Fatty acid synthase inhibitor, C75, blocks resistin-induced increases in lipid accumulation by human macrophages

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Increasing adiposity (overweight and obesity) is associated with insulin resistance and increased risk of type II diabetes mellitus and cardiovascular disease. Adipose tissue is a highly active endocrine tissue, producing bioactive proteins called adipokines, such as leptin, apelin, adiponectin and resistin, which may link obesity and atherogenesis. Resistin, originally discovered in a search for novel adipocyte-derived molecules linking obesity and insulin-resistant diabetes [1], belongs to a new gene family of small cysteine-rich secretory proteins called ‘resistin-like molecules’ or RELMs. In rodents, resistin derives largely from adipose tissue and mice deficient in resistin (Retn [-/-]) are protected from obesity-associated insulin resistance [2]. In humans, expression of RETN, which shows significant sequence and tissue divergence from its murine counterpart, lies under the control of the myeloid-specific nuclear transcription factor CCAAT/enhancer-binding protein epsilon and is upregulated during monocyte–macrophage differentiation [3].

Original languageEnglish
Pages (from-to)1271-1274
Number of pages4
JournalDiabetes, Obesity and Metabolism
Issue number12
Publication statusPublished - 1 Oct 2008



  • obesity
  • atherosclerosis
  • anti-obesity drugs

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