Affiliation:
1. Department of Biological Sciences, Texas Tech University, 2500 Broadway, Lubbock, TX 79409, USA
2. Obesity Research Institute, Texas Tech University, 2500 Broadway, Lubbock, TX 79409, USA
Abstract
The excess consumption of a high-fat diet has been identified as one of the factors contributing to obesity. Women are at higher risk of adult obesity than men, predisposing them to a different set of detrimental disease conditions. Furthermore, aging studies show that physiological decline also has a serious impact on changes in the endocrine properties of white adipose tissue. However, there is still relatively little known about the factors associated with obesity and aging and their compounding impacts on women’s health. To investigate changes in adipocytokine secretion profiles, obesity was induced in female C3H/HeJ mice through the long-term consumption of a high-fat diet. Weight gain measurements and the Echo MRI analysis of fat composition showed that increases were due solely to the high fat content in the diet. Adipocytokine secretions were analyzed in media conditioned from harvested visceral fat tissue that was organ-cultured ex vivo. Adipocytokine analysis performed across diets and ages showed that there were significant increases in Adiponectin and Leptin secretion in high-fat diets, accelerating increases in Resistin secretion in high-fat diets. Aging induced the increased secretion of Lipcalin-2, Pentraxin-3, Serpin E1, MCP-1, and ICAM-1, regardless of diet. Furthermore, the comparisons of organoid-cultured protein secretions and flash-frozen tissue samples differed greatly, suggesting the WAT organoid cultures may yield information that is more reflective of in situ conditions. Taken together, our results show that high-fat diets and aging in C3H/HeJ female mice significantly impact secretions from adipose tissue, which may contribute to women’s health issues.
Funder
Texas Tech Association of Biologists Grants-in-Aid
Department of Biological Sciences at Texas Tech University
Empirical Foods Inc.
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