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Dexamethasone treatment alters levels of insulin, leptin, and adiponectin but does not have metabolic effects across generations

ABSTRACT: Genome-wide expression analysis of sperms did not identify significant transcriptome changes upon dexamethasone treatment in mice. These results are consistent with the observation that dexamethasone treatment of parental male mice did not induce metabolic changes in the F1 generation.

ORGANISM(S): Mus musculus

PROVIDER: GSE67290 | GEO | 2015/11/25

SECONDARY ACCESSION(S): PRJNA279415

REPOSITORIES: GEO

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Dexamethasone treatment alters levels of insulin, leptin, and adiponectin but does not have metabolic effects across generations

Project description:Genome-wide expression analysis of sperms did not identify significant transcriptome changes upon dexamethasone treatment in mice. These results are consistent with the observation that dexamethasone treatment of parental male mice did not induce metabolic changes in the F1 generation. We performed gene expression microarray analysis of sperms derived from dexamethasone-treated (n=8) or control mice (n=7).

2015-11-25 | E-GEOD-67290 | biostudies-arrayexpress

Dexamethasone treatment alters insulin, leptin, and adiponectin levels in male mice as observed in DIO but does not lead to alterations of metabolic phenotypes in the offspring.

Project description:Epigenetic inheritance (EI) of metabolic phenotypes via the paternal lineage has been shown in rodent models of diet-induced obesity (DIO). However, the factors involved in soma-to-germline information transfer remain elusive. Here, we address the role of alterations in insulin, leptin, and adiponectin levels for EI of metabolic phenotypes by treating C57BL/6NTac male mice (F0) with the synthetic glucocorticoid dexamethasone and generating offspring (F1) either by in vitro fertilization or by natural fecundation. Dexamethasone treatment slightly alters F0 body composition by increasing fat mass and decreasing lean mass, and significantly improves glucose tolerance. Moreover, it increases insulin and leptin levels and reduces adiponectin levels in F0 fathers as observed in mouse models of DIO. However, these paternal changes of metabolic hormones do not alter metabolic parameters, such as body weight, body composition and glucose homeostasis in male and female F1 mice even when these are challenged with a high-fat diet. Accordingly, sperm transcriptomes are not altered by dexamethasone treatment. Our results suggest that neither increased glucocorticoid, insulin, and leptin levels, nor decreased adiponectin levels in fathers are sufficient to confer soma-to-germline information transfer in EI of obesity via the paternal lineage.

| S-EPMC4731435 | biostudies-literature

Rat liver: Dexamethasone treatment vs. Control

Project description:Sixteen male Sprague-Dawley rats were randomly allocated into 2 groups (8 rats per group) as follows: the control group (CON) and the dexamethasone-treated group (DEXA). Dexamethasone-treated rats received a daily intraperitoneal injection of 1.5 mg/kg of dexamethasone for 5 days. All rats were fasted during the night following the fifth day. On the sixth day, the animals were killed by decapitation. In order to focus our investigation on metabolism-related genes, we developed a metabolism dedicated microarray tool: the Mitoligo. Using this microarray tool, we were able to determine that energy metabolism was deeply modified by dexamethasone treatment. Dexamethasone treatment to rats induces a complete switch of the metabolism toward a maximal rate of ATP synthesis. In this study, we show that substrate supplying for oxidative phosphorylation is greatly enhanced. We also confirm that oxidative phosphorylation capacity is increased by dexamethasone treatment. Keywords: hormonal treatment

2008-01-13 | GSE9035 | GEO

c3h10t1/2 with dexamethasone

Project description:determine genes regulated by dexamethasone in c3h10t1/2 cells after 90 minutes of treatment compared to vehicle Keywords: treatment comparison microarray

2008-03-21 | GSE10900 | GEO

Effects of Dexamethasone in COVID-19 patients

Project description:Dexamethasone improves the survival of COVID-19 patients in need of supplemental oxygen therapy. Hospitalized COVID-19 patients eligible for dexamethasone therapy were recruited from the general care ward in several centers in Greece and the Netherlands and whole blood transcriptomic analysis was performed before and after starting dexamethasone treatment. Peripheral blood mononuclear cells (PBMCs) were isolated from healthy individuals and COVID-19 patients and stimulated with inactivated SARS-CoV-2 ex vivo in the presence or absence of dexamethasone and their transcriptome was assessed.

