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Chronic over-nutrition and dysregulation of GSK3 in diseases

Xunxian Liu1, Zemin Yao1

  • 1Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, University of Ottawa, 451 Smyth Road, Ottawa, ON K1H 8M5 Canada.

Nutrition & Metabolism
|August 6, 2016
PubMed

Insights

Aging reduces cellular response to hormones, accelerating aging and disease. Chronic overnutrition and factors like perilipin 2 (PLIN2) dysregulate glycogen synthase kinase 3 (GSK3) signaling, impacting metabolic homeostasis.

Area of Science:

  • Cellular biology
  • Metabolic regulation
  • Aging research

Background:

  • Aging is associated with a loss of cellular response to hormonal regulation, crucial for metabolic homeostasis.
  • Chronic over-nutrition can lead to cellular insensitivity to hormonal signals, potentially accelerating aging and disease development.
  • Glycogen synthase kinase 3 (GSK3) is a key regulator of cellular processes, including growth, survival, regeneration, and death.

Purpose of the Study:

  • To review environmental and nutritional factors influencing glycogen synthase kinase 3 (GSK3) regulation.
  • To elucidate the role of the phosphoinositide 3-kinase (PI3K)/phosphoinositide-dependent kinase-1 (PDK1)/Akt signaling pathway in GSK3 regulation.
  • To highlight the newly identified function of perilipin 2 (PLIN2) in modulating GSK3 activity and downstream pathways.

Main Methods:

  • Literature review of current understanding on GSK3 regulation.
  • Analysis of the PI3K/PDK1/Akt/GSK3 signaling axis.
  • Examination of perilipin 2 (PLIN2) association with GSK3.

Main Results:

  • The PI3K/PDK1/Akt pathway regulates GSK3 activity via serine-phosphorylation, leading to its inactivation.
  • Perilipin 2 (PLIN2) directly associates with GSK3, influencing its activation state.
  • Environmental and nutritional factors contribute to the dysregulation of the PI3K/PDK1/Akt/GSK3 axis.

Conclusions:

  • Dysregulation of GSK3, influenced by nutrition and environmental factors, contributes to aging and metabolic diseases.
  • PLIN2 emerges as a novel regulator of GSK3 activity and its downstream signaling.
  • Understanding these regulatory mechanisms is critical for developing interventions against age-related metabolic dysfunction.

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