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Author Spotlight: Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator
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Obesity of G2e3 Knockout Mice Suggests That Obesity-Associated Variants Near Human G2E3 Decrease G2E3 Activity.

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Inactivating the G2/M-phase-specific E3 ubiquitin protein ligase (G2E3) gene in mice causes obesity and glucose intolerance. This suggests that reduced G2E3 function in humans may contribute to obesity risk associated with specific gene variants.

Keywords:
PRKD1Prkd1SNPgene trapglucose tolerancehomologous recombination

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Area of Science:

  • Genetics
  • Metabolic Research
  • Obesity Studies

Background:

  • Single nucleotide polymorphisms (SNPs) near human PRKD1 and G2E3 genes are linked to obesity.
  • No prior studies have demonstrated a direct link between the inactivation of G2E3 or PRKD1 and changes in body fat.
  • Obesity-associated genes are often conserved between humans and mice, making mouse models valuable for investigation.

Purpose of the Study:

  • To investigate whether the inactivation of G2e3 or Prkd1 genes in mice leads to obesity.
  • To determine if G2e3 or Prkd1 gene inactivation causes changes in body fat percentage and glucose homeostasis in mice.
  • To infer the potential role of G2E3 gene function in human obesity based on conserved gene function.

Main Methods:

  • Generation of G2e3 and Prkd1 knockout (KO) mouse lines using gene trapping and homologous recombination.
  • Measurement of body fat in adult KO and wild-type (WT) mice using Dual-energy X-ray absorptiometry (DEXA) and Quantitative Magnetic Resonance (QMR).
  • Assessment of glucose homeostasis via oral glucose tolerance tests (OGTTs) in mice fed a high-fat diet (HFD).

Main Results:

  • G2e3 KO mice exhibited significantly increased body weight (11%), body fat (65%), and % body fat (48%) compared to WT littermates.
  • Lean body mass was not significantly affected in G2e3 KO mice.
  • G2e3 KO mice demonstrated impaired glucose tolerance during OGTTs, while Prkd1 KO mice showed no significant differences in body fat or glucose tolerance compared to WT mice.

Conclusions:

  • Inactivation of the G2e3 gene in mice results in significant obesity and glucose intolerance.
  • The Prkd1 gene knockout did not lead to obesity or glucose intolerance in the studied mice.
  • These findings suggest that reduced functional G2E3 is likely responsible for the obesity observed in individuals with specific G2E3/PRKD1 genetic variants.