AI Article Synopsis
- Adiponectin (AdN) is an adipokine that usually helps insulin sensitivity, but its levels drop in cases of obesity and insulin resistance.
- Research using CRH transgenic mice, which are models for Cushing syndrome, revealed that these mice had higher plasma AdN levels despite lower AdN expression in adipose tissue compared to normal counterparts.
- The findings indicate that changes in AdN are likely not the primary cause of insulin resistance in Cushing syndrome; instead, glucocorticoids may elevate plasma AdN while diminishing its expression in fat cells.
Article Abstract
Adiponectin (AdN), an adipokine derived from the adipose tissue, has an insulin-sensitizing effect, and plasma AdN is shown to be decreased in obesity and/or insulin resistant state. To clarify whether changes in AdN are also responsible for the development of glucocorticoid-induced insulin resistance, we examined AdN concentration in plasma and AdN expression in the adipose tissue, using corticotropin-releasing hormone (CRH) transgenic mouse (CRH-Tg), an animal model of Cushing syndrome. We found, unexpectedly, that plasma AdN levels in CRHTg were significantly higher than those in wild-type littermates (wild-type: 19.7+/-2.5, CRH-Tg: 32.4+/-3.1 microg/mL, p<0.01). On the other hand, AdN mRNA and protein levels were significantly decreased in the adipose tissue of CRH-Tg. Bilateral adrenalectomy in CRH-Tg eliminated both their Cushing's phenotype and their increase in plasma AdN levels (wild-type/sham: 9.4+/-0.5, CRH-Tg/sham: 15.7+/-2.0, CRH-Tg/ADX: 8.5+/-0.4 microg/mL). These results strongly suggest that AdN is not a major factor responsible for the development of insulin resistance in Cushing syndrome. Our data also suggest that glucocorticoid increases plasma AdN levels but decreases AdN expression in adipocytes, the latter being explained possibly by the decrease in AdN metabolism in the Cushing state.
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| http://dx.doi.org/10.1507/endocrj.k09e-038 | DOI Listing |
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