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Dual regulation of TxNIP by ChREBP and FoxO1 in liver

Benedicte Noblet1, Fadila Benhamed1, InSug O-Sullivan2,3

  • 1Université de Paris, Institut Cochin, CNRS, INSERM, 75014 Paris, France.

Iscience
|March 22, 2021
PubMed

Insights

Thioredoxin-interacting protein (TxNIP) regulation in liver cells was investigated. Hepatic TxNIP expression is controlled by ChREBP and FoxO1, correlating with fasting and nutrient restriction.

Area of Science:

  • Metabolism and endocrinology
  • Molecular biology
  • Cellular regulation

Background:

  • Thioredoxin-interacting protein (TxNIP) is implicated in type 2 diabetes and linked to hyperglycemia in pancreatic beta cells.
  • Hepatic regulation of TxNIP, particularly in response to physiological stimuli and hyperglycemia, remains less understood.
  • Transcription factors ChREBP (Carbohydrate Responsive Element Binding Protein) and FoxO1 (Forkhead box protein O1) are key regulators of glucose and fasting responses in gene expression.

Purpose of the Study:

  • To elucidate the regulatory mechanisms of Txnip in hepatocytes.
  • To investigate Txnip regulation in response to physiological stimuli and hyperglycemia using a mouse model.
  • To understand the roles of ChREBP and FoxO1 in hepatic Txnip expression.

Main Methods:

  • Utilized genetically modified mice to study Txnip regulation in liver cells.
  • Investigated the influence of hyperglycemia in a db/db mouse model.
  • Focused on the roles of ChREBP and FoxO1 transcription factors.

Main Results:

  • Hepatic TxNIP expression is upregulated by both ChREBP and FoxO1 in liver cells.
  • Txnip expression in the liver shows a strong correlation with fasting states.
  • Identified TxNIP as a key player in the physiological adaptation to nutrient restriction.

Conclusions:

  • Both ChREBP and FoxO1 are critical regulators of hepatic Txnip expression.
  • TxNIP plays a significant role in the liver's response to fasting and nutrient restriction.
  • Understanding TxNIP regulation in the liver offers insights into metabolic diseases like type 2 diabetes.
Keywords:
EndocrinologyMolecular BiologyMolecular Physiology

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