Expression of resistin in the adipose tissue is modulated by various factors including peroxisome proliferator-activated receptor alpha
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Updated: Aug 9, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
1Department of Biochemistry, Meiji Pharmaceutical University, Kiyose, Tokyo, Japan.
Aim:
Resistin has been suggested to link obesity to diabetes by antagonizing insulin action. However, this model is based on limited observations and how resistin links the two complex processes is not known. In this study, we investigated the effects of various factors on the expression of resistin and examined the generality of the proposal.
Methods:
Total RNA was isolated from the adipose tissues of lean, obese and peroxisome proliferator-activated receptor (PPAR)alpha-null mice fed a control diet or that contained a PPAR ligand, and analysed by Northern blotting using cDNAs for resistin, leptin, aP2 and other mRNAs as probes. For quantitative analysis, an image analyser was used.
Results:
Basal expression of resistin mRNA was suppressed by obesity, but the extent of suppression differed significantly among the mouse strains and types of adipose tissue examined. Anti-diabetic thiazolidinediones induced resistin expression in the lean mice and showed smaller effects in obese mice. Furthermore, PPARalpha was shown to play an important role in constitutive expression of resistin in the adipose tissue.
Conclusion:
Our results indicated that diverse factors modulate the expression of resistin in the adipose tissues of mice, and suggested that resistin is not a master hormone linking obesity to diabetes.
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