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Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets
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Apontes, Pasha, Liu, Zhongbo, Su, Kai, Benard, Outhiriaradjou, Youn, Dou Y., Li, Xisong, Li, Wei, Mirza, Raihan H., Bastie, Claire C., Jelicks, Linda A., Pessin, Jeffrey E., Muzumdar, Radhika H., Sauve, Anthony A. and Chi, Yuling (2014) Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. Diabetes, 63 (11). pp. 3626-3636. doi:10.2337/db14-0006 ISSN 0012-1797.
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Official URL: http://dx.doi.org/10.2337/db14-0006
Abstract
Excessive dietary fat intake causes systemic metabolic toxicity, manifested in weight gain, hyperglycemia, and insulin resistance. In addition, carbohydrate utilization as a fuel is substantially inhibited. Correction or reversal of these effects during high-fat diet (HFD) intake is of exceptional interest in light of widespread occurrence of diet-associated metabolic disorders in global human populations. Here we report that mangiferin (MGF), a natural compound (the predominant constituent of Mangifera indica extract from the plant that produces mango), protected against HFD-induced weight gain, increased aerobic mitochondrial capacity and thermogenesis, and improved glucose and insulin profiles. To obtain mechanistic insight into the basis for these effects, we determined that mice exposed to an HFD combined with MGF exhibited a substantial shift in respiratory quotient from fatty acid toward carbohydrate utilization. MGF treatment significantly increased glucose oxidation in muscle of HFD-fed mice without changing fatty acid oxidation. These results indicate that MGF redirects fuel utilization toward carbohydrates. In cultured C2C12 myotubes, MGF increased glucose and pyruvate oxidation and ATP production without affecting fatty acid oxidation, confirming in vivo and ex vivo effects. Furthermore, MGF inhibited anaerobic metabolism of pyruvate to lactate but enhanced pyruvate oxidation. A key target of MGF appears to be pyruvate dehydrogenase, determined to be activated by MGF in a variety of assays. These findings underscore the therapeutic potential of activation of carbohydrate utilization in correction of metabolic syndrome and highlight the potential of MGF to serve as a model compound that can elicit fuel-switching effects.
| Item Type: | Journal Article | ||||||
|---|---|---|---|---|---|---|---|
| Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School |
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| Journal or Publication Title: | Diabetes | ||||||
| Publisher: | American Diabetes Association | ||||||
| ISSN: | 0012-1797 | ||||||
| Official Date: | 21 May 2014 | ||||||
| Dates: |
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| Volume: | 63 | ||||||
| Number: | 11 | ||||||
| Page Range: | pp. 3626-3636 | ||||||
| DOI: | 10.2337/db14-0006 | ||||||
| Status: | Peer Reviewed | ||||||
| Publication Status: | Published |
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