The effects of leptin deficiency on cold-induced energy expenditure
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE59517 | GEO | 2015/06/15
SECONDARY ACCESSION(S): PRJNA255493
REPOSITORIES: GEO
Similar Datasets
Project description:At 24 °C Lep-/- mice are hyperphagic compared to the Lep+/+ mice. Reducing the ambient temperature from 24 to 6 °C (3 °C per day) was accompanied by a graded parallel increase in food intake in both control and Lep-/- mice. The rate of increase in food intake per degree Celsius reduction in ambient temperature by the control mice and Lep-/- mice was essentially indistinguishable. Since the body composition of Lep+/+ and Lep-/- mice was unchanged during cold exposure, thermogenesis is fueled solely by food intake. Accordingly, we predicted that the same changes in gene expression associated with the central regulation of thermogenesis by the hypothalamus must occur in both Lep+/+ and Lep-/- mice during the transition from 24 to 6 °C. Microarray analysis of gene expression was performed on hypothalamic tissue dissected from Lep-/- and Lep+/+ mice kept at different temperature conditions, that is, in mice maintained at 24°C and in mice in which the ambient temperature had been reduced to 6 °C over 6 days.
2015-06-15 | E-GEOD-59517 | biostudies-arrayexpress
Project description:Decreased ambient temperature, from birth to weaning, significantly reduced fat mass (FM) and adiposity in developing mice. Changes in FM content in 10 day-old mice raised at 17°C were not accompanied by precocious induction of brown adipocytes in inguinal white adipose tissue (WAT). Brown phenotype was induced in 21 day-old mice independently of ambient temperature (17°C or 29°C) however the expression of Ucp1 and other brown fat biomarker genes was greater in animals raised at 17°C suggesting increased adaptive thermogenesis. Accordingly, we predict that the induction of brown adipocytes in WAT follows a strict developmental program and the number of potential brown adipocytes in WAT is determined genetically.
2015-05-03 | GSE62350 | GEO
Project description:Although mitochondrial dysfunctions are implicated in the pathogenesis of obesity, the molecular mechanisms underlying obesity-related metabolic abnormalities are still not well established. To acquire a comprehensive picture of mitochondrial molecular changes within metabolically active tissues, we focused on hepatic and muscle whole cellular transcriptome and mitochondrial proteome alterations in 16 and 48 weeks old high fat diet (HFD)-feed wild type C57BL/6J and hyperphagic, genetically modified mice with leptin dysfunction (ob/ob and db/db). On transcriptome level, the most discriminative hepatic alterations distinguished between genetically modified and wild type mice, and between overnight fasted and non-fasted mice, while the muscle transcriptional alterations related mainly to the fasting state. The fractions of uniquely different proteins were consistently higher in hyperphagic than in HFD-fed mice and in fasted than non-fasted mice . The liver samples revealed overall higher number of differentially expressed RNAs and proteins than muscle samples. Differentially expressed genes and proteins in the liver, but not in the muscle, could be assigned to several Gene Ontology terms, including oxidation-reduction and several metabolic processes. Thus, altered expression of genes and proteins accompanied the state of obesity and was quantitatively different in the liver and muscle. Our parallel microarray- and quantitative mitochondrial mass spectrometry-based study performed on hepatic and muscle samples identified a higher number of differentially expressed proteins than any other studies investigating obesity-related proteomes. However, even with our integrated transcriptomic and proteomic approach still many details and dynamics of a chain of metabolic events leading to obesity-related mitochondrial dysfunctions remain unresolved . 48 samples each of liver and muscle (total samples: 96). Samples splitted equally according to 3 criterions: age (24 young/24 old), fasting status (24 fasted/24 non fasted), and strain+diet (12 each: B6.V-Lep ob/J+D12450B, B6.BKS(D)-Lep rdb/J+D12450B, C57BL/6J+D12450B, C57BL/6J+D12492). Overall 3 replicates for each strain+diet/age/fasting_status combination. Low fat diet = D12450B; high fat diet = D12492.
2013-05-01 | E-GEOD-43691 | biostudies-arrayexpress
Project description:Decreased ambient temperature, from birth to weaning, significantly reduced fat mass (FM) and adiposity in developing mice. Changes in FM content in 10 day-old mice raised at 17°C were not accompanied by precocious induction of brown adipocytes in inguinal white adipose tissue (WAT). Brown phenotype was induced in 21 day-old mice independently of ambient temperature (17°C or 29°C) however the expression of Ucp1 and other brown fat biomarker genes was greater in animals raised at 17°C suggesting increased adaptive thermogenesis. Accordingly, we predict that the induction of brown adipocytes in WAT follows a strict developmental program and the number of potential brown adipocytes in WAT is determined genetically. Microarray analysis of gene expression was performed on inguinal white adipose tissue dissected from 10 and 21 day-old mice kept at different temperature conditions, that is, in mice maintained at 17°C or 29oC during early post-natal development.
2015-05-03 | E-GEOD-62350 | biostudies-arrayexpress
Project description:On August 22 – 25, 2017, 3 colonies of Montipora capitata with a diameter of ~ 24 cm were collected from the inner lagoon surrounding the Hawaii Institute of Marine Biology (HIMB). The corals were acclimated in outdoor flow-through tanks at HIMB that were supplied with ambient seawater and covered with shade-cloth to mimic PAR levels on the reef. Each colony was split in half with a hammer and chisel to produce two colonies of identical genotype, so that each genotype would experience both ambient and increased temperatures. On August 28 - 29, the corals were equally divided among the experimental tanks, at ambient (n=3) or increased (n=3) temperature. Throughout the temperature treatment, corals were randomly rotated among tanks to minimize potential tank effects. On September 1, the temperature in the increased temperature tanks was turned up 2°C per day, 1°C at 0900 and 1°C at 1400, for four days, reaching an average temperature of 30 °C. The ambient tanks averaged 25 °C. On September 26, the heaters were turned off and the temperature returned to ambient levels by Sept. 29.
