mmpc-logo mmpc-logo
twitter-logo    bluesky-logo
| Create Account | login
Publication
Distinct Roles for JNK and IKK Activation in Agouti-Related Peptide Neurons in
the Development of Obesity and Insulin Resistance.
Authors Tsaousidou E, Paeger L, Belgardt BF, Pal M, Wunderlich CM, Brönneke H, Collienne
U, Hampel B, Wunderlich FT, Schmidt-Supprian M, Kloppenburg P, Brüning JC
Submitted By Submitted Externally on 7/24/2015
Status Published
Journal Cell reports
Year 2014
Date Published 11/20/2014
Volume : Pages 9 : 1495 - 1506
PubMed Reference 25456138
Abstract Activation of c-Jun N-terminal kinase 1 (JNK1)- and inhibitor of nuclear factor
kappa-B kinase 2 (IKK2)-dependent signaling plays a crucial role in the
development of obesity-associated insulin and leptin resistance not only in
peripheral tissues but also in the CNS. Here, we demonstrate that constitutive
JNK activation in agouti-related peptide (AgRP)-expressing neurons of the
hypothalamus is sufficient to induce weight gain and adiposity in mice as a
consequence of hyperphagia. JNK activation increases spontaneous action
potential firing of AgRP cells and causes both neuronal and systemic leptin
resistance. Similarly, activation of IKK2 signaling in AgRP neurons also
increases firing of these cells but fails to cause obesity and leptin
resistance. In contrast to JNK activation, IKK2 activation blunts insulin
signaling in AgRP neurons and impairs systemic glucose homeostasis.
Collectively, these experiments reveal both overlapping and nonredundant effects
of JNK- and IKK-dependent signaling in AgRP neurons, which cooperate in the
manifestation of the metabolic syndrome.




Menu

Home
Contact
About MMPC
Animal Husbandry
Tests Data
Search Data
Analysis
Clients
MMPC Centers

Newsletter

Interested in receiving MMPC News?
twitter-logo Mouse Phenotyping
@NationalMMPC



2017 National MMPC. All Rights Reserved.