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Intrinsic High Aerobic Capacity in Male Rats Protects Against Diet-Induced Insulin Resistance
Low aerobic capacity increases the risk for insulin resistance but the mechanisms are unknown. In this study, we tested susceptibility to acute (3-day) high-fat, high-sucrose diet (HFD)-induced insulin resistance in male rats selectively bred for divergent intrinsic aerobic capacity, that is, high-c...
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| Published in: | Endocrinology (Philadelphia) 2019-05, Vol.160 (5), p.1179-1192 |
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| creator | Morris, E Matthew Meers, Grace M E Ruegsegger, Gregory N Wankhade, Umesh D Robinson, Tommy Koch, Lauren G Britton, Steven L Rector, R Scott Shankar, Kartik Thyfault, John P |
| description | Low aerobic capacity increases the risk for insulin resistance but the mechanisms are unknown. In this study, we tested susceptibility to acute (3-day) high-fat, high-sucrose diet (HFD)-induced insulin resistance in male rats selectively bred for divergent intrinsic aerobic capacity, that is, high-capacity running (HCR) and low-capacity running (LCR) rats. We employed hyperinsulinemic-euglycemic clamps, tracers, and transcriptome sequencing of skeletal muscle to test whether divergence in aerobic capacity impacted insulin resistance through systemic and tissue-specific metabolic adaptations. An HFD evoked decreased insulin sensitivity and insulin signaling in muscle and liver in LCR rats, whereas HCR rats were protected. An HFD led to increased glucose transport in skeletal muscle (twofold) of HCR rats while increasing glucose transport into adipose depots of the LCR rats (twofold). Skeletal muscle transcriptome revealed robust differences in the gene profile of HCR vs LCR on low-fat diet and HFD conditions, including robust differences in specific genes involved in lipid metabolism, adipogenesis, and differentiation. HCR transcriptional adaptations to an acute HFD were more robust than for LCR and included genes driving mitochondrial energy metabolism. In conclusion, intrinsic aerobic capacity robustly impacts systemic and skeletal muscle adaptations to HFD-induced alterations in insulin resistance, an effect that is likely driven by baseline differences in oxidative capacity, gene expression profile, and transcriptional adaptations to an HFD. |
| doi_str_mv | 10.1210/en.2019-00118 |
| format | article |
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In this study, we tested susceptibility to acute (3-day) high-fat, high-sucrose diet (HFD)-induced insulin resistance in male rats selectively bred for divergent intrinsic aerobic capacity, that is, high-capacity running (HCR) and low-capacity running (LCR) rats. We employed hyperinsulinemic-euglycemic clamps, tracers, and transcriptome sequencing of skeletal muscle to test whether divergence in aerobic capacity impacted insulin resistance through systemic and tissue-specific metabolic adaptations. An HFD evoked decreased insulin sensitivity and insulin signaling in muscle and liver in LCR rats, whereas HCR rats were protected. An HFD led to increased glucose transport in skeletal muscle (twofold) of HCR rats while increasing glucose transport into adipose depots of the LCR rats (twofold). Skeletal muscle transcriptome revealed robust differences in the gene profile of HCR vs LCR on low-fat diet and HFD conditions, including robust differences in specific genes involved in lipid metabolism, adipogenesis, and differentiation. HCR transcriptional adaptations to an acute HFD were more robust than for LCR and included genes driving mitochondrial energy metabolism. In conclusion, intrinsic aerobic capacity robustly impacts systemic and skeletal muscle adaptations to HFD-induced alterations in insulin resistance, an effect that is likely driven by baseline differences in oxidative capacity, gene expression profile, and transcriptional adaptations to an HFD.