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Related Experiment Videos

Increased insulin sensitivity in Gsalpha knockout mice.

S Yu1, A Castle, M Chen

  • 1Metabolic Diseases Branch and Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.

The Journal of Biological Chemistry
|March 29, 2001
PubMed
Summary
This summary is machine-generated.

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Mice with altered Gnas gene expression show increased insulin sensitivity, regardless of obesity. This study demonstrates that G(s)-coupled pathways negatively regulate insulin signaling in vivo.

Area of Science:

  • Endocrinology
  • Metabolic Research
  • Genetics

Background:

  • The stimulatory guanine nucleotide-binding protein (G(s)) is crucial for hormone-stimulated cAMP generation.
  • The Gnas gene, encoding the G(s) alpha-subunit, is imprinted, leading to different phenotypes in mice with maternal (m-/+) or paternal (+/p-) allele disruption.
  • m-/+ mice are obese, while +/p- mice are leaner, indicating opposite effects on energy metabolism.

Purpose of the Study:

  • To investigate the impact of Gnas gene imprinting on insulin sensitivity and glucose metabolism.
  • To explore the relationship between altered energy metabolism, obesity, and insulin sensitivity in Gnas mutant mice.
  • To determine the role of G(s)-coupled pathways in regulating insulin signaling.

Main Methods:

  • Generation of Gnas imprinting mutant mice (m-/+ and +/p-).

Related Experiment Videos

  • Assessment of glucose homeostasis, insulin sensitivity, and glucose uptake in skeletal muscle.
  • Measurement of G(s)alpha and GLUT4 expression in muscle tissue.

    • Main Results:

    • Both m-/+ and +/p- mice exhibited enhanced insulin sensitivity, characterized by low fasting glucose/insulin, improved glucose tolerance, and exaggerated hypoglycemic response.
    • Obesity in m-/+ mice was paradoxically accompanied by increased insulin sensitivity, challenging typical associations.
    • Skeletal muscles showed significantly increased 2-deoxyglucose uptake upon maximal insulin stimulation, linked to reduced G(s)alpha expression in both mutant groups.

    Conclusions:

    • G(s)-coupled pathways exert negative regulation on insulin signaling.
    • Altered G(s)alpha expression in muscle is a key factor in enhanced insulin sensitivity in Gnas imprinting mutants.
    • This study provides the first in vivo evidence of G(s)-coupled pathways negatively regulating insulin signaling using a genetically modified model.