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Renal mineralocorticoid receptor expression is reduced in lipoatrophy
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Renal mineralocorticoid receptor expression is reduced in lipoatrophy
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Journal Article
Renal mineralocorticoid receptor expression is reduced in lipoatrophy
2019
Overview
Obesity is a condition characterized by adipose tissue hypertrophy; it is estimated that the obesity epidemic accounted for 4 million deaths in 2015 and that 70% of these were due to cardiovascular disease (CVD). One of the mechanisms linking obesity to CVD is the ability of adipose tissue to secrete circulating factors. We hypothesized that adipose tissue and its secretory products may influence mineralocorticoid receptor (MR) expression. Here, we showed that expression of MR and its downstream targets (Cnksr3, Scnn1b, and Sgk1) were significantly reduced in the kidneys of peroxisome proliferator‐activated receptor‐γ null (PpargΔ/Δ) and A‐ZIP/F‐1 (AZIPtg/+) lipoatrophic mice with respect to their controls. Intriguingly, MR expression was also found to be significantly reduced in the kidneys of genetically obese ob/ob mice. Our data suggest that adipose tissue contributes to the regulation of MR expression. Given that leptin deficiency seems to be the major feature shared by PpargΔ/Δ, AZIPtg/+, and ob/ob mice, we speculate that adipose tissue modulates MR expression through the leptin system. In the kidneys of mouse models of lipoatrophy, we found a significant reduction of mineralocorticoid receptor (MR) expression and its downstream targets. Likewise, there was a significant reduction of MR protein expression in the kidneys of genetically obese ob/ob mice. Given that leptin deficiency is the common feature of these strains, we speculate that leptin might regulate kidney MR expression.
