Difference between revisions of "Hoeks 2011 PLoS One"
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{{Publication | {{Publication | ||
|title=Hoeks J, de Wilde J, Hulshof MF, van den Berg SA, Schaart G, van Dijk KW, Smit E, Mariman EC (2011) High fat diet-induced changes in mouse muscle mitochondrial phospholipids do not impair mitochondrial respiration despite insulin resistance. PLoS One 6: e27274. | |title=Hoeks J, de Wilde J, Hulshof MF, van den Berg SA, Schaart G, van Dijk KW, Smit E, Mariman EC (2011) High fat diet-induced changes in mouse muscle mitochondrial phospholipids do not impair mitochondrial respiration despite insulin resistance. PLoS One 6:e27274. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/22140436 PMID: 22140436 | |info=[http://www.ncbi.nlm.nih.gov/pubmed/22140436 PMID: 22140436 Open Access] | ||
|authors=Hoeks J, de Wilde J, Hulshof MF, van den Berg SA, Schaart G, van Dijk KW, Smit E, Mariman EC | |authors=Hoeks J, de Wilde J, Hulshof MF, van den Berg SA, Schaart G, van Dijk KW, Smit E, Mariman EC | ||
|year=2011 | |year=2011 | ||
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CONCLUSIONS/INTERPRETATION: Our findings do not support the concept that prolonged HF feeding leads to increased saturation of skeletal muscle mitochondrial phospholipids resulting in a decrease in mitochondrial fat oxidative capacity and (muscle) insulin resistance. | CONCLUSIONS/INTERPRETATION: Our findings do not support the concept that prolonged HF feeding leads to increased saturation of skeletal muscle mitochondrial phospholipids resulting in a decrease in mitochondrial fat oxidative capacity and (muscle) insulin resistance. | ||
|keywords=Mitochondrial phospholipids, high-fat diet, muscle insulin resistance, Type 2 diabetes mellitus ย | |keywords=Mitochondrial phospholipids, high-fat diet, muscle insulin resistance, Type 2 diabetes mellitus | ||
|mipnetlab=NL_Maastricht_Schrauwen P | |mipnetlab=NL_Maastricht_Schrauwen P | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Mouse | |organism=Mouse | ||
|tissues=Skeletal muscle | |tissues=Skeletal muscle | ||
|preparations=Isolated | |preparations=Isolated mitochondria | ||
|topics= | |diseases=Diabetes | ||
|topics=Fatty acid | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k | |||
}} | }} |
Latest revision as of 14:45, 13 February 2015
Hoeks J, de Wilde J, Hulshof MF, van den Berg SA, Schaart G, van Dijk KW, Smit E, Mariman EC (2011) High fat diet-induced changes in mouse muscle mitochondrial phospholipids do not impair mitochondrial respiration despite insulin resistance. PLoS One 6:e27274. |
Hoeks J, de Wilde J, Hulshof MF, van den Berg SA, Schaart G, van Dijk KW, Smit E, Mariman EC (2011) PLoS One
Abstract: BACKGROUND: Type 2 diabetes mellitus and muscle insulin resistance have been associated with reduced capacity of skeletal muscle mitochondria, possibly as a result of increased intake of dietary fat. Here, we examined the hypothesis that a prolonged high-fat diet consumption (HFD) increases the saturation of muscle mitochondrial membrane phospholipids causing impaired mitochondrial oxidative capacity and possibly insulin resistance.
METHODOLOGY: C57BL/6J mice were fed an 8-week or 20-week low fat diet (10 kcal%; LFD) or HFD (45 kcal%). Skeletal muscle mitochondria were isolated and fatty acid (FA) composition of skeletal muscle mitochondrial phospholipids was analyzed by thin-layer chromatography followed by GC. High-resolution respirometry was used to assess oxidation of pyruvate and fatty acids by mitochondria. Insulin sensitivity was estimated by HOMA-IR.
PRINCIPAL FINDINGS: At 8 weeks, mono-unsaturated FA (16โถ1n7, 18โถ1n7 and 18โถ1n9) were decreased (-4.0%, p<0.001), whereas saturated FA (16โถ0) were increased (+3.2%, p<0.001) in phospholipids of HFD vs. LFD mitochondria. Interestingly, 20 weeks of HFD descreased mono-unsaturated FA while n-6 poly-unsaturated FA (18โถ2n6, 20โถ4n6, 22โถ5n6) showed a pronounced increase (+4.0%, p<0.001). Despite increased saturation of muscle mitochondrial phospholipids after the 8-week HFD, mitochondrial oxidation of both pyruvate and fatty acids were similar between LFD and HFD mice. After 20 weeks of HFD, the increase in n-6 poly-unsaturated FA was accompanied by enhanced maximal capacity of the electron transport chain (+49%, p = 0.002) and a tendency for increased ADP-stimulated respiration, but only when fuelled by a lipid-derived substrate. Insulin sensitivity in HFD mice was reduced at both 8 and 20 weeks.
CONCLUSIONS/INTERPRETATION: Our findings do not support the concept that prolonged HF feeding leads to increased saturation of skeletal muscle mitochondrial phospholipids resulting in a decrease in mitochondrial fat oxidative capacity and (muscle) insulin resistance. โข Keywords: Mitochondrial phospholipids, high-fat diet, muscle insulin resistance, Type 2 diabetes mellitus
โข O2k-Network Lab: NL_Maastricht_Schrauwen P
Labels:
Pathology: Diabetes
Organism: Mouse Tissue;cell: Skeletal muscle Preparation: Isolated mitochondria
Regulation: Fatty acid Coupling state: OXPHOS
HRR: Oxygraph-2k