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Glucocorticoids Down-Regulate Glucose Uptake Capacity and Insulin-Signaling Proteins in Omental But Not Subcutaneous Human Adipocytes
Abstract
Visceral adiposity is associated with insulin resistance and type 2 diabetes. This study explores the metabolic differences between s.c. and visceral fat depots with respect to effects in vitro of glucocorticoids and insulin on glucose uptake. Adipocytes from human s.c. and omental fat depots were obtained during abdominal surgery in 18 nondiabetic subjects. Cells were isolated, and metabolic studies were performed directly after the biopsies and after a culture period of 24 h with or without dexamethasone. After washing, basal and insulin-stimulated [14C]glucose uptake as well as cellular content of insulin signaling proteins and glucose transporter 4 (GLUT4) was assessed. Omental adipocytes had an approximately 2-fold higher rate of insulin-stimulated glucose uptake compared with s.c. adipocytes (P < 0.01). Dexamethasone treatment markedly inhibited (by approximately 50%; P < 0.05) both basal and insulin-stimulated glucose uptake in omental adipocytes but had no consistent effect in s.c. adipocytes. The cellular content of insulin receptor substrate 1 and phosphatidylinositol 3-kinase did not differ significantly between the depots, but the expression of protein kinase B (PKB) tended to be increased in omental compared with s.c. adipocytes (P = 0.09). Dexamethasone treatment decreased the expression of insulin receptor substrate 1 (by approximately 40%; P < 0.05) and PKB (by approximately 20%; P < 0.05) in omental but not in s.c. adipocytes. In contrast, dexamethasone pretreatment had no effect on insulin-stimulated Ser473 phosphorylation of PKB. GLUT4 expression was approximately 4-fold higher in omental than s.c. adipocytes (P < 0.05). Dexamethasone treatment did not alter the expression of GLUT4. In conclusion, human omental adipocytes display approximately 2-fold higher glucose uptake rate compared with s.c. adipocytes, and this could be explained by a higher GLUT4 expression. A marked suppression is exerted by glucocorticoids on glucose uptake and on the expression of insulin signaling proteins in omental but not in s.c. adipocytes. These findings may be of relevance for the interaction between endogenous glucocorticoids and visceral fat in the development of insulin resistance.
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“GCs were shown to interfere with insulin signalling in vitro and in vivo in rodents in liver [38], adipose tissue [39] and skeletal muscle [40].”
From Low-dose glucocorticoid treatment affects multiple aspects of intermediary metabolism in healthy humans: a randomised controlled trial (2011) · cites this paper as [39]
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Self-citation
Metadata
- Authors
- Lundgren, M., Burén, J., Ruge, T., Myrnäs, T., & Eriksson, J. W.
- Affiliations
- Departments of Medicine (M.L., J.B., T.R., J.W.E.); SE-901 85, Sweden
- Surgery (T.M.), Umeå University Hospital, Umeå SE-901 85, Sweden
- Corresponding author
- Eriksson, J. W.
- ORCID
- Ruge, T.
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2004-06-01
- Volume
- 89
- Issue
- 6
- Pages
- 2989-2997
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W2015237552
- Semantic Scholar
- 3ac8ca39fe13f06f9ca60a9ec018ce4f020beaba
- Cited by
- 163
- References
- 58
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 3 · 2022: 9 · 2021: 7 · 2020: 3 · 2019: 4 · 2018: 7 · 2017: 5 · 2016: 13 · 2015: 6 · 2014: 7 · 2013: 11 · 2012: 8
- FWCI
- 7.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- glucocorticoids, dexamethasone, glucose uptake, insulin signaling, omental adipocytes, subcutaneous adipocytes, visceral adipose tissue, GLUT4, IRS-1, phosphatidylinositol 3-kinase, Akt, insulin resistance, type 2 diabetes, adipocyte metabolism, insulin-stimulated glucose uptake
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Biological Transport, Carbon Radioisotopes, Cells, Cultured, Dexamethasone, Female, Glucocorticoids, Glucose, Humans, Insulin, Male, Middle Aged, Monosaccharide Transport Proteins, Muscle Proteins, Omentum, Signal Transduction, Adipocytes, Subcutaneous Tissue, Glucose Transporter Type 4
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