The Role of Gender Differences and Menopause in Obesity-Related Renal Disease, Renal Inflammation and Lipotoxicity

The pathogenesis of obesity-related-renal disease is unknown. Menopause can promote renal disease in obese women, but this interaction is unclear. In a previous study, we observed that obese male and female mice developed albuminuria, hyperfiltration, and glomerulomegaly, and these changes were more severe in those obese ovariectomized females. In this study, we also evaluated renal inflammation and lipotoxicity in that animal model. For six months, 43 males and 36 females C57BL6/J mice were randomized to standard diet (SD) or high fat diet (HFD). A group of female animals on SD or HFD was ovariectomized to simulate menopause. We evaluated cytokines: NF-kappa beta p65, IL-1 beta, MCP-1, TNF-alpha, total lipid content, lipid classes, and fatty acid profile in total lipid and individual lipid classes in renal tissue and urine. We found that obese males and females showed higher NF-kappa beta p-65, TNF-alpha and MCP-1 in renal tissue, and obese females ovariectomized had higher IL-1 beta and TNF-alpha compared with not-ovariectomized. Also, obese animals showed lower proinflammatory and higher anti-inflammatory fatty acids in kidney total lipids, while obese females ovariectomized had a more exacerbated pattern. In brief, obesity induces inflammation and an unbalanced lipidic profile in renal tissue. This pattern seems to be enhanced in obesity after menopause.

Automated summary

The pathogenesis of obesity-related-renal disease is not clear, and the interaction between menopause and renal disease in obese women is still unknown. In this study, obese male and female mice developed albuminuria, hyperfiltration, and glomerulomegaly, and these changes were more severe in obese ovariectomized females. Obesity induced inflammation and an unbalanced lipidic profile in renal tissue, and this pattern seems to be enhanced in obesity after menopause.