</description><identifier>ISSN: 1945-7170</identifier><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2019-00118</identifier><identifier>PMID: 31144719</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Adaptation ; Adipogenesis ; Adipogenesis - genetics ; Aerobic capacity ; Animals ; Clamps ; Diet ; Diet, High-Fat ; Disease susceptibility ; Divergence ; Endocrinology ; Energy metabolism ; Energy Metabolism - genetics ; Gene expression ; Gene Expression Profiling - methods ; Genes ; Genetic aspects ; Glucose ; Glucose transport ; Health aspects ; High fat diet ; Impact resistance ; Insulin ; Insulin resistance ; Insulin Resistance - genetics ; Lipid metabolism ; Lipid Metabolism - genetics ; Lipids ; Liver ; Liver - metabolism ; Low fat diet ; Male ; Metabolism ; Mitochondria ; Muscle, Skeletal - metabolism ; Muscles ; Musculoskeletal system ; Nutrient deficiency ; Oxidation resistance ; Physical Conditioning, Animal - physiology ; Rats ; Risk factors ; Robustness ; Running - physiology ; Sequence Analysis, RNA - methods ; Skeletal muscle ; Sucrose ; Sugar ; Testing ; Tracers ; Transcription ; Transcription (Genetics) ; Type 2 diabetes</subject><ispartof>Endocrinology (Philadelphia), 2019-05, Vol.160 (5), p.1179-1192</ispartof><rights>Copyright © 2019 Endocrine Society.</rights><rights>COPYRIGHT 2019 Oxford University Press</rights><rights>Copyright © 2019 Endocrine Society</rights><rights>Copyright © 2019 Endocrine Society 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-1c7f6e5a09168402bec24f38ed0ef1e9658f0fbd735f3a24584ca3f0db4987833</citedby><cites>FETCH-LOGICAL-c482t-1c7f6e5a09168402bec24f38ed0ef1e9658f0fbd735f3a24584ca3f0db4987833</cites><orcidid>0000-0001-7920-7466</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,786,790,891,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31144719$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morris, E Matthew</creatorcontrib><creatorcontrib>Meers, Grace M E</creatorcontrib><creatorcontrib>Ruegsegger, Gregory N</creatorcontrib><creatorcontrib>Wankhade, Umesh D</creatorcontrib><creatorcontrib>Robinson, Tommy</creatorcontrib><creatorcontrib>Koch, Lauren G</creatorcontrib><creatorcontrib>Britton, Steven L</creatorcontrib><creatorcontrib>Rector, R Scott</creatorcontrib><creatorcontrib>Shankar, Kartik</creatorcontrib><creatorcontrib>Thyfault, John P</creatorcontrib><title>Intrinsic High Aerobic Capacity in Male Rats Protects Against Diet-Induced Insulin Resistance</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Low aerobic capacity increases the risk for insulin resistance but the mechanisms are unknown. In this study, we tested susceptibility to acute (3-day) high-fat, high-sucrose diet (HFD)-induced insulin resistance in male rats selectively bred for divergent intrinsic aerobic capacity, that is, high-capacity running (HCR) and low-capacity running (LCR) rats. We employed hyperinsulinemic-euglycemic clamps, tracers, and transcriptome sequencing of skeletal muscle to test whether divergence in aerobic capacity impacted insulin resistance through systemic and tissue-specific metabolic adaptations. An HFD evoked decreased insulin sensitivity and insulin signaling in muscle and liver in LCR rats, whereas HCR rats were protected. An HFD led to increased glucose transport in skeletal muscle (twofold) of HCR rats while increasing glucose transport into adipose depots of the LCR rats (twofold). Skeletal muscle transcriptome revealed robust differences in the gene profile of HCR vs LCR on low-fat diet and HFD conditions, including robust differences in specific genes involved in lipid metabolism, adipogenesis, and differentiation. HCR transcriptional adaptations to an acute HFD were more robust than for LCR and included genes driving mitochondrial energy metabolism. In conclusion, intrinsic aerobic capacity robustly impacts systemic and skeletal muscle adaptations to HFD-induced alterations in insulin resistance, an effect that is likely driven by baseline differences in oxidative capacity, gene expression profile, and transcriptional adaptations to an HFD.