2023-07-26 | GSE227585 | GEO

c3h10t1/2 with dexamethasone

Project description:determine genes regulated by dexamethasone in c3h10t1/2 cells after 90 minutes of treatment compared to vehicle Keywords: treatment comparison microarray c3h10t1/2 cells were treated with vehicle or 1uM dexamethasone for 90 minutes (3 biological replicates of each) RNA samples were isolated from RNeasy kit (Qiagen) hybridized all samples to a pool of RNA from vehicle and treated c3h10t1/2 cells

2010-05-25 | E-GEOD-10900 | biostudies-arrayexpress

FKBP5 expression in human adipose tissue increases following dexamethasone exposure and is associated with insulin resistance

Project description:Glucocorticoid excess is linked to central obesity, adipose tissue insulin resistance and type 2 diabetes mellitus. The aim of our study was to investigate the effects of dexamethasone on gene expression in human subcutaneous and omental adipose tissue, in order to identify potential novel mechanisms and biomarkers for glucocorticoid-induced insulin resistance in adipose tissue. Dexamethasone changed the expression of 527 genes in both subcutaneous and omental adipose tissue. FKBP5 and CNR1 were the most responsive genes in both depots (~7-fold increase). Dexamethasone increased FKBP5 gene and protein expression in a dose-dependent manner in both depots, but FKBP5 protein levels were 10-fold higher in omental than subcutaneous adipose tissue. FKBP5 gene expression in subcutaneous adipose tissue was positively correlated with serum insulin, HOMA-IR and subcutaneous adipocyte diameter, while fold change in gene expression by dexamethasone was negatively correlated with clinical markers of insulin resistance, i.e. HbA1c, BMI, HOMA-IR and serum insulin. Only one gene, SERTM1, clearly differed in response to dexamethasone between the two depots. Dexamethasone at high concentrations, influences gene expression in both subcutaneous and omental adipose tissue in a similar pattern and promotes gene expression of FKBP5, a gene that may be implicated in glucocorticoid-induced insulin resistance.

2014-08-18 | GSE42902 | GEO

Associations of body mass index and insulin resistance with leptin, adiponectin, and the leptin-to-adiponectin ratio across ethnic groups: the Multi-Ethnic Study of Atherosclerosis (MESA).

Project description:PurposeAssociations of adiponectin and leptin and their ratio with body mass index (BMI) and homeostasis model assessment of insulin resistance (HOMA-IR) have been investigated in different ethnic groups but variability in both assays and statistical methods have made cross-study comparisons difficult. We examined associations among these variables across four ethnic groups in a single study.MethodsAdiponectin and leptin were measured in a subset of participants from the Multi-Ethnic Study of Atherosclerosis study. We calculated associations (using both partial correlations and adjusted linear regression) in each ethnic group and then compared the magnitude of these associations across groups.ResultsAfter we excluded individuals with type 2 diabetes, there were 714 white, 219 Chinese, 332 African-American, and 405 Hispanic subjects in the study sample. Associations of BMI with adiponectin and leptin differed significantly (P < .05) across the ethnic groups in regression analyses, whereas associations of HOMA-IR with adiponectin and leptin did not differ across ethnic groups. The leptin-to-adiponectin ratio was not associated with a greater amount of adiposity or HOMA-IR variance than leptin or adiponectin in any ethnic group.ConclusionsGiven the consistency of HOMA-IR and adipokine associations, the differing means of adiponectin and leptin across ethnic groups may help to explain ethnic differences in mean insulin resistance.

| S-EPMC3459265 | biostudies-literature

Leptin/Adiponectin Ratios Using Either Total Or High-Molecular-Weight Adiponectin as Biomarkers of Systemic Insulin Sensitivity in Normoglycemic Women.

Project description:Plasma leptin/adiponectin ratio (LAR) is negatively associated with insulin sensitivity indexes. High-molecular-weight adiponectin (HMWA) was proposed as the most biologically active form of this insulin-sensitizing adipokine. There are no studies assessing the relative merits of leptin/HMWA ratio over LAR as a biomarker of systemic insulin sensitivity. A standard 2-hour oral glucose tolerance test (OGTT; 75 g of glucose) and a short minimal-model intravenous glucose tolerance test (IVGTT; 0.3 g/kg body weight) were performed in 58 Chilean normoglycemic women (age: 27 ± 6.3 years, BMI 23.6 ± 3.2 kg/m2). LAR was negatively associated with HOMA-S (r = -0.49; p < 0.0001), Matsuda-ISICOMP (r = -0.54; p < 0.0001), and the calculated sensitivity index (CSi) derived from IVGTT (r = -0.38; p = 0.007). In comparison to LAR, leptin/HMWA ratio did not increase neither the linear fit (r2) nor the magnitude of association with insulin sensitivity indexes (slope of multiple linear regression). The discriminatory capacity of both ratios to classify insulin-resistant versus insulin-sensitive subjects was similar for HOMA-S (p = 0.84), Matsuda-ISICOMP (p = 0.43), or CSi (p = 0.50). In conclusion, LAR showed consistent negative associations with different systemic insulin sensitivity indexes. The use of HMWA to generate leptin/HMWA ratio did not show any advantage over LAR as a biomarker of systemic insulin sensitivity in normoglycemic women.

| S-EPMC5463152 | biostudies-literature

Trancriptional signatures of dexamethasone-treated sarcoidosis monocytes.

Project description:The goal of this study was to determine the effect of dexamethasone treatment on trancriptional sigantures and pathways of sarcoidosis monocytes.

2020-05-20 | GSE150049 | GEO

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