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Insulin and insulin-like growth factor-1 can modulate the phosphoinositide-3-kinase/Akt/FoxO1 pathway in SZ95 sebocytes in vitro
Abstract
A recent hypothesis suggests that a high glycaemic load diet-associated increase of insulin-like growth factor-1 (IGF-1) and insulin may promote acne by reducing nuclear localization of the forkhead box-O1 (FoxO1) transcription factor via activation of the phosphoinositide-3-kinase (PI3K)/Akt pathway. Using SZ95 sebocytes as a model, we investigated the effect of the most important insulinotropic western dietary factors, IGF-1 and insulin on acne. SZ95 sebocytes were stimulated with different concentrations of IGF-1 and insulin (0.001, 0.01, 0.1 and 1 μM) for 15 to 120 min ± PI3K inhibitor LY294002 (50 μM). Cytoplasmic and nuclear protein expression of p-Akt and p-FoxO1 as well as FoxO transcriptional activity was analysed. In addition, the proliferation and differentiation of sebocytes and their TLR2/4 expression were determined. We found that high concentrations of IGF-1 and insulin differentially stimulate the PI3K/Akt/FoxO1 pathway by an early up-regulation of cytoplasmic p-Akt and delayed up-regulation of p-FoxO1 resulting in FoxO1 shift to the cytoplasm and the reduction of FoxO transcriptional activity, physiological serum concentration had no effect. IGF-1 at concentrations of 0.1 and 1 μM significantly reduced proliferation but increased differentiation of sebocytes to a greater extent than insulin (0.1 and 1 μM), but up-regulated TLR2/4 expression to comparable extent. These data provide the first in vitro evidence that FoxO1 principally might be involved in the regulation of growth-factor-stimulatory effects on sebaceous lipogenesis and inflammation in the pathological condition of acne. However, the in vivo significance under physiological conditions remains to be elucidated.
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“The presence of the IGF-1 receptor in sebocytes has been described and was shown to activate the PI3K/ Akt/FoxO1 pathway”
From Sebaceous-immunobiology is orchestrated by sebum lipids (2017) · cites this paper as [84]
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“thus providing evidence that FoxO1 may be a key factor in the regulation of growth-factor stimulatory effects on sebaceous lipogenesis and inflammation in response to elevated IGF-1 and insulin levels.84”
From Sebaceous-immunobiology is orchestrated by sebum lipids (2017) · cites this paper as [84]
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Metadata
- Authors
- Mirdamadi, Y., Thielitz, A., Wiede, A., Goihl, A., Papakonstantinou, E., Hartig, R., Zouboulis, C. C., Reinhold, D., Simeoni, L., Bommhardt, U., Quist, S., & Gollnick, H.
- Affiliations
- Otto-von-Guericke-Universität Magdeburg (DE)
- Städtisches Klinikum Dessau (DE)
- Corresponding author
- Gollnick, Harald
- Venue
- Molecular and Cellular Endocrinology
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 415
- Pages
- 32-44
- ISSN
- 0303-7207 (ISSN-L)
- OpenAlex
- W1080640958
- Cited by
- 109
- References
- 54
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 7 · 2023: 5 · 2022: 10 · 2021: 14 · 2020: 14 · 2019: 6 · 2018: 13 · 2017: 17 · 2016: 9 · 2015: 1
- FWCI
- 14.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular and Cellular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Department Dermatology & Venereology Otto-von-Guericke University Magdeburg/Germany
- Topics
- Health Sciences › Medicine › Dermatology › Acne and Rosacea Treatments and Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › FOXO transcription factor regulation
- Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
- Keywords
- insulin, insulin-like growth factor I, FOXO1, PI3K/Akt signaling, sebocytes, acne, lipogenesis, TLR2/4, LY294002
- MeSH terms
- Forkhead Box Protein O1, Acne Vulgaris, Cell Differentiation, Cell Line, Gene Expression Regulation, Humans, Insulin, Insulin-Like Growth Factor I, Models, Biological, Signal Transduction, Phosphatidylinositol 3-Kinases, Cell Proliferation, Lipogenesis, Proto-Oncogene Proteins c-akt, Toll-Like Receptor 2, Toll-Like Receptor 4, Forkhead Transcription Factors, In Vitro Techniques
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