</description><subject>Adaptation</subject><subject>Adipogenesis</subject><subject>Adipogenesis - genetics</subject><subject>Aerobic capacity</subject><subject>Animals</subject><subject>Clamps</subject><subject>Diet</subject><subject>Diet, High-Fat</subject><subject>Disease susceptibility</subject><subject>Divergence</subject><subject>Endocrinology</subject><subject>Energy metabolism</subject><subject>Energy Metabolism - genetics</subject><subject>Gene expression</subject><subject>Gene Expression Profiling - methods</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Glucose</subject><subject>Glucose transport</subject><subject>Health aspects</subject><subject>High fat diet</subject><subject>Impact resistance</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Lipid metabolism</subject><subject>Lipid Metabolism - genetics</subject><subject>Lipids</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Low fat diet</subject><subject>Male</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscles</subject><subject>Musculoskeletal system</subject><subject>Nutrient deficiency</subject><subject>Oxidation resistance</subject><subject>Physical Conditioning, Animal - physiology</subject><subject>Rats</subject><subject>Risk factors</subject><subject>Robustness</subject><subject>Running - physiology</subject><subject>Sequence Analysis, RNA - methods</subject><subject>Skeletal muscle</subject><subject>Sucrose</subject><subject>Sugar</subject><subject>Testing</subject><subject>Tracers</subject><subject>Transcription</subject><subject>Transcription (Genetics)</subject><subject>Type 2 diabetes</subject><issn>1945-7170</issn><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNptktFrFDEQxoNYbK0--ioLvviy10yS3c2-CMdV7UGLUvRRQjY7uabsJWeSFfrfm7O1tlLykJnkN98ww0fIG6ALYEBP0C8Yhb6mFEA-I0fQi6buoKPPH8SH5GVK1wURQvAX5JBDiTroj8iPtc_R-eRMdeY2V9USYxhKstI7bVy-qZyvLvSE1aXOqfoaQ0ZTguVGl6JcnTrM9dqPs8GxWvs0T4W_xORS1t7gK3Jg9ZTw9d19TL5_-vhtdVaff_m8Xi3PayMkyzWYzrbYaNpDKwVlAxomLJc4UrSAfdtIS-0wdryxXDPRSGE0t3QcRC87yfkx-XCru5uHLY4Gy1B6UrvotjreqKCdevzj3ZXahF-qLf0pb4rA-zuBGH7OmLLaumRwmrTHMCfFGGeiayWDgr77D70Oc_RlPMV42zCQPfB_1KYsTzlvQ-lr9qJq2UIjemD9vu3iCaqcEbfOBI_WlfdHBfVtgYkhpYj2fkagau8HhV7t_aD--KHwbx8u5p7-awD-G9ZTruI</recordid><startdate>20190501</startdate><enddate>20190501</enddate><creator>Morris, E Matthew</creator><creator>Meers, Grace M E</creator><creator>Ruegsegger, Gregory N</creator><creator>Wankhade, Umesh D</creator><creator>Robinson, Tommy</creator><creator>Koch, Lauren G</creator><creator>Britton, Steven L</creator><creator>Rector, R Scott</creator><creator>Shankar, Kartik</creator><creator>Thyfault, John P</creator><general>Oxford University Press</general><general>Endocrine 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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7920-7466</orcidid></search><sort><creationdate>20190501</creationdate><title>Intrinsic High Aerobic Capacity in Male Rats Protects Against Diet-Induced Insulin Resistance</title><author>Morris, E Matthew ; Meers, Grace M E ; Ruegsegger, Gregory N ; Wankhade, Umesh D ; Robinson, Tommy ; Koch, Lauren G ; Britton, Steven L ; Rector, R Scott ; Shankar, Kartik ; Thyfault, John P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-1c7f6e5a09168402bec24f38ed0ef1e9658f0fbd735f3a24584ca3f0db4987833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adaptation</topic><topic>Adipogenesis</topic><topic>Adipogenesis - genetics</topic><topic>Aerobic capacity</topic><topic>Animals</topic><topic>Clamps</topic><topic>Diet</topic><topic>Diet, High-Fat</topic><topic>Disease susceptibility</topic><topic>Divergence</topic><topic>Endocrinology</topic><topic>Energy metabolism</topic><topic>Energy Metabolism - genetics</topic><topic>Gene expression</topic><topic>Gene Expression Profiling - methods</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Glucose</topic><topic>Glucose transport</topic><topic>Health aspects</topic><topic>High fat diet</topic><topic>Impact resistance</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - genetics</topic><topic>Lipid metabolism</topic><topic>Lipid Metabolism - genetics</topic><topic>Lipids</topic><topic>Liver</topic><topic>Liver - metabolism</topic><topic>Low fat diet</topic><topic>Male</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscles</topic><topic>Musculoskeletal system</topic><topic>Nutrient deficiency</topic><topic>Oxidation resistance</topic><topic>Physical Conditioning, Animal - physiology</topic><topic>Rats</topic><topic>Risk factors</topic><topic>Robustness</topic><topic>Running - physiology</topic><topic>Sequence Analysis, RNA - methods</topic><topic>Skeletal