Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hypothalamic oxidative stress provokes leptin and insulin resistance

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE92236 | GEO | 2017/02/06

SECONDARY ACCESSION(S): PRJNA356974

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Hypothalamic oxidative stress provokes leptin and insulin resistance [hypothlamus]

Project description:The relationship between loss of hypothalamic function and onset of diabetes mellitus remains elusive. Therefore, we generated a targeted oxidative-stress murine model utilizing conditional knockout of selenocysteine-tRNA (Trsp) using rat insulin promoter-driven-Cre (RIP-Cre). These Trsp-knockout (TrspRIPKO) mice exhibit deletion of Trsp in both hypothalamic cells and pancreatic β-cells leading to increased hypothalamic oxidative stress and severe insulin resistance. Leptin signals were suppressed and numbers of proopiomelanocortin-positive neurons in the hypothalamus were decreased. In contrast, a Trsp-knockout mouse (TrspIns1KO) expressing Cre specifically in pancreatic β-cells, but not in the hypothalamus, did not display insulin and leptin resistance, demonstrating a critical role of the hypothalamus in the onset of diabetes mellitus. Nrf2 (NF-E2-related-factor-2) regulates antioxidant gene expression. Gene-driven increase in Nrf2 signaling suppressed hypothalamic oxidative stress and improved insulin and leptin resistance in TrspRIPKO mice. Thus, Nrf2 harbors the potential to prevent the onset of diabetic mellitus by reducing hypothalamic oxidative damage.

2017-02-06 | GSE92235 | GEO

Hypothalamic oxidative stress provokes leptin and insulin resistance [Islets]

2017-02-06 | GSE92234 | GEO

Hypothalamic oxidative stress provokes leptin and insulin resistance

Project description:Hypothalamic oxidative stress provokes leptin and insulin resistance

| PRJNA356974 | ENA

Towards epigenetic understanding and therapy of insulin resistance by intranuclear insulin

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-05-23 | E-GEOD-57928 | biostudies-arrayexpress

Hypothalamic REV-ERBs Control Circadian Food Intake and Leptin Sensitivity

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-10-11 | GSE148644 | GEO

Irx3 and Irx5 regulate hypothalamic postnatal neurogenesis and leptin sensitivity

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-18 | GSE154981 | GEO

The epigenetic signature of systemic insulin resistance in obese women

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-08-01 | E-GEOD-76399 | biostudies-arrayexpress

Cancer anorexia: the role of serotonin in hypothalamic resistance of the neuropeptide Y system

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-10-31 | E-GEOD-57190 | biostudies-arrayexpress

Pervasive genomic transcription during oxidative stress generates thousands of previously uncharacterized lncRNAs

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-05-27 | E-GEOD-55172 | biostudies-arrayexpress

Leptin regulation of Hsp60 impacts hypothalamic insulin signaling.

Project description:Type 2 diabetes is characterized by insulin resistance and mitochondrial dysfunction in classical target tissues such as muscle, fat, and liver. Using a murine model of type 2 diabetes, we show that there is hypothalamic insulin resistance and mitochondrial dysfunction due to downregulation of the mitochondrial chaperone HSP60. HSP60 reduction in obese, diabetic mice was due to a lack of proper leptin signaling and was restored by leptin treatment. Knockdown of Hsp60 in a mouse hypothalamic cell line mimicked the mitochondrial dysfunction observed in diabetic mice and resulted in increased ROS production and insulin resistance, a phenotype that was reversed with antioxidant treatment. Mice with a heterozygous deletion of Hsp60 exhibited mitochondrial dysfunction and hypothalamic insulin resistance. Targeted acute downregulation of Hsp60 in the hypothalamus also induced insulin resistance, indicating that mitochondrial dysfunction can cause insulin resistance in the hypothalamus. Importantly, type 2 diabetic patients exhibited decreased expression of HSP60 in the brain, indicating that this mechanism is relevant to human disease. These data indicate that leptin plays an important role in mitochondrial function and insulin sensitivity in the hypothalamus by regulating HSP60. Moreover, leptin/insulin crosstalk in the hypothalamus impacts energy homeostasis in obesity and insulin-resistant states.

| S-EPMC3809782 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data