Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomics of Gipr-expressing cells in mouse hypothalamus tissue [dataset 1]

ABSTRACT: We purified Gipr-expressing cells from mouse hypothalamus by FACS and identified cell types distinguished by transcripts.

ORGANISM(S): Mus musculus

PROVIDER: GSE199036 | GEO | 2022/04/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptomics of Gipr-expressing cells in mouse hypothalamus tissue [dataset 2]

Project description:We purified Gipr-expressing cells from mouse hypothalamus by FACS and identified cell types distinguished by transcripts.

2022-04-27 | GSE199215 | GEO

Transcriptomics of Rxfp4-expressing cells in mouse hypothalamus tissue

Project description:We purified Rxfp4-expressing cells from mouse hypothalamus by FACS and identified cell types distinguished by transcripts.

2022-11-21 | GSE178897 | GEO

Transcriptomics of Glp1r-expressing cells in mouse hypothalamus tissue

Project description:We purified Glp1r-expressing cells from mouse hypothalamus by FACS and identified cell types distinguished by transcripts.

2022-04-27 | GSE199216 | GEO

Transcriptomics of Gipr-expressing cells in mouse hypothalamus tissue [dataset 1]

Project description:Transcriptomics of Gipr-expressing cells in mouse hypothalamus tissue [dataset 1]

| PRJNA818166 | ENA

Transcriptomics of Gipr-expressing cells in mouse hypothalamus tissue [dataset 2]

Project description:Transcriptomics of Gipr-expressing cells in mouse hypothalamus tissue [dataset 2]

| PRJNA818971 | ENA

Glucose-dependent Insulinotropic polypeptide receptor-expressing cells in the hypothalamus regulate food intake

Project description:Ambiguity regarding the role of glucose-dependent insulinotropic polypeptide (GIP) in obesity arises from conflicting reports asserting that both GIP receptor (GIPR) agonism and antagonism are effective strategies for inhibiting weight gain. To enable identification and manipulation of Gipr-expressing (Gipr) cells we created GIPR-Cre knock-in mice. As GIPR-agonists have recently been reported to suppress food intake we aimed to identify central mediators of this effect. Gipr cells were identified in the arcuate, dorsomedial, and paraventricular nuclei of the hypothalamus, as confirmed by RNAscope in mouse and human. Single cell RNAseq identified clusters of hypothalamic Gipr cells exhibiting transcriptomic signatures for mural, glial and neuronal cells, the latter expressing somatostatin, but little proopiomelanocortin or agouti-related peptide. Activation of Gq-DREADDs in hypothalamic Gipr cells suppressed food intake in vivo, which was not obviously additive with concomitant GLP1R activation. These data identify hypothalamic GIPR as a target for the regulation of energy balance.

2019-07-24 | GSE134726 | GEO

Hypothalamic and dorsal vagal glucose-dependent insulinotropic polypeptide receptor (GIPR) neurons employ distinct mechanisms to affect feeding

Project description:Central glucose-dependent insulinotropic polypeptide (GIP) receptor (GIPR) signalling is critical for GIP-based therapeutics to lower body weight, but pathways leveraged by GIPR agonism pharmacology in the brain remain incompletely understood. We explored the role of Gipr neurons in the hypothalamus and dorsal vagal complex (DVC)—brain regions critical to the control of energy balance. Hypothalamic expression of Gipr expression was not necessary for the synergistic effect of GIPR/ agonism combined with GLP-1R co-agonism on body weight. While chemogenetic stimulation of both hypothalamic and DVC Gipr neurons suppressed food intake, activation of DVC Gipr neurons reduced ambulatory activity and induced conditioned taste avoidance, while there was no effect of a short-acting GIPR agonist (SAGIPRA). Within the DVC, Gipr neurons of the nucleus tractus solitarius (NTS), but not the area postrema (AP), projected to the parabrachial nucleus and paraventricular hypothalamic nucleusdistal brain regions. ScRNAseq and FISH analysis showed that Gipr neurons in the NTS and AP Gipr neurons were transcriptomically distinct. Peripherally-dosed fluorescent GIPR agonists (GIPRAs) revealed that GIPRA access was restricted to circumventricular organs in the CNS. Together tThese data demonstrate that while the hypothalamus, AP and NTS are key sites for Gipr expression, these subpopulations of Gipr neurons in the hypothalamus, AP and NTS differ in their connectivity, transcriptomic profile, peripheral accessibility to peripherally administered GIPRAs, and the appetite controlling pathways they employ. These results highlight the heterogeneity of the central GIPR signalling axis, and suggest that studies aimed at understandinginto the effects of GIP pharmacology on feeding behaviour should consider the interplay of multiple regulatory pathways.

2023-04-07 | GSE228192 | GEO

Comparison of testes gene expression in Gipr–/– and Gipr+/+

Project description:The aim is to compare gene expression profiles of Gipr–/– mice testes with those of Gipr+/+ mice testes.

2016-09-30 | GSE72504 | GEO

Single cell RNA sequencing of Gipr- and Glp1r-expressing cells in the mouse hypothalamus

Project description:Single cell RNA sequencing of Gipr- and Glp1r-expressing cells in the mouse hypothalamus

| PRJNA819265 | ENA

Single cell transcriptomic analysis of KLB expressing cells in the hypothalamus

Project description:Using a custom primer set for cDNA library construction we performed single cell RNA sequencing on FACs sorted tdTomato positive cells from single cell suspensions prepared from the hypothalamus of mice expressing cre-recombinase under the endogenus KLB promoter that were crossed with tdTomato reporter mice (Ai14). We then performed unbiased clustering analysis on 1,904 cells using the single cell transcriptomes to identify 12 different cell types which express KLB in the hypothalamus including neuronal and non-neuronal cell types. This information was then used to delete KLB in specific cell populations to determine the direct target of FGF21 in the brain responsible for suppression of sucrose preference.

2020-07-07 | GSE150923 | GEO

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