular remodelling during weight regain

Adipocyte. 2019 Dec;8(1):190-200. doi: 10.1080/21623945.2019.1608757.

Abstract

Long-term weight loss maintenance is a problem of overweight and obesity. Changes of gene expression during weight loss (WL) by calorie restriction (CR) are linked to the risk of weight regain (WR). However, detailed information on genes/proteins involved in the mechanism is still lacking. Therefore, we developed an in-vitro model system for glucose restriction (GR) and refeeding (RF) to uncover proteome differences between GR with RF vs normal feeding, of which we explored the relation with WR after WL. Human Simpson-Golabi-Behmel Syndrome cells were subjected to changing levels of glucose to mimic the condition of CR and RF. Proteome profiling was performed by liquid chromatography tandem mass spectrometry. This in-vitro model revealed 44 proteins differentially expressed after GR and RF versus feeding including proteins of the focal adhesions. Four proteins showed a persistent up- or down-regulation: liver carboxylesterase (CES1), mitochondrial superoxide dismutase [Mn] (SOD2), alpha-crystallin B-chain (CRYAB), alpha-enolase (ENO1). In-vivo weight loss-induced RNA expression changes linked CES1, CRYAB and ENO1 to WR. Moreover, of these 44 proteins, CES1 and glucosidase II alpha subunit (GANAB) during follow up correlated with WR. Correlation clustering of in-vivo protein expression data indicated an interaction of these proteins with structural components of the focal adhesions and cytoplasmic filaments in the adipocytes.

Keywords: fat-regain; SGBS adipocytes; focal adhesion; proteomics; weight regain.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / cytology
  • Adipocytes / metabolism*
  • Biomarkers, Tumor / genetics
  • Biomarkers, Tumor / metabolism*
  • Carboxylic Ester Hydrolases / genetics
  • Carboxylic Ester Hydrolases / metabolism*
  • Cells, Cultured
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Glucose / deficiency*
  • Glucose / metabolism
  • Glucosidases / genetics
  • Glucosidases / metabolism*
  • Humans
  • Phosphopyruvate Hydratase / genetics
  • Phosphopyruvate Hydratase / metabolism*
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*
  • Weight Gain*
  • alpha-Crystallin B Chain / genetics
  • alpha-Crystallin B Chain / metabolism*

Substances

  • Biomarkers, Tumor
  • CRYAB protein, human
  • DNA-Binding Proteins
  • Tumor Suppressor Proteins
  • alpha-Crystallin B Chain
  • Carboxylic Ester Hydrolases
  • CES1 protein, human
  • GANAB protein, human
  • Glucosidases
  • ENO1 protein, human
  • Phosphopyruvate Hydratase
  • Glucose

Grants and funding

The Yoyo study was supported by The Netherlands Organization for Scientific Research (NWO TOP grant 200500001). Qi Qiao is supported by the Chinese Scholarship Council (File No. 201707720057).