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CHROMIUM PICOLINATE INHIBITS RESISTIN SECRETION IN INSULIN‐RESISTANT 3T3‐L1 ADIPOCYTES VIA ACTIVATION OF AMP‐ACTIVATED PROTEIN KINASE
Author(s) -
Wang YiQun,
Dong Yi,
Yao MingHui
Publication year - 2009
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2009.05164.x
Subject(s) - resistin , ampk , adiponectin , medicine , endocrinology , 3t3 l1 , protein kinase a , secretion , chemistry , insulin , amp activated protein kinase , adipogenesis , insulin resistance , adipose tissue , biology , kinase , biochemistry
SUMMARY1 Chromium picolinate (CrPic) has been recommended as an alternative therapeutic regimen for Type 2 diabetes mellitus (T2DM). However, the molecular mechanism underlying the action of CrPic is poorly understood. 2 Using normal and insulin‐resistant 3T3‐L1 adipocytes, we examined the effects of CrPic on the gene transcription and secretion of adiponectin and resistin. In addition, using immunoblotting, ELISA and real‐time reverse transcription–polymerase chain reaction (RT‐PCR), we investigated the effects of 10 nmol/L CrPic for 24 h on AMP‐activated protein kinase (AMPK) to determine whether this pathway contributed to the regulation of adiponectin and resistin expression and secretion. 3 Chromium picolinate did not modulate the expression of adiponectin and resistin; however, it did significantly inhibit the secretion of resistin, but not adiponectin, by normal and insulin‐resistant 3T3‐L1 adipocytes in vitro . Furthermore, although CrPic markedly elevated levels of phosphorylated AMPK and acetyl CoA carboxylase in 3T3‐L1 adipocytes, it had no effect on the levels of AMPK α‐1 and α‐2 mRNA transcripts. Importantly, inhibition of AMPK by 2 h pretreatment of cells with 20 µmol/L compound C completely abolished the CrPic‐induced suppression of resistin secretion. 4 In conclusion, the data suggest that CrPic inhibits resistin secretion via activation of AMPK in normal and insulin‐resistant 3T3‐L1 adipocytes.