Anti-inflammatory effects of oestrogen mediate the sexual dimorphic response to lipid-induced insulin resistance
Open accessAbstract
Key points: Oestrogen has been shown to play an important role in the regulation of metabolic homeostasis and insulin sensitivity in both human and rodent studies. Insulin sensitivity is greater in premenopausal women compared with age‐matched men, and metabolism‐related cardiovascular diseases and type 2 diabetes are less frequent in these same women. Both female and male mice treated with oestradiol are protected against obesity‐induced insulin resistance. The protection against obesity‐induced insulin resistance is associated with reduced ectopic lipid content in liver and skeletal muscle. These results were associated with increased insulin‐stimulated suppression of white adipose tissue lipolysis and reduced inflammation. Oestrogen has been shown to play an important role in the regulation of metabolic homeostasis and insulin sensitivity in both human and rodent studies. Overall, females are protected against obesity‐induced insulin resistance; yet, the mechanisms responsible for this protection are not well understood. Therefore, the aim of the present work was to evaluate the underlying mechanism(s) by which female mice are protected against obesity‐induced insulin resistance compared with male mice. We studied male and female mice in age‐matched or body weight‐matched conditions. They were fed a high‐fat diet (HFD) or regular chow for 4 weeks. We also studied HFD male mice treated with oestradiol or vehicle. Both HFD female and HFD male mice treated with oestradiol displayed increased whole‐body insulin sensitivity, associated with reduction in ectopic hepatic and muscle lipid content compared to HFD male mice. Reductions in ectopic lipid content in these mice were associated with increased insulin‐stimulated suppression of white adipose tissue (WAT) lipolysis. Both HFD female and HFD male mice treated with oestradiol also displayed striking reductions in WAT inflammation, represented by reductions in plasma and adipose tissue tumour necrosis factor α and interleukin 6 concentrations. Taken together these data support the hypothesis that HFD female mice are protected from obesity‐induced insulin resistance due to oestradiol‐mediated reductions in WAT inflammation, leading to improved insulin‐mediated suppression of WAT lipolysis and reduced ectopic lipid content in liver and skeletal muscle.
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Estrogen replacement reverses some of the detrimental metabolic effects of ovariectomy.
“Estrogen treatment promotes anti-inflammatory and insulin sensitizing effects in both male and female mice (80, 81), and estrogen replacement reverses some of the detrimental metabolic effects of ovariectomy (80, 82–84).”
From Metabolic impact of endogenously produced estrogens by adipose tissue in females and males across the lifespan (2025) · cites this paper as [80]
The Introduction (page unavailable) reports increased fat mass after ovariectomy and improved systemic metabolism with ERα activation in high-fat-fed ovariectomized mice. That supports the general idea that restoring oestrogen signalling can improve metabolic outcomes, but the paper does not report an experiment in which oestrogen replacement reverses effects of ovariectomy; its own oestradiol-treatment experiment used male mice (Methods, page unavailable). (LLM, conf=0.83)
Experimental — accuracy not yet measuredEstrogen treatment promotes anti-inflammatory and insulin sensitizing effects in both male and female mice.
“Estrogen treatment promotes anti-inflammatory and insulin sensitizing effects in both male and female mice (80, 81), and estrogen replacement reverses some of the detrimental metabolic effects of ovariectomy (80, 82–84).”
From Metabolic impact of endogenously produced estrogens by adipose tissue in females and males across the lifespan (2025) · cites this paper as [80]
The Methods (Animal care and protocol) describe oestradiol treatment in male mice only. The Discussion reports improved insulin sensitivity and reduced inflammation in oestradiol-treated males and in females, but it does not report estrogen treatment of female mice. The treatment claim is therefore supported for males, not for both sexes. (LLM, conf=0.88)
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- Authors
- Camporez, J. P., Lyu, K., Goldberg, E. L., Zhang, D., Cline, G. W., Jurczak, M. J., Dixit, V. D., Petersen, K. F., & Shulman, G. I.
- Affiliations
- Universidade de São Paulo (BR)
- Yale University (US)
- University of Pittsburgh (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Camporez, João Paulo
- ORCID
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2019-07-04
- Volume
- 597
- Issue
- 15
- Pages
- 3885-3903
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC6876753
- OpenAlex
- W2953132933
- Cited by
- 71
- References
- 57
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 13 · 2023: 17 · 2022: 9 · 2021: 11 · 2020: 7 · 2019: 4
- FWCI
- 5.90
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK‐116774, P30 DK‐45735, R01 AG‐23686, K01 DK‐099402)
- American Diabetes Association (1‐14‐10 Merck)
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (88887.144251/2017‐00)
- Conselho Nacional de Desenvolvimento Científico e Tecnológico (211490/2013‐4)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- estradiol, estrogen, insulin resistance, obesity, sex differences, high-fat diet, adipose tissue inflammation, lipolysis, ectopic fat deposition, liver lipids, skeletal muscle lipids, TNF-α, interleukin-6, insulin sensitivity, type 2 diabetes
- MeSH terms
- Animals, Body Weight, Cell Line, Cells, Cultured, Estrogens, Female, Insulin Resistance, Lipolysis, Liver, Male, Mice, Inbred C57BL, Sex Characteristics, Tumor Necrosis Factor-alpha, Interleukin-6, Muscle, Skeletal, Mice, Adipose Tissue, White, Diet, High-Fat
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