Inactivation of NF-κB2 (p52) restrains hepatic glucagon response via preserving PDE4B induction.

Abstract:

:Glucagon promotes hepatic gluconeogenesis and maintains whole-body glucose levels during fasting. The regulatory factors that are involved in fasting glucagon response are not well understood. Here we report a role of p52, a key activator of the noncanonical nuclear factor-kappaB signaling, in hepatic glucagon response. We show that p52 is activated in livers of HFD-fed and glucagon-challenged mice. Knockdown of p52 lowers glucagon-stimulated hyperglycemia, while p52 overexpression augments glucagon response. Mechanistically, p52 binds to phosphodiesterase 4B promoter to inhibit its transcription and promotes cAMP accumulation, thus augmenting the glucagon response through cAMP/PKA signaling. The anti-diabetic drug metformin and ginsenoside Rb1 lower blood glucose at least in part by inhibiting p52 activation. Our findings reveal that p52 mediates glucagon-triggered hepatic gluconeogenesis and suggests that pharmacological intervention to prevent p52 processing is a potential therapeutic strategy for diabetes.

journal_name

Nat Commun

journal_title

Nature communications

authors

Zhang WS,Pan A,Zhang X,Ying A,Ma G,Liu BL,Qi LW,Liu Q,Li P

doi

10.1038/s41467-019-12351-x

subject

Has Abstract

pub_date

2019-09-20 00:00:00

pages

4303

issue

1

issn

2041-1723

pii

10.1038/s41467-019-12351-x

journal_volume

10

pub_type

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