Glucocorticoid Modulation of Insulin Signaling in Human Subcutaneous Adipose Tissue
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CONTEXT: Glucocorticoid (GC) excess is characterized by central obesity, insulin resistance, and in some cases, type 2 diabetes. However, the impact of GC upon insulin signaling in human adipose tissue has not been fully explored. OBJECTIVE: We have examined the effect of GC upon insulin signaling in both human sc primary preadipocyte cultures and a novel human immortalized sc adipocyte cell line (Chub-S7) and contrasted this with observations in primary cultures of human skeletal muscle. DESIGN AND SETTING: This is an in vitro study characterizing the impact of GC upon insulin signaling in human tissues. PATIENTS: Biopsy specimens were from healthy volunteers who gave their full and informed written consent. INTERVENTIONS: Combinations of treatments, including GC, RU38486, and wortmannin, were used. MAIN OUTCOME MEASURES: Insulin signaling cascade gene and protein expression and insulin-stimulated glucose uptake were determined. RESULTS: In human adipocytes, pretreatment with GC induced a dose-dependent [1.0 (control); 1.2 +/- 0.1 (50 nm); 2.2 +/- 0.2 (250 nm), P < 0.01 vs. control; 3.4 +/- 0.2 (1000 nm), P < 0.001 vs. control] and time-dependent [1.0 (1 h); 3.2 +/- 2.0 (6 h); 9.1 +/- 5.9 (24 h), P < 0.05 vs. 1 h; 4.5 +/- 2.2 (48 h)] increase in insulin-stimulated protein kinase B/akt phosphorylation. In addition, whereas insulin receptor substrate (IRS)-1 protein expression did not change, IRS-1 tyrosine phosphorylation increased. Furthermore, GC induced IRS-2 mRNA expression (2.8-fold; P < 0.05) and increased insulin-stimulated glucose uptake [1.0 (control) 1.8 +/- 0.1 (insulin) vs. 2.8 +/- 0.2 (insulin + GC); P < 0.05]. In contrast, in primary cultures of human muscle, GC decreased insulin-stimulated glucose uptake [1.0 (control) 1.9 +/- 0.2 (insulin) vs. GC 1.3 +/- 0.1 (insulin + GC); P < 0.05]. CONCLUSIONS: We have demonstrated tissue-specific regulation of insulin signaling by GC. Within sc adipose tissue, GCs augment insulin signaling, yet in muscle GCs cause insulin resistance. We propose that enhanced insulin action in adipose tissue increases adipocyte differentiation, thereby contributing to GC-induced obesity.
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Glucocorticoids induce insulin resistance in liver and muscle but sensitize insulin signaling in adipose tissues.
“Although glucocorticoids induce insulin resistance (IR) in liver and muscle, they are known to sensitize insulin signaling in adipose tissues (26).”
From Mechanistic inferences on metabolic dysfunction in posttraumatic stress disorder from an integrated model and multiomic analysis: role of glucocorticoid receptor sensitivity (2019) · cites this paper as [26]
The Discussion reports glucocorticoid-induced insulin resistance in human muscle cultures and reduced insulin-signaling markers in rodent liver. It also reports enhanced insulin signaling in human subcutaneous adipose cells, but says the study cannot address intra-abdominal adipose tissue and that insulin-stimulated glucose uptake in adipose tissue as a whole remains unclear. The claim therefore overgeneralizes the adipose finding. (LLM, conf=0.88)
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- Authors
- Gathercole, L. L., Bujalska, I. J., Stewart, P. M., & Tomlinson, J. W.
- Affiliations
- University of Birmingham (GB)
- Corresponding author
- Tomlinson, Jeremy W.
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2007-11-01
- Volume
- 92
- Issue
- 11
- Pages
- 4332-4339
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- PMC
- PMC7611650
- OpenAlex
- W2104246562
- Semantic Scholar
- 680257296a944dee3f38e8e5ecd8d6ed2b9aafdd
- Cited by
- 73
- References
- 47
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 1 · 2023: 3 · 2022: 6 · 2021: 1 · 2020: 4 · 2019: 3 · 2018: 4 · 2017: 5 · 2016: 4 · 2015: 6 · 2014: 1 · 2013: 8 · 2012: 5
- FWCI
- 2.95
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
- Funders
- Wellcome Trust (075322/Z/04/Z)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- glucocorticoids, insulin signaling, subcutaneous adipose tissue, insulin resistance, insulin-stimulated glucose uptake, Akt phosphorylation, IRS-1 tyrosine phosphorylation, skeletal muscle, mifepristone, wortmannin, preadipocytes, type 2 diabetes, abdominal obesity
- MeSH terms
- Cell Line, Dose-Response Relationship, Drug, Glucocorticoids, Glucose, Humans, Insulin, Insulin Resistance, Receptors, Glucocorticoid, RNA, Messenger, Stem Cells, Signal Transduction, Adipocytes, Muscle Fibers, Skeletal, Reverse Transcriptase Polymerase Chain Reaction, Myoblasts, Subcutaneous Fat, Lipid Metabolism
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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