ArticleAmerican journal of physiology. Endocrinology and metabolism2012
Glucocorticoids antagonize tumor necrosis factor-α-stimulated lipolysis and resistance to the antilipolytic effect of insulin in human adipocytes.
Article in American journal of physiology. Endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Walnuts change lipoprotein composition suppressing TNFα-stimulated cytokine production by diabetic adipocyte.The Journal of nutritional biochemistry · 2019Trial
- Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct.Diabetes, obesity & metabolism · 2017Trial
- Acute Hypercortisolemia Exerts Depot-Specific Effects on Abdominal and Femoral Adipose Tissue Function.The Journal of clinical endocrinology and metabolism · 2017Trial
- Dousing the flame: reviewing the mechanisms of inflammatory programming during stress-induced intrauterine growth restriction and the potential for ω-3 polyunsaturated fatty acid intervention.Frontiers in physiology · 2023Review
- Impact of blood perilipin A levels on obesity and metabolic health.BMC research notes · 2022Observational
- Article
- Contributions of white and brown adipose tissues to the circadian regulation of energy metabolism.Endocrinology · 2021Review
- Article
- RBP4 increases lipolysis in human adipocytes and is associated with increased lipolysis and hepatic insulin resistance in obese women.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Rosiglitazone remodels the lipid droplet and britens human visceral and subcutaneous adipocytes ex vivo.Journal of lipid research · 2019Article
- How does leptin restore euglycemia in insulin-deficient diabetes?The Journal of clinical investigation · 2017Article
- Low expression of the GILZ may contribute to adipose inflammation and altered adipokine production in human obesity.Journal of lipid research · 2016Article
- Silencing Mediator of Retinoid and Thyroid Hormone Receptors (SMRT) regulates glucocorticoid action in adipocytes.Molecular and cellular endocrinology · 2015Article
- Inflammation and Nutritional Science for Programs/Policies and Interpretation of Research Evidence (INSPIRE).The Journal of nutrition · 2015Review
- The glucocorticoid receptor, not the mineralocorticoid receptor, plays the dominant role in adipogenesis and adipokine production in human adipocytes.International journal of obesity (2005) · 2014Article
- Loss of the TNFα function inhibits Wnt/β-catenin signaling, exacerbates obesity development in adolescent spontaneous obese mice.Molecular and cellular biochemistry · 2014Article
- Prolonged efficiency of siRNA-mediated gene silencing in primary cultures of human preadipocytes and adipocytes.Obesity (Silver Spring, Md.) · 2014Article
- Mechanisms of glucocorticoid-induced insulin resistance: focus on adipose tissue function and lipid metabolism.Endocrinology and metabolism clinics of North America · 2014Review
- Deconstructing the roles of glucocorticoids in adipose tissue biology and the development of central obesity.Biochimica et biophysica acta · 2014Review
- Optimal protocol for the differentiation and metabolic analysis of human adipose stromal cells.Methods in enzymology · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
High concentrations of TNF within obese adipose tissue increase basal lipolysis and antagonize insulin signaling. Adipocytes of the obese are also exposed to elevated levels of glucocorticoids (GCs), which antagonize TNF actions in many cell types. We tested the hypothesis that TNF decreases sensitivity to the antilipolytic effect of insulin and that GCs antagonize this effect in differentiated human adipocytes. Lipolysis and expression levels of lipolytic proteins were measured after treating adipocytes with TNF, dexamethasone (DEX), or DEX + TNF for up to 48 h. TNF not only increased basal lipolysis, it caused resistance to the antilipolytic effects of insulin in human adipocytes. DEX alone did not significantly affect lipolysis. Cotreatment with DEX blocked TNF induction of basal lipolysis and insulin resistance by antagonizing TNF stimulation of PKA-mediated phosphorylation of hormone-sensitive lipase (HSL) at Ser⁵⁶³ and Ser⁶⁶⁰ and perilipin. TNF did not affect perilipin, HSL, or phosphodiesterase-3B mass but paradoxically suppressed adipose tissue triglyceride lipase expression, and this effect was blocked by DEX. The extent to which GCs can restrain the lipolytic actions of TNF may both diminish the potentially deleterious effects of excess lipolysis and contribute to fat accumulation in obesity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.