Difference between revisions of "Den Besten 2015 Diabetes"
(Created page with "{{Publication |title=den Besten G, Bleeker A, Gerding A, van Eunen K, Havinga R, van Dijk TH, Oosterveer MH, Jonker JW, Groen AK, Reijngoud DJ, Bakker BM (2015) Short-chain fatty...") Ā |
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{{Publication | {{Publication | ||
|title=den Besten G, Bleeker A, Gerding A, van Eunen K, Havinga R, van Dijk TH, Oosterveer MH, Jonker JW, Groen AK, Reijngoud DJ, Bakker BM (2015) Short-chain fatty acids protect against high-fat diet-induced obesity via a PPARĪ³-dependent switch from lipogenesis to fat oxidation. Diabetes [Epub ahead of print]. Ā | |title=den Besten G, Bleeker A, Gerding A, van Eunen K, Havinga R, van Dijk TH, Oosterveer MH, Jonker JW, Groen AK, Reijngoud DJ, Bakker BM (2015) Short-chain fatty acids protect against high-fat diet-induced obesity via a PPARĪ³-dependent switch from lipogenesis to fat oxidation. Diabetes [Epub ahead of print]. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/25695945 PMID:25695945] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/25695945 PMID:25695945] | ||
|authors=den Besten G, Bleeker A, Gerding A, van Eunen K, Havinga R, van Dijk TH, Oosterveer MH, Jonker JW, Groen AK, Reijngoud DJ, Bakker BM | |authors=den Besten G, Bleeker A, Gerding A, van Eunen K, Havinga R, van Dijk TH, Oosterveer MH, Jonker JW, Groen AK, Reijngoud DJ, Bakker BM | ||
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|journal=Diabetes | |journal=Diabetes | ||
|abstract=Short-chain fatty acids (SCFAs) are the main products of dietary fiber fermentation and are believed to drive the fiber-related prevention of the metabolic syndrome. Here we show that dietary SCFAs induce a peroxisome proliferator-activated receptor (PPAR) Ī³-dependent switch from lipid synthesis to utilization. Dietary SCFA supplementation prevented and reversed high-fat diet-induced metabolic abnormalities in mice by decreasing PPARĪ³ expression and activity. This increased the expression of mitochondrial uncoupling protein 2 and raised the AMP/ATP ratio, thereby stimulating oxidative metabolism in liver and adipose tissue via AMP-activated protein kinase. The SCFA-induced reduction in body weight and stimulation of insulin sensitivity were absent in mice with adipose-specific disruption of PPARĪ³. Similarly, SCFA-induced reduction of hepatic steatosis was absent in mice lacking hepatic PPARĪ³. These results demonstrate that adipose and hepatic PPARĪ³ are critical mediators of the beneficial effects of SCFA on the metabolic syndrome, with clearly distinct and complementary roles. Our findings indicate that SCFAs may be used therapeutically as cheap and selective PPARĪ³ modulators. | |abstract=Short-chain fatty acids (SCFAs) are the main products of dietary fiber fermentation and are believed to drive the fiber-related prevention of the metabolic syndrome. Here we show that dietary SCFAs induce a peroxisome proliferator-activated receptor (PPAR) Ī³-dependent switch from lipid synthesis to utilization. Dietary SCFA supplementation prevented and reversed high-fat diet-induced metabolic abnormalities in mice by decreasing PPARĪ³ expression and activity. This increased the expression of mitochondrial uncoupling protein 2 and raised the AMP/ATP ratio, thereby stimulating oxidative metabolism in liver and adipose tissue via AMP-activated protein kinase. The SCFA-induced reduction in body weight and stimulation of insulin sensitivity were absent in mice with adipose-specific disruption of PPARĪ³. Similarly, SCFA-induced reduction of hepatic steatosis was absent in mice lacking hepatic PPARĪ³. These results demonstrate that adipose and hepatic PPARĪ³ are critical mediators of the beneficial effects of SCFA on the metabolic syndrome, with clearly distinct and complementary roles. Our findings indicate that SCFAs may be used therapeutically as cheap and selective PPARĪ³ modulators. | ||
|mipnetlab=NL Groningen Reijngoud RJ | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
Revision as of 15:25, 20 April 2015
| den Besten G, Bleeker A, Gerding A, van Eunen K, Havinga R, van Dijk TH, Oosterveer MH, Jonker JW, Groen AK, Reijngoud DJ, Bakker BM (2015) Short-chain fatty acids protect against high-fat diet-induced obesity via a PPARĪ³-dependent switch from lipogenesis to fat oxidation. Diabetes [Epub ahead of print]. |
den Besten G, Bleeker A, Gerding A, van Eunen K, Havinga R, van Dijk TH, Oosterveer MH, Jonker JW, Groen AK, Reijngoud DJ, Bakker BM (2015) Diabetes
Abstract: Short-chain fatty acids (SCFAs) are the main products of dietary fiber fermentation and are believed to drive the fiber-related prevention of the metabolic syndrome. Here we show that dietary SCFAs induce a peroxisome proliferator-activated receptor (PPAR) Ī³-dependent switch from lipid synthesis to utilization. Dietary SCFA supplementation prevented and reversed high-fat diet-induced metabolic abnormalities in mice by decreasing PPARĪ³ expression and activity. This increased the expression of mitochondrial uncoupling protein 2 and raised the AMP/ATP ratio, thereby stimulating oxidative metabolism in liver and adipose tissue via AMP-activated protein kinase. The SCFA-induced reduction in body weight and stimulation of insulin sensitivity were absent in mice with adipose-specific disruption of PPARĪ³. Similarly, SCFA-induced reduction of hepatic steatosis was absent in mice lacking hepatic PPARĪ³. These results demonstrate that adipose and hepatic PPARĪ³ are critical mediators of the beneficial effects of SCFA on the metabolic syndrome, with clearly distinct and complementary roles. Our findings indicate that SCFAs may be used therapeutically as cheap and selective PPARĪ³ modulators.
ā¢ O2k-Network Lab: NL Groningen Reijngoud RJ
Labels: MiParea: Exercise physiology;nutrition;life style, Patients
Pathology: Obesity
Organism: Mouse Tissue;cell: Liver, Fat Preparation: Isolated mitochondria
Coupling state: LEAK, OXPHOS
Labels, [Epub ahead of print]