muscle</topic><topic>Sucrose</topic><topic>Sugar</topic><topic>Testing</topic><topic>Tracers</topic><topic>Transcription</topic><topic>Transcription (Genetics)</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morris, E Matthew</creatorcontrib><creatorcontrib>Meers, Grace M E</creatorcontrib><creatorcontrib>Ruegsegger, Gregory N</creatorcontrib><creatorcontrib>Wankhade, Umesh D</creatorcontrib><creatorcontrib>Robinson, Tommy</creatorcontrib><creatorcontrib>Koch, Lauren G</creatorcontrib><creatorcontrib>Britton, Steven L</creatorcontrib><creatorcontrib>Rector, R Scott</creatorcontrib><creatorcontrib>Shankar, Kartik</creatorcontrib><creatorcontrib>Thyfault, John P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morris, E Matthew</au><au>Meers, Grace M E</au><au>Ruegsegger, Gregory N</au><au>Wankhade, Umesh D</au><au>Robinson, Tommy</au><au>Koch, Lauren G</au><au>Britton, Steven L</au><au>Rector, R Scott</au><au>Shankar, Kartik</au><au>Thyfault, John P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intrinsic High Aerobic Capacity in Male Rats Protects Against Diet-Induced Insulin Resistance</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2019-05-01</date><risdate>2019</risdate><volume>160</volume><issue>5</issue><spage>1179</spage><epage>1192</epage><pages>1179-1192</pages><issn>1945-7170</issn><issn>0013-7227</issn><eissn>1945-7170</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Low aerobic capacity increases the risk for insulin resistance but the mechanisms are unknown. In this study, we tested susceptibility to acute (3-day) high-fat, high-sucrose diet (HFD)-induced insulin resistance in male rats selectively bred for divergent intrinsic aerobic capacity, that is, high-capacity running (HCR) and low-capacity running (LCR) rats. We employed hyperinsulinemic-euglycemic clamps, tracers, and transcriptome sequencing of skeletal muscle to test whether divergence in aerobic capacity impacted insulin resistance through systemic and tissue-specific metabolic adaptations. An HFD evoked decreased insulin sensitivity and insulin signaling in muscle and liver in LCR rats, whereas HCR rats were protected. An HFD led to increased glucose transport in skeletal muscle (twofold) of HCR rats while increasing glucose transport into adipose depots of the LCR rats (twofold). Skeletal muscle transcriptome revealed robust differences in the gene profile of HCR vs LCR on low-fat diet and HFD conditions, including robust differences in specific genes involved in lipid metabolism, adipogenesis, and differentiation. HCR transcriptional adaptations to an acute HFD were more robust than for LCR and included genes driving mitochondrial energy metabolism. In conclusion, intrinsic aerobic capacity robustly impacts systemic and skeletal muscle adaptations to HFD-induced alterations in insulin resistance, an effect that is likely driven by baseline differences in oxidative capacity, gene expression profile, and transcriptional adaptations to an HFD.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>31144719</pmid><doi>10.1210/en.2019-00118</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-7920-7466</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Oxford Journals Online |
| subjects | Adaptation Adipogenesis Adipogenesis - genetics Aerobic capacity Animals Clamps Diet Diet, High-Fat Disease susceptibility Divergence Endocrinology Energy metabolism Energy Metabolism - genetics Gene expression Gene Expression Profiling - methods Genes Genetic aspects Glucose Glucose transport Health aspects High fat diet Impact resistance Insulin Insulin resistance Insulin Resistance - genetics Lipid metabolism Lipid Metabolism - genetics Lipids Liver Liver - metabolism Low fat diet Male Metabolism Mitochondria Muscle, Skeletal - metabolism Muscles Musculoskeletal system Nutrient deficiency Oxidation resistance Physical Conditioning, Animal - physiology Rats Risk factors Robustness Running - physiology Sequence Analysis, RNA - methods Skeletal muscle Sucrose Sugar Testing Tracers Transcription Transcription (Genetics) Type 2 diabetes |
| title | Intrinsic High Aerobic Capacity in Male Rats Protects Against Diet-Induced Insulin Resistance |
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