Plasma adiponectin levels are increased despite insulin resistance in corticotropin-releasing hormone transgenic mice, an animal model of Cushing syndrome

Masayuki Shinahara, Mitsuru Nishiyama, Yasumasa Iwasaki, Shuichi Nakayama, Toru Noguchi, Machiko Kambayashi, Yasushi Okada, Masayuki Tsuda, Mary P. Stenzel-Poore, Kozo Hashimoto, Yoshio Terada

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

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 CRH-Tg were significantly higher than those in wild-type littermates (wild-type: 19.7±2.5, CRH-Tg: 32.4±3.1μg/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±0.4μg/ 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.

Original languageEnglish (US)
Pages (from-to)879-886
Number of pages8
JournalEndocrine Journal
Volume56
Issue number7
DOIs
StatePublished - Nov 9 2009

Keywords

  • Adiponectin
  • Cushing syndrome
  • Glucocorticoid
  • Insulin resistance
  • Obesity

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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