Role of glucocorticoids in the regulation of lipogenesis

Berdanier, Carolyn D.

doi:10.1096/fasebj.3.10.2666232

Cited by 91 publications

(35 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Glucocorticoids act to modulate intermediary metabolism in a nutritionally dependent manner, stimulating lipogenesis and TG formation in the fed state (7,8) and WAT lipolysis in the fasted state (9 -11). Glucocorticoid levels fluctuate throughout the day in accordance with this, displaying their largest peak in the morning following an overnight fast (12).…”

Section: ؊/؊mentioning

confidence: 99%

Angiopoietin-like 4 (Angptl4) Protein Is a Physiological Mediator of Intracellular Lipolysis in Murine Adipocytes

Gray

Lam

Yang

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Angiopoietin-like 4 (Angptl4) is a secreted protein involved in triacylglycerol homeostasis. Results: Angptl4 was required for fasting, glucocorticoids, and catecholamines to stimulate cAMP-dependent signaling and triacylglycerol hydrolysis in murine fat, a response reproduced by treating adipocytes with purified ANGPTL4. Conclusion: Angptl4 is a physiological mediator of lipolysis. Significance: This finding may impact aberrant lipolytic states like insulin resistance.

show abstract

Section: ؊/؊mentioning

confidence: 99%

Angiopoietin-like 4 (Angptl4) Protein Is a Physiological Mediator of Intracellular Lipolysis in Murine Adipocytes

Gray

Lam

Yang

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…During adipogenesis, glucocorticoids are required to induce the adipogenic transcriptional program allowing the differentiation of preadipocytes to mature adipocytes (Hauner et al 1989). In the final step of differentiation, glucocorticoids promote also the lipid uptake and lipid storage in mature adipocytes (Berdanier 1989, Fried et al 1993. In mice, adipocyte-specific amplification of glucocorticoids through selective overexpression of 11βHSD1, the enzyme converting the inactive cortisone to active cortisol, induces central obesity and associated metabolic disorders (Masuzaki et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Adipocyte glucocorticoid receptor has a minor contribution in adipose tissue growth

Desarzens

Faresse

2016

Journal of Endocrinology

View full text Add to dashboard Cite

The glucocorticoids bind and activate both the glucocorticoid receptor (GR) as well as the mineralocorticoid receptor in adipocytes. Despite several studies to determine the function of these two receptors in mediating glucocorticoids effects, their relative contribution in adipose tissue expansion and obesity is unclear. To investigate the effect of GR in adipose tissue function, we generated an adipocyte-specific Gr-knockout mouse model (Gr ad-ko ). These mice were submitted either to a standard diet or a high-fat high sucrose diet. We found that adipocyte-specific deletion of Gr did not affect body weight gain or adipose tissue formation and distribution. However, the lack of Gr in adipocyte promotes a diet-induced inflammation determined by higher pro-inflammatory genes expression and macrophage infiltration in the fat pads. Surprisingly, the adipose tissue inflammation in Gr ad-ko mice was not correlated with insulin resistance or dyslipidemia, but with disturbed glucose tolerance. Our data demonstrate that adipocyte-specific ablation of Gr in vivo may affect the adipose tissue function but not its expansion during a high calorie diet.

show abstract

“…In liver, these agents influence the expression of serum proteins that regulate immune/inflammatory responses (Morand and Leech, 1999). Expression of liver enzymes involved in metabolic effects, such as gluconeogenesis and lipid metabolism, is also altered (Berdanier, 1989;Andrews and Walker, 1999). In addition, CS modify the metabolism of many endogenous and exogenous substrates (Prough et al, 1996).…”

mentioning

confidence: 99%

Modeling of Corticosteroid Pharmacogenomics in Rat Liver Using Gene Microarrays

Jin¹,

Almon²,

DuBois³

et al. 2003

J Pharmacol Exp Ther

143

129

View full text Add to dashboard Cite

Corticosteroid (CS) pharmacogenomics was studied using gene microarrays in rat liver. Methylprednisolone (MPL) was administered intravenously at 50 mg/kg. Rats were sacrificed and liver excised at 17 time points over 72 h. RNAs from individual livers were used to query Affymetrix GeneChips that contain sequences for 8000 genes. Cluster analysis revealed six temporal patterns consisting of 197 CS-responsive probes representing 143 genes. Based on our fifth-generation model of CS pharmacokinetics/pharmacodynamics (PK/PD), mechanistic models were developed to describe the time pattern for each CS-responsive gene. Two clusters showed increased expression with different effect duration. PK/PD models assuming CS stimulation of mRNA synthesis were applied. Another two clusters showed an initial decline followed by delayed increase, suggesting two mechanisms might be involved jointly. The initial suppression was captured by CS inhibition of mRNA synthesis or stimulation of degradation. CS may also stimulate the production of a biosignal (transcription factors or other hormones), which can cause secondary induction of the target mRNA. One cluster showed a very abrupt increase in message followed by rapid decrease. These genes were lymphocytic in origin and were modeled combining the fast gene induction effect of CS in lymphoid cells and its direct lymphocyte trafficking effect. Another cluster showed reduction persisting for 18 h, which was described by CS inhibition of mRNA synthesis. Our results reveal the marked diversity of genes regulated by CS via a limited array of mechanisms. These PK/PD models provide quantitation of CS pharmacogenomics and new hypotheses regarding understanding of diverse mechanisms of CS receptor-gene mediated action.

show abstract

Role of glucocorticoids in the regulation of lipogenesis

Cited by 91 publications

References 31 publications

Angiopoietin-like 4 (Angptl4) Protein Is a Physiological Mediator of Intracellular Lipolysis in Murine Adipocytes

Angiopoietin-like 4 (Angptl4) Protein Is a Physiological Mediator of Intracellular Lipolysis in Murine Adipocytes

Adipocyte glucocorticoid receptor has a minor contribution in adipose tissue growth

Modeling of Corticosteroid Pharmacogenomics in Rat Liver Using Gene Microarrays

Contact Info

Product

Resources

About