Obesity
|
0.100 |
Biomarker
|
disease |
BEFREE |
KEY MESSAGES: JNK1 is a link between obesity/type 2 diabetes and cognitive loss Inhibition of JNK1 is neuroprotective JNK1 constitutes a therapeutic strategy for cognitive loss.
|
31797011 |
2019 |
Obesity
|
0.100 |
Biomarker
|
disease |
BEFREE |
p53 in AgRP neurons is required for protection against diet-induced obesity via JNK1.
|
30143607 |
2018 |
Obesity
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, the UDCA-LPE mediated inhibition of p-JNK1 represents a powerful tool to control intestinal absorption of fatty acids and, thus may be employed as a drug to treat obesity.
|
28602806 |
2017 |
Obesity
|
0.100 |
Biomarker
|
disease |
BEFREE |
Whereas current evidence indicates that JNK1/2 inhibition may improve insulin sensitivity in obesity, the role of JNK in the progression from insulin resistance to diabetes, and its complications is largely unresolved.
|
28180059 |
2017 |
Obesity
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, by use of novel and highly selective JNK inhibitors, we investigated the actions of JNK in the control of feeding and body weight homeostasis.In lean mice, intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) administration of SR-3306, a brain-penetrant and selective pan-JNK (JNK1/2/3) inhibitor, reduced food intake and body weight.Moreover, i.p. and i.c.v. administrations of SR11935, a brain-penetrant and JNK2/3 isoform-selective inhibitor, exerted similar anorectic effects as SR3306, which suggests JNK2 or JNK3 mediates aspect of the anorectic effect by pan-JNK inhibition.Furthermore, daily i.p. injection of SR3306 (7 days) prevented the increases in food intake and weight gain in lean mice upon high-fat diet feeding, and this injection paradigm reduced high-fat intake and obesity in diet-induced obese (DIO) mice.
|
28165482 |
2017 |
Obesity
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These data suggest that adipose inflammation under conditions of obesity suppresses adipolin expression via JNK-dependent down-regulation of KLF15 in adipocytes.
|
24358263 |
2013 |
Obesity
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, these findings indicate that inhibiting adipogenic differentiation of hAMSCs by artemisinic acid occurs primarily through reduced expression of C/EBP δ, which is mediated by the inhibition of JNK and suggest that aremisinic acid may be used as a complementary treatment option for obesity associated with metabolic syndrome.
|
22396222 |
2012 |
Obesity
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In vivo, SIRT1 undergoes an extensive degradation in hepatocytes in obesity as a consequence of persistent activation of JNK1.
|
21540183 |
2011 |
Obesity
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We recently reported that p38MAPK and Jun N-terminal kinase (JNK), but not ERK and inhibitory-kappaB kinase beta, are more highly expressed and activated in human omental (OM) adipose tissue in obesity.
|
19351724 |
2009 |
Obesity
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Adipose-derived JNK1/2 activity was not associated with obesity (all P> 0.1), although it was inversely related to M (r = -0.54, P < 0.05) and explained 29% of its variance.
|
19258436 |
2009 |
Obesity
|
0.100 |
Biomarker
|
disease |
BEFREE |
Phosphorylation of eukaryotic initiation factor 2alpha but not of c-Jun N-terminal kinase 1 or c-jun was increased with obesity.
|
18728164 |
2008 |
Obesity
|
0.100 |
Biomarker
|
disease |
BEFREE |
A sustained increase in JNK activity was observed in dietary and genetic models of obesity in mice, whereas JNK deficiency prevented obesity-induced insulin resistance.
|
17050683 |
2006 |
Obesity
|
0.100 |
Biomarker
|
disease |
BEFREE |
Functional in vivo interactions between JNK1 and JNK2 isoforms in obesity and insulin resistance.
|
16818881 |
2006 |