Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of human skeletal muscle in response to stabilized weight loss.

ABSTRACT: Background: Diet induced weight reduction promotes a decrease in resting energy expenditure that could partly explain the difficulty to maintain reduced body mass. Whether this reduction remains after stabilized weight loss is still controversial. The molecular mechanisms are unknown. Objective: To investigate the effect of a stabilized 10%-weight loss on resting metabolic rate, body composition and skeletal muscle gene expression profile in obese women. Design: Obese women were successively submitted to a 4-w very low-calorie diet, a 3-6-wk low-calorie diet, and a 4-wk weight maintenance program to achieve a 10% weight loss. Resting energy expenditure, body composition, plasma parameters and skeletal muscle transcriptome were compared before weight loss and during stabilized weight reduction. Results: Energy restriction caused an 11% weight loss. Stabilization to the new weight was accompanied by an 11% decrease of the resting metabolic rate normalized to the body cellular mass which was below that of lean subjects. The range of the changes in the skeletal muscle transcriptome was modest. The main regulated genes were that of slow/oxidative fiber markers which were overexpressed and the gene encoding the glucose metabolism inhibitor PDK4 which was down-regulated. The knowledge based approach, gene set enrichment analysis, identified pathways related to insulin and interleukin 6 and long term calorie restriction adaptations during weight loss. Set of arrays that are part of repeated experiments Keywords: Biological Replicate

ORGANISM(S): Homo sapiens

PROVIDER: GSE9917 | GEO | 2008/03/26

SECONDARY ACCESSION(S): PRJNA103913

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of human skeletal muscle from morbidly obese patients before and after gastric bypass surgery to identify genes responsive to weight loss.

Project description:Obesity results from a chronic imbalance between energy intake and energy expenditure, with excess calories stored as fat. As such, weight loss has long been considered as a primary goal of treatment for obesity. A surgical treatment of severe obesity such as gastric bypass provides the most dramatic reductions in body weight, and a well-known effect of weight loss is an improvement in insulin sensitivity. However, the molecular mechanism underlying this association remains unclear. Thus, we profiled skeletal muscle of morbidly obese patients before and after gastric bypass surgery. Results from this project will provide global patterns of gene expression with weight loss, which help to understand the pathogenesis of obesity at the molecular level. Experiment Overall Design: To identify responsive genes to weight loss.

2007-10-26 | E-GEOD-5109 | biostudies-arrayexpress

Effect of in utero undernutrition on skeletal muscle gene expression

Project description:In utero undernutrition is associated with obesity and insulin resistance, although its effect on skeletal muscle remains poorly defined. We report that, in mice, adult offspring from undernourished dams have decreased energy expenditure, decreased skeletal muscle mitochondrial content, and altered energetics in isolated mitochondria and permeabilized muscle fibers. Strikingly, when these mice are put on a 40% calorie restricted diet they lose half as much weight as calorie restricted controls. Our results reveal for the first time that in utero undernutrition alters metabolic physiology having a profound effect on skeletal muscle energetics and response to calorie restriction in adulthood. We have used a mouse model of low birth weight generated through 50% food restriction of mouse dams during the third week of gestation. We have studied in utero food restricted offspring and control offspring that were not food restricted in utero in both the ad libitum and calorie restricted states. Gene expression profiling was performed on tibialis anterior muscle from 8 mice per group, pooled in pairs.

2014-08-01 | E-GEOD-53520 | biostudies-arrayexpress

Effect of in utero undernutrition on skeletal muscle gene expression

2014-08-01 | GSE53520 | GEO

Cancer-cell-secreted miR-204-5p induces leptin signaling pathway in white adipose tissue to promote cancer-associated cachexia

Project description:Cachexia is a wasting disorder of adipose tissues that leads to profound weight loss and frailty. One key characteristic of cachexia is elevated resting energy expenditure, which has been linked to increased fat lipolysis and thermogenesis.

2024-07-23 | GSE239524 | GEO

Gastric Bypass Human Obese Muscle

2006-06-20 | GSE5109 | GEO

Effects of ad libitum feeding on canine skeletal muscle gene expression

Project description:Skeletal muscle, as a large and insulin sensitive tissue, is an important contributor to metabolic homeostasis and energy expenditure. Obese dogs exhibit skeletal muscle insulin resistance, but the causes of these changes are unclear. Thus, we used canine microarrays to analyze gene expression profiles of skeletal muscle tissue collected from obese dogs, after 24 wk of ad libitum feeding. Skeletal muscle tissue samples were collected from 9 intact female beagles (4 yr-old; 4 control; 5 ad libitum) after 24 wk of ad libitum feeding.

