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      Galanin inhibits leptin expression and secretion in rat adipose tissue and 3T3-L1 adipocytes.

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          Abstract

          In addition to serving as a fat depot, adipose tissue is also considered as an important endocrine organ that synthesizes and secretes a number of factors. Leptin is an adipocyte-derived hormone that plays a vital role in energy balance. Expression of leptin is regulated by dietary status and hormones. In the present study, we report that galanin, an orexigenic peptide, inhibits leptin expression and secretion in rat adipose tissue and in 3T3-L1 adipocytes. Treatment with galanin (25 micro g/animal) induced approximately 46% down-regulation of leptin secretion at 15 min, followed by 40, 37 and 47% decreases in leptin secretion at 1, 2 and 4 h respectively. Although Northern blot analysis of adipose tissue from the same animals showed that leptin mRNA expression in adipose tissue was unaffected by galanin treatment for 2 h, galanin treatment for 4 h led to decline of leptin mRNA expression in a dose-dependent manner. Meanwhile, treating the rats with galanin had no effect on leptin mRNA expression in the hypothalamus. The inhibitory action of the galanin on leptin mRNA and protein levels was also observed in vitro. When incubated with 10 nM galanin for 48 h, leptin mRNA expression and protein secretion also decreased in 3T3-L1 adipocytes. On the other hand, galanin was found not only to express in rat adipose tissue, but also to increase about 8-fold after fasting. Based on these data, we speculate that increased galanin expression in rat adipose tissue after fasting may be involved in reducing leptin expression and secretion in fasting rats.

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          Author and article information

          Journal
          J Mol Endocrinol
          Journal of molecular endocrinology
          Bioscientifica
          0952-5041
          0952-5041
          Aug 2004
          : 33
          : 1
          Affiliations
          [1 ] Ruijin Hospital, Shanghai Institute of Endocrinology, Shanghai Second Medical University, Shanghai, China 200025.
          Article
          10.1677/jme.0.0330011
          15291739
          8d16af34-99d8-4db3-b5da-7425353e1f59
          History

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