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Links from GEO DataSets

Items: 4

1.
Full record GDS3316

Leptin deficiency effect on lungs

Analysis of lungs from leptin-deficient (ob/ob) mutants treated with saline or leptin. Leptin deficiency results in low lung volumes and an attenuated chemical control of breathing. Results provide insight into molecular mechanisms by which leptin alters respiratory system structure and function.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 protocol sets
Platform:
GPL339
Series:
GSE10915
6 Samples
Download data: CEL
2.

Comparative analysis of gene expression in ob/ob leptin-treated and ob/ob saline-treated lungs.

(Submitter supplied) We hypothesize that gene expression in the lungs of these differentially-treated mice are divergent thus contributing to the disparity in their phenotypes. More specifically, (1) Effects of Leptin-treatment of ob/ob postnatal mice lungs are known to be volume-dependent from 2 to 10 wks of age, and are independent of the hypometabolism associated with leptin deficiency. ; (2) Leptin is critical to postnatal lung remodeling, particularly related to enlarged alveolar surface area. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS3316
Platform:
GPL339
6 Samples
Download data: CEL
Series
Accession:
GSE10915
ID:
200010915
3.

Expression data from leptin administration to Lepob/Lepob mice and Lepmkyo/Lepmkyo rats

(Submitter supplied) Leptin-responsive genes in the pathway of a leptin signal from the hypothalamus to the liver has not been detected. We used microarray to detailed the expression of gene in liver in the status of leptin deficiency, and leptin administration. As leptin deficient status, we use Lepmkyo/Lepmkyo rats or Lepob/Lepob mice and their wild type littermates.
Organism:
Rattus norvegicus; Mus musculus
Type:
Expression profiling by array
Platforms:
GPL1355 GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE42532
ID:
200042532
4.

Skeletal glucocorticoid signaling determines aging-related leptin resistance and obesity

(Submitter supplied) Aging contributes to many chronic conditions, including central obesity, insulin resistance and osteoporosis, which are also critical features of glucocorticoid excess. To investigate tissue-specific sites of glucocorticoid (GC) action during aging, we disrupted GC signalling in mouse osteoblasts via transgenic overexpression of the GC-inactivating enzyme, 11β-hydroxysteroid-dehydrogenase type 2 (11β-HSD2). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL17400
24 Samples
Download data: CEL
Series
Accession:
GSE141448
ID:
200141448
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