Redox regulation of insulin sensitivity due to enhanced fatty acid utilization in the mitochondria
Obesity enhances the risk for the development of type 2 diabetes and cardiovascular disease. Loss in insulin sensitivity and diminished ability of muscle to take up and use glucose are characteristics of type 2 diabetes. Paradoxically, regulatory mechanisms that promote utilization of fatty acids ap...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2013-09, Vol.305 (5), p.H634-H643 |
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| container_end_page | H643 |
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| container_issue | 5 |
| container_start_page | H634 |
| container_title | American journal of physiology. Heart and circulatory physiology |
| container_volume | 305 |
| creator | Rindler, Paul M Crewe, Clair L Fernandes, Jolyn Kinter, Michael Szweda, Luke I |
| description | Obesity enhances the risk for the development of type 2 diabetes and cardiovascular disease. Loss in insulin sensitivity and diminished ability of muscle to take up and use glucose are characteristics of type 2 diabetes. Paradoxically, regulatory mechanisms that promote utilization of fatty acids appear to initiate diet-induced insulin insensitivity. In this review, we discuss recent findings implicating increased mitochondrial production of the prooxidant H2O2 due to enhanced utilization of fatty acids, as a signal to diminish reliance on glucose and its metabolites for energy. In the short term, the ability to preferentially use fatty acids may be beneficial, promoting a metabolic shift that ensures use of available fat by skeletal muscle and heart while preventing intracellular glucose accumulation and toxicity. However, with prolonged consumption of high dietary fat and ensuing obesity, the near exclusive dependence on fatty acid oxidation for production of energy by the mitochondria drives insulin resistance, diabetes, and cardiovascular disease. |
| doi_str_mv | 10.1152/ajpheart.00799.2012 |
| format | Article |
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Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>Obesity enhances the risk for the development of type 2 diabetes and cardiovascular disease. Loss in insulin sensitivity and diminished ability of muscle to take up and use glucose are characteristics of type 2 diabetes. Paradoxically, regulatory mechanisms that promote utilization of fatty acids appear to initiate diet-induced insulin insensitivity. In this review, we discuss recent findings implicating increased mitochondrial production of the prooxidant H2O2 due to enhanced utilization of fatty acids, as a signal to diminish reliance on glucose and its metabolites for energy. In the short term, the ability to preferentially use fatty acids may be beneficial, promoting a metabolic shift that ensures use of available fat by skeletal muscle and heart while preventing intracellular glucose accumulation and toxicity. However, with prolonged consumption of high dietary fat and ensuing obesity, the near exclusive dependence on fatty acid oxidation for production of energy by the mitochondria drives insulin resistance, diabetes, and cardiovascular disease.</description><subject>Animals</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular Diseases - epidemiology</subject><subject>Diabetes</subject><subject>Diabetes Mellitus - epidemiology</subject><subject>Energy Metabolism - physiology</subject><subject>Fatty acids</subject><subject>Fatty Acids - metabolism</subject><subject>Glucose - metabolism</subject><subject>Humans</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - physiology</subject><subject>Mitochondria</subject><subject>Mitochondria, Muscle - metabolism</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Obesity - metabolism</subject><subject>Oxidation</subject><subject>Oxidation-Reduction</subject><subject>Risk assessment</subject><subject>Risk Factors</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1LXDEUxUOpdEbbv6BQAt1088Z8TL6WRawKgiC6fmSS-zoZ3iTTJK-of73RcVy4unDu7xwu9yD0nZIFpYKd2s1uDTbXBSHKmAUjlH1C87ZhHRXcfEZzwiXvJOViho5L2RBChJL8C5oxrgyTis3R6hZ8esAZ_k6jrSFFnAYcYpnGEHGBWEIN_0N9xH4CXBOGuLbRgceDrU21Lng81TCGp727ueoa8DbU5NYp-hzsV3Q02LHAt7d5gu7_nN-dXXbXNxdXZ7-vO8eNqZ23QmmulPTUWVCcOHBNGAilzOkBlhq01UZrLb3X1Ak6aCGdkCuhQRjBT9Cvfe4up38TlNpvQ3EwjjZCmkpPl8xIvmSSNPTnB3STphzbdY3ihBNtuGoU31Mup1IyDP0uh63Njz0l_UsF_aGC_rWC_qWC5vrxlj2ttuDfPYef82deL4TJ</recordid><startdate>20130901</startdate><enddate>20130901</enddate><creator>Rindler, Paul M</creator><creator>Crewe, Clair L</creator><creator>Fernandes, Jolyn</creator><creator>Kinter, Michael</creator><creator>Szweda, Luke I</creator><general>American Physiological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20130901</creationdate><title>Redox regulation of insulin sensitivity due to enhanced fatty acid utilization in the mitochondria</title><author>Rindler, Paul M ; Crewe, Clair L ; Fernandes, Jolyn ; Kinter, Michael ; Szweda, Luke I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c399t-da5783776d1cae730cec783f0112c8fe48e8a898886dd81c51f856c56b58e5953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular Diseases - epidemiology</topic><topic>Diabetes</topic><topic>Diabetes Mellitus - epidemiology</topic><topic>Energy Metabolism - physiology</topic><topic>Fatty acids</topic><topic>Fatty Acids - metabolism</topic><topic>Glucose - metabolism</topic><topic>Humans</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - physiology</topic><topic>Mitochondria</topic><topic>Mitochondria, Muscle - metabolism</topic><topic>Obesity</topic><topic>Obesity - complications</topic><topic>Obesity - metabolism</topic><topic>Oxidation</topic><topic>Oxidation-Reduction</topic><topic>Risk assessment</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rindler, Paul M</creatorcontrib><creatorcontrib>Crewe, Clair L</creatorcontrib><creatorcontrib>Fernandes, Jolyn</creatorcontrib><creatorcontrib>Kinter, Michael</creatorcontrib><creatorcontrib>Szweda, Luke I</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. 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Loss in insulin sensitivity and diminished ability of muscle to take up and use glucose are characteristics of type 2 diabetes. Paradoxically, regulatory mechanisms that promote utilization of fatty acids appear to initiate diet-induced insulin insensitivity. In this review, we discuss recent findings implicating increased mitochondrial production of the prooxidant H2O2 due to enhanced utilization of fatty acids, as a signal to diminish reliance on glucose and its metabolites for energy. In the short term, the ability to preferentially use fatty acids may be beneficial, promoting a metabolic shift that ensures use of available fat by skeletal muscle and heart while preventing intracellular glucose accumulation and toxicity. 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| identifier | ISSN: 0363-6135 |
| ispartof | American journal of physiology. Heart and circulatory physiology, 2013-09, Vol.305 (5), p.H634-H643 |
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| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Cardiovascular disease Cardiovascular Diseases - epidemiology Diabetes Diabetes Mellitus - epidemiology Energy Metabolism - physiology Fatty acids Fatty Acids - metabolism Glucose - metabolism Humans Insulin resistance Insulin Resistance - physiology Mitochondria Mitochondria, Muscle - metabolism Obesity Obesity - complications Obesity - metabolism Oxidation Oxidation-Reduction Risk assessment Risk Factors |
| title | Redox regulation of insulin sensitivity due to enhanced fatty acid utilization in the mitochondria |
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