Effect of 1,5-Anhydro-D-Fructose on the Inhibition of Adipogenesis in 3T3-L1 Adipocytes

• Published in: Natural product communications 2012-11, Vol.7 (11), p.1501-1506
• Main Authors: Kojima-Yuasa, Akiko, Deguchi, Yohei, Konishi, Yotaro, Matsui-Yuasa, Isao
• Format: Article
• Language: English
• Subjects: 3T3 Cells; Adipocytes - drug effects; Adipocytes - metabolism; Adipogenesis - drug effects; AMP-Activated Protein Kinases - metabolism; Animals; Anti-Obesity Agents - pharmacology; CCAAT-Enhancer-Binding Proteins - metabolism; Drug Evaluation, Preclinical; Fructose - analogs & derivatives; Fructose - pharmacology; Glycerolphosphate Dehydrogenase - metabolism; Mice; PPAR gamma - metabolism
• ISSN: 1934-578X; 1555-9475
• DOI: 10.1177/1934578X1200701123

1,5-Anhydro-D-fructose (1,5-AF) is a monosaccharide that shares a structural similarity to glucose. 1,5-AF is found in fungi, algae, Escherichia coli and rat liver and is produced by the degradation of starch and glycogen, which is catalyzed by the enzyme α-1,4-glucan lyase. However, the physiological role of 1,5-AF in mammalian tissues is not well understood. Here, we investigated the anti-obesity potential of 1,5-AF on adipogenesis in 3T3-L1 adipocytes. 1,5-AF caused a significant decrease in GPDH activity in 3T3-L1 preadipocytes and mature adipocytes without eliciting cytotoxicity, and inhibited cellular lipid accumulation through down-regulation of transcription factors such as PPARγ and C/EBPα. 1,5-AF also induced dose-dependent phosphorylation of AMP-activated protein kinase (AMPK), a cellular energy sensor. However, the total AMPK protein content remained unchanged. Furthermore, 1,5-AF increased the levels of reactive oxygen species, an important upstream signal for AMPK activation in 3T3-L1 adipocytes. Our results show that 1,5-AF exerts anti-obesity action in vitro and suggest that 1,5-AF is potentially a novel preventative agent for obesity and other metabolic diseases.