Difference between revisions of "Attane 2012 Diabetes"
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{{Publication | {{Publication | ||
|title=Attané C, Foussal C, Le Gonidec S, Benani A, Daviaud D, Wanecq E, Guzmán-Ruiz R, Dray C, Bezaire V, Rancoule C, Kuba K, Ruiz-Gayo M, Levade T, Penninger J, Burcelin R, Pénicaud L, Valet P, Castan-Laurell I (2012) Apelin treatment increases complete fatty acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice. Diabetes 61: 310- | |title=Attané C, Foussal C, Le Gonidec S, Benani A, Daviaud D, Wanecq E, Guzmán-Ruiz R, Dray C, Bezaire V, Rancoule C, Kuba K, Ruiz-Gayo M, Levade T, Penninger J, Burcelin R, Pénicaud L, Valet P, Castan-Laurell I (2012) Apelin treatment increases complete fatty acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice. Diabetes 61:310-20. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/22210322 PMID:22210322] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/22210322 PMID:22210322] | ||
|authors=Attane C, Foussal C, Le Gonidec S, Benani A, Daviaud D, Wanecq E, | |authors=Attane C, Foussal C, Le Gonidec S, Benani A, Daviaud D, Wanecq E, Guzman-Ruiz R, Dray C, Bezaire V, Rancoule C, Kuba K, Ruiz-Gayo M, Levade T, Penninger J, Burcelin R, Penicaud L, Valet P, Castan-Laurell I | ||
|year=2012 | |year=2012 | ||
|journal=Diabetes | |journal=Diabetes | ||
|abstract=Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice. However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed. Thus, the aim of the current study was to determine the impact of chronic treatment on lipid use, especially in skeletal muscles. High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice. Indirect calorimetry experiments showed that apelin-treated mice had a better use of lipids. The complete FAO, the oxidative capacity, and mitochondrial biogenesis were increased in soleus of apelin-treated mice. The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK. Finally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnitines and enhanced insulin-stimulated glucose uptake in soleus. Thus, by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contribute to insulin sensitivity improvement. | |abstract=Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice. However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed. Thus, the aim of the current study was to determine the impact of chronic treatment on lipid use, especially in skeletal muscles. High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice. Indirect calorimetry experiments showed that apelin-treated mice had a better use of lipids. The complete FAO, the oxidative capacity, and mitochondrial biogenesis were increased in soleus of apelin-treated mice. The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK. Finally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnitines and enhanced insulin-stimulated glucose uptake in soleus. Thus, by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contribute to insulin sensitivity improvement. | ||
|keywords=Fatty acid oxidation, Apelin, Insulin resistance | |keywords=Fatty acid oxidation, Apelin, Insulin resistance | ||
|mipnetlab= | |mipnetlab=FR Toulouse Casteilla L, FR Toulouse Dray C | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
| | |diseases=Diabetes | ||
|injuries=Mitochondrial | |injuries=Mitochondrial disease | ||
|organism=Mouse | |organism=Mouse | ||
|tissues=Skeletal muscle | |tissues=Skeletal muscle | ||
|topics=Fatty acid | |||
|instruments=Oxygraph-2k | |||
}} | }} |
Latest revision as of 17:00, 26 March 2018
Attané C, Foussal C, Le Gonidec S, Benani A, Daviaud D, Wanecq E, Guzmán-Ruiz R, Dray C, Bezaire V, Rancoule C, Kuba K, Ruiz-Gayo M, Levade T, Penninger J, Burcelin R, Pénicaud L, Valet P, Castan-Laurell I (2012) Apelin treatment increases complete fatty acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice. Diabetes 61:310-20. |
Attane C, Foussal C, Le Gonidec S, Benani A, Daviaud D, Wanecq E, Guzman-Ruiz R, Dray C, Bezaire V, Rancoule C, Kuba K, Ruiz-Gayo M, Levade T, Penninger J, Burcelin R, Penicaud L, Valet P, Castan-Laurell I (2012) Diabetes
Abstract: Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice. However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed. Thus, the aim of the current study was to determine the impact of chronic treatment on lipid use, especially in skeletal muscles. High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice. Indirect calorimetry experiments showed that apelin-treated mice had a better use of lipids. The complete FAO, the oxidative capacity, and mitochondrial biogenesis were increased in soleus of apelin-treated mice. The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK. Finally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnitines and enhanced insulin-stimulated glucose uptake in soleus. Thus, by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contribute to insulin sensitivity improvement. • Keywords: Fatty acid oxidation, Apelin, Insulin resistance
• O2k-Network Lab: FR Toulouse Casteilla L, FR Toulouse Dray C
Labels:
Pathology: Diabetes
Stress:Mitochondrial disease
Organism: Mouse
Tissue;cell: Skeletal muscle
Regulation: Fatty acid
HRR: Oxygraph-2k