IRS2 and PTP1B: Two opposite modulators of hepatic insulin signalling.

Abstract:

:Type 2 Diabetes mellitus (T2D) is the most common endocrine disorder associated to metabolic syndrome (MS) and occurs when insulin secretion can no compensate peripheral insulin resistance. Among peripheral tissues, the liver controls glucose homeostasis due to its ability to consume and produce glucose. The molecular mechanism underlying hepatic insulin resistance is not completely understood; however, it involves the impairment of the insulin signalling network. Among the critical nodes of hepatic insulin signalling, insulin receptor substrate 2 (IRS2) and protein tyrosine phosphatase 1B (PTP1B) modulate the phosphatidylinositol (PI) 3-kinase/Akt/Foxo1 pathway that controls the suppression of gluconeogenic genes. In this review, we will focus on recent findings regarding the molecular mechanism by which IRS2 and PTP1B elicit opposite effects on carbohydrate metabolism in the liver in response to insulin. Finally, we will discuss the involvement of the critical nodes of insulin signalling in non-alcoholic fatty liver disease (NAFLD) in humans.

journal_name

Arch Physiol Biochem

authors

Valverde AM,González-Rodríguez A

doi

10.3109/13813455.2011.557386

subject

Has Abstract

pub_date

2011-07-01 00:00:00

pages

105-15

issue

3

eissn

1381-3455

issn

1744-4160

journal_volume

117

pub_type

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