2022-01-19 | PXD021243 | Pride
Project description:Insufficient mitochondrial quantity in brown adipose tissue (BAT) causes defective thermogenesis and positive energy balance, which is coupled with the development of obesity. Whether disturbance of mitochondrial quality affects BAT function remains unknown. Here, we describe that the brown adipocyte-specific Leucine-rich PPR motif-containing protein knockout mice (LrpprcBKO) exhibited mitochondrial electron transport chain (ETC) proteome imbalance and a complete loss of the -adrenergic-stimulated thermogenesis at room temperature (RT), due to specific reduction of mtDNA-encoded genes. However, the LrpprcBKO mice were lean at normal chow and were protected against high-fat-diet-induced metabolic abnormalities, such as obesity, insulin resistance, adipose inflammation, hepatic steatosis, and hypertriglyceridemia. The beige adipocytes in inguinal white adipose tissue were expanded in LrpprcBKO mice at RT, but not at thermoneutrality. However, BAT thermogenic defects and metabolic benefits were present in LrpprcBKO mice regardless of ambient temperatures. Collectively, our results reveal that a thermogenesis-incapable BAT with mitochondrial ETC proteome imbalance can improve systemic metabolism, suggesting BAT’s contributions to thermoregulation and systemic metabolism can be uncoupled.
2021-10-07 | PXD008798 | Pride
Project description:We isolated mutants in Arabidopsis with enhanced ambient temperature response. Microarray analysis was performed to understand the extent to which ambient temperature transcriptome is perturbed in the mutants in comparison with the WT at non inductive 12 ºC and after shift to inductive 27 ºC for 2 h and 24 h. We performed global transcript profiling to understand the regulation of of gene expression underlying ambient temperature response.
2010-01-08 | GSE18624 | GEO
Project description:Ambient temperature affects energy intake and expenditure to maintain homeostasis in a continuously fluctuating environment. Here, mice with an adipose-specific defect in fatty acid oxidation (Cpt2A-/-) were subjected to varying temperature to determine the role of adipose bioenergetics to environmental adaptation. Cpt2A-/- brown adipose tissue (BAT) failed to induce thermogenic genes such as Ucp1 and Pgc1α in response to adrenergic stimulation, which is exacerbated by increasing temperature. Thermoneutrality induced a mitochondrial DNA stress in Cpt2A-/- BAT that resulted in a loss of classical interscapular BAT, but did not affect body weight gain or glucose tolerance in response to a high-fat diet. In this dataset, we include the expression data obtained from dissected mouse interscapular brown adipose tissue from mice acclimatized to thermoneutrality (30C) with and without beta3adrenergic stimulation with and without the deletion of carnitine palmitoyltransferase 2 (i.e., adipose unable to beta-oxidize long chain fatty acids in mitochondria). WildType and Cpt2A KnockOut mice were treated either with or without beta3adrenergic stimulation, thus four classes. Three biologic replicates were compared per class, thus twelve mice.
2016-02-04 | E-GEOD-72210 | biostudies-arrayexpress
Project description:We tested if minor changes in environmental temperature during pregnancy can severely alter the phenotype of the offspring already in the next generation. Genome-wide expression profiling of liver samples obtained from adult male mice offspring identified several alterations in the hepatic transcriptomic landscape, thus demonstrating that even minor differences in the demand for maternal thermogenesis profoundly and permanently alter hepatic gene activity in the adult offspring. Liver gene expression data of offspring from dams that were kept at different ambient temperatures (30°C, 23°C, 18°C, 10°C) only during pregnancy.
2020-11-09 | GSE145142 | GEO
Project description:Background: Anorexia is a common symptom among cancer patients and contributes to malnutrition and strongly impinges on quality of life. Cancer-induced anorexia is thought to be caused by an inability of food intake-regulating systems in the hypothalamus to respond adequately to negative energy balance during tumour growth. Here, we show that this impaired response of food-intake control is likely to be mediated by altered serotonin signalling and by failure in post-transcriptional neuropeptide Y (NPY) regulation. Methods: Two tumour cachectic mouse models with different food intake behaviours were used: a C26-colon adenocarcinoma model with increased food intake and a Lewis lung carcinoma model with decreased food intake. This contrast in food intake behaviour between tumour-bearing (TB) mice in response to growth of the two different tumours was used to distinguish between processes involved in cachexia and mechanisms that might be important in food intake regulation. The hypothalamus was used for transcriptomics (affymetrix chips). Results: In both models, hypothalamic expression of orexigenic NPY was significantly higher compared with controls, suggesting that this change does not directly reflect food intake status but might be linked to negative energy balance in cachexia. Expression of genes involved in serotonin signalling showed to be different between C26-TB mice and Lewis lung carcinoma-TB mice and was inversely associated with food intake. In vitro, using hypothalamic cell lines, serotonin repressed neuronal hypothalamic NPY secretion while not affecting messenger NPY expression, suggesting that serotonin signalling can interfere with NPY synthesis, transport, or secretion. Conclusions: Altered serotonin signalling is associated with changes in food intake behaviour in cachectic TB mice. Serotonins' inhibitory effect on food intake under cancer cachectic conditions is probably via affecting the NPY system. Therefore, serotonin regulation might be a therapeutic target to prevent the development of cancer-induced eating disorders.
2014-10-31 | GSE57189 | GEO