Forkhead box class O family member proteins: The biology and pathophysiological roles in diabetes

Kyoichiro Tsuchiya, Yoshihiro Ogawa

Research output: Contribution to journalReview article

17 Citations (Scopus)

Abstract

Forkhead box class O family member proteins (FoxOs) of transcription factors are essential regulators of cellular homeostasis, including glucose and lipid metabolism, oxidative stress response and redox signaling, cell cycle progression, and apoptosis. Altered FoxO1 expression and activity have been associated with glucose intolerance, dyslipidemia and complications of diabetes. In the liver, they direct carbons to glucose or lipid utilization, thus providing a unifying mechanism for the two abnormalities of the diabetic liver: excessive glucose production, and increased lipid synthesis and secretion. In the pancreas, FoxO1 is necessary to maintain β-cell differentiation, and could be promising targets for β-cell regeneration. In endothelial cells, FoxOs strongly promote atherosclerosis through suppressing nitric oxide production and enhancing inflammatory responses. In the present review, we summarize the basic biology and pathophysiological significance of FoxOs in diabetes.

Original languageEnglish
Pages (from-to)726-734
Number of pages9
JournalJournal of Diabetes Investigation
Volume8
Issue number6
DOIs
Publication statusPublished - Nov 2017

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Glucose
Lipids
Proteins
Glucose Intolerance
Liver
Diabetes Complications
Dyslipidemias
Lipid Metabolism
Oxidation-Reduction
Regeneration
Cell Differentiation
Pancreas
Atherosclerosis
Cell Cycle
Nitric Oxide
Oxidative Stress
Homeostasis
Transcription Factors
Carbon
Endothelial Cells

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Forkhead box class O family member proteins : The biology and pathophysiological roles in diabetes. / Tsuchiya, Kyoichiro; Ogawa, Yoshihiro.

In: Journal of Diabetes Investigation, Vol. 8, No. 6, 11.2017, p. 726-734.

Research output: Contribution to journalReview article

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