Oestrogen alters adipocyte biology and protects female mice from adipocyte inflammation and insulin resistance
Open accessAbstract
Aims: Obesity is associated with insulin resistance, liver steatosis and low‐grade inflammation. The role of oestrogen in sex differences in the above co‐morbidities is not fully understood. Our aim was to assess the role oestrogen has in modulating adipocyte size, adipose tissue oxidative stress, inflammation, insulin resistance and liver steatosis. Methods: To determine the role oestrogen has in the above co‐morbidities related to obesity, we randomized C57BL/6J mice into four groups (15 mice per group): (i) male, (ii) non‐ovariectomized female (novx), (iii) ovariectomized female (ovx) and (iv) ovariectomized female mice supplemented with 17 β estradiol (ovx‐E). Mice received either a low‐fat (LF) or a high‐fat (HF) diet for 10 weeks. Outcomes measured were bodyweight, body fat, adipocyte diameter, adipose tissue lipolysis markers, adipose tissue oxidative stress, inflammation, insulin resistance and liver steatosis. Results: Male and ovx‐female mice consuming the HF diet had a higher propensity of gaining weight, specifically in the form of body fat. Oestrogen protected female mice from adipocyte hypertrophy and from developing adipose tissue oxidative stress and inflammation. Moreover, novx‐female and ovx‐female+E mice had higher phosphorylated levels of protein kinase A and hormone sensitive lipase, markers associated with lipolysis. Additionally, male and ovx female mice had a higher propensity of developing liver steatosis and insulin resistance. In contrast, oestrogen protected female mice from developing liver steatosis and from becoming insulin resistant. Conclusion: We show that oestrogen protects female mice from adipocyte hypertrophy and adipose tissue oxidative stress and inflammation. Furthermore, oestrogen prevented female mice from developing liver steatosis and from becoming insulin resistant.
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Estrogen prevented female mice from developing liver steatosis and from becoming insulin resistant.
“Furthermore, estrogen prevented female mice from developing liver steatosis and from becoming insulin resistant [72, 138].”
From Estrogen deficiency and the origin of obesity during menopause (2014) · cites this paper as [138]
Administration of estrogens to ovariectomized female mice significantly reduces mRNA of IL6, TNFα, and CD68.
“Administration of estrogens to ovariectomized female mice reduces significantly the mRNA of IL6, TNFα, and CD68.”
From Estrogen deficiency and the origin of obesity during menopause (2014) · cites this paper as [138]
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- Authors
- Stubbins, R. E., Najjar, K., Holcomb, V. B., Hong, J., & Núñez, N. P.
- Affiliations
- The University of Texas at Austin (US)
- Venue
- Diabetes, Obesity and Metabolism
- Publisher
- Wiley
- Published
- 2011-11-22
- Volume
- 14
- Issue
- 1
- Pages
- 58-66
- ISSN
- 1462-8902 (ISSN-L)
- 1463-1326
- PMC
- PMC3236284
- OpenAlex
- W2166652825
- Cited by
- 204
- References
- 41
- Citations by year
- 2026: 4 · 2025: 13 · 2024: 7 · 2023: 15 · 2022: 8 · 2021: 18 · 2020: 19 · 2019: 16 · 2018: 10 · 2017: 14 · 2016: 16 · 2015: 18 · 2014: 17 · 2013: 19 · 2012: 9
- FWCI
- 11.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Diabetes Obesity and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Cancer Society
- Centre National d’Etudes Spatiales
- National Institutes of Health (5k22ca127519-03)
- National Cancer Institute (K22 CA127519, 1K22 CA127519-01A1)
- National Institute of Environmental Health Sciences (R01ES009145, ES09145, P30ES007784, ES 007784)
- 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 › Genetics › Estrogen and related hormone effects
- Keywords
- estrogen, estradiol, adipocyte hypertrophy, adipose tissue inflammation, insulin resistance, hepatic steatosis, oxidative stress, lipolysis, hormone-sensitive lipase, protein kinase A, ovariectomy, sex differences, obesity, high-fat diet, adipocyte size
- MeSH terms
- Adipose Tissue, Animals, Blood Glucose, Body Weight, Estrogens, Fatty Liver, Female, Hypertrophy, Inflammation, Insulin Resistance, Lipolysis, Male, Mice, Inbred C57BL, Obesity, Ovariectomy, Random Allocation, Triglycerides, Adipocytes, Diet, Fat-Restricted, Mice, Diet, High-Fat
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