2012-01-15 | E-GEOD-29279 | biostudies-arrayexpress

Early Leptin Intervention Reverses Perturbed Energy Balance Regulating Hypothalamic Neuropeptides in the Pre- and Postnatal Calorie Restricted Offspring

Project description:Pre- and postnatal calorie restriction is associated with postnatal growth restriction, reduced circulating leptin concentrations and perturbed energy balance. Hypothalamic regulation of energy balance demonstrates enhanced orexigenic (NPY, AgRP) and diminished anorexigenic (POMC, CART) neuropeptide expression (PN21) setting the stage for subsequent development of obesity. Leptin replenishment during the early postnatal period (PN2-PN8) led to reversing the hypothalamic orexigenic:anorexigenic neuropeptide ratio at PN21 by only reducing the orexigenic (NPY, AgRP) without affecting the anorexigenic (POMC, CART) neuropeptide expression. This hypothalamic effect was mediated via enhanced leptin receptor (ObRb) signaling that involved increased pSTAT3 but reduced PTP1B. This was further confirmed by an increase in body weight at PN21 in response to intracerebroventricular administration of antisense ObRb oligonucleotides (PN2-PN8). The change in the hypothalamic neuropeptide balance in response to leptin administration caused increased oxygen consumption, carbon dioxide production and physical activity which resulted in increased milk intake (PN14) with no change in body weight. This is in contrast to the reduction in milk intake with no effect on energy expenditure and physical activity observed in controls. We conclude that pre- and postnatal calorie restriction perturbs hypothalamic neuropeptide regulation of energy balance setting the stage for hyperphagia and reduced energy expenditure, hallmarks of obesity. Leptin in turn reverses this phenotype by increasing hypothalamic ObRb signaling (sensitivity) and affecting only the orexigenic arm of the neuropeptide balance.

2014-12-31 | GSE55384 | GEO

Gene Expression in Adipose Tissue during Weight Loss

Project description:We investigated the regulation of adipose tissue (AT) gene expression during different phases of a dietary weight loss program and its relationship with insulin sensitivity. Obese women followed a weight reduction program composed of an energy restriction phase (ER) with a 4-week very-low-calorie diet and a weight stabilization period (WS) composed of a 2-month low-calorie diet followed by 3 to 4 months of a weight maintenance diet. At each time point, body composition, plasma parameters and glucose disposal rate were assessed and subcutaneous AT biopsies were performed. Variations in mRNA levels were determined using DNA microarrays and reverse transcription-quantitative PCR. Distinct sets of AT genes are regulated during calorie restriction and weight stabilization revealing an unexpected temporal pattern in the link between AT and insulin sensitivity during weight loss.

2009-05-12 | GSE11975 | GEO

Effects of ad libitum feeding on canine skeletal muscle gene expression

2012-01-15 | GSE29279 | GEO

A chaperone-assisted mechanism of outer mitochondrial membrane TOM70 insertion protective against diet-induced obesity

Project description:Outer mitochondrial membrane (OMM) proteins communicate with the cytosol and other organelles including the endoplasmic reticulum (ER). This communication is important in thermogenic adipocytes to increase energy expenditure that controls body temperature and weight. However, the regulatory mechanisms of OMM protein insertion are poorly understood. Herein, stress-induced cytosolic chaperone PPID (peptidyl-prolyl isomerase D/cyclophilin 40/Cyp40) drives OMM insertion of the mitochondrial import receptor TOM70 regulating body temperature and weight in obese mice, and respiratory/thermogenic function in brown adipocytes. PPID PPIase activity and C-terminal tetratricopeptide repeats (TPR), which show specificity towards TOM70 core and C-tail domains, facilitate OMM insertion. Our results provide an unprecedented role for ER-stress-activated chaperones in controlling energy metabolism through a selective OMM protein insertion mechanism with implications in adaptation to cold temperatures and high-calorie diets.

2024-10-03 | PXD053607 | Pride

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