Lamellar events related to insulin‐like growth factor‐1 receptor signalling in two models relevant to endocrinopathic laminitis
Summary Background Insulin dysregulation, obesity, and exposure to high‐nonstructural carbohydrate (NSC) forage are risk factors for equine metabolic syndrome‐associated laminitis (EMSAL); high systemic insulin concentrations in EMSAL are proposed to induce cellular dysregulation in the digital lame...
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| Veröffentlicht in: | Equine veterinary journal 2017-09, Vol.49 (5), p.643-654 |
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| creator | Lane, H. E. Burns, T. A. Hegedus, O. C. Watts, M. R. Weber, P. S. Woltman, K. A. Geor, R. J. McCutcheon, L. J. Eades, S. C. Mathes, L. E. Belknap, J. K. |
| description | Summary
Background
Insulin dysregulation, obesity, and exposure to high‐nonstructural carbohydrate (NSC) forage are risk factors for equine metabolic syndrome‐associated laminitis (EMSAL); high systemic insulin concentrations in EMSAL are proposed to induce cellular dysregulation in the digital lamellae through activation of the insulin‐like growth factor‐1 receptor.
Objectives
To use a dietary challenge model (DCM) and a euglycaemic–hyperinsulinaemic clamp (EHC) model to assess lamellar growth factor‐related signalling.
Study design
Lamellar phospho (P)‐protein concentrations of signalling proteins important in growth factor‐related signalling were assessed in 2 models: 1) lean and obese ponies on a low‐ or high‐NSC diet; and 2) EHC model using Standardbred horses.
Methods
Ponies stratified for body condition (lean [LN, n = 11] and obese [OB, n = 11]) were exposed to a low‐NSC diet (LO, n = 5 per group for LN LO and OB LO) or a high NSC diet (HI, n = 6 per group for LN HI and OB HI groups) for 7 days. For the EHC model, horses were administered insulin (constant rate infusion [6 mIU/kg bwt/min] combined with 50% dextrose, EHC group, n = 8)] or saline (0.57 mL/kg bwt/h, CON group, n = 8) for 48 h. Immunoblotting was employed to assess concentrations of activated/phosphorylated and total protein for members of the PI3K/Akt/mTORC1 and Ras/ERK pathways in lamellar samples from both models.
Results
In the DCM, lamellar P‐(Ser 240/244) RPS6 was increased in OB HI ponies (vs. OB LO, P |
| doi_str_mv | 10.1111/evj.12663 |
| format | Article |
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Background
Insulin dysregulation, obesity, and exposure to high‐nonstructural carbohydrate (NSC) forage are risk factors for equine metabolic syndrome‐associated laminitis (EMSAL); high systemic insulin concentrations in EMSAL are proposed to induce cellular dysregulation in the digital lamellae through activation of the insulin‐like growth factor‐1 receptor.
Objectives
To use a dietary challenge model (DCM) and a euglycaemic–hyperinsulinaemic clamp (EHC) model to assess lamellar growth factor‐related signalling.
Study design
Lamellar phospho (P)‐protein concentrations of signalling proteins important in growth factor‐related signalling were assessed in 2 models: 1) lean and obese ponies on a low‐ or high‐NSC diet; and 2) EHC model using Standardbred horses.
Methods
Ponies stratified for body condition (lean [LN, n = 11] and obese [OB, n = 11]) were exposed to a low‐NSC diet (LO, n = 5 per group for LN LO and OB LO) or a high NSC diet (HI, n = 6 per group for LN HI and OB HI groups) for 7 days. For the EHC model, horses were administered insulin (constant rate infusion [6 mIU/kg bwt/min] combined with 50% dextrose, EHC group, n = 8)] or saline (0.57 mL/kg bwt/h, CON group, n = 8) for 48 h. Immunoblotting was employed to assess concentrations of activated/phosphorylated and total protein for members of the PI3K/Akt/mTORC1 and Ras/ERK pathways in lamellar samples from both models.
Results
In the DCM, lamellar P‐(Ser 240/244) RPS6 was increased in OB HI ponies (vs. OB LO, P<0.05); positive correlations existed (P<0.05; r>0.5) between Day 7 basal serum insulin concentrations and lamellar concentrations of P‐p70S6K and P‐(Ser 240/244) RPS6. In the EHC model, lamellar concentrations of P‐Akt, P‐p70S6K, P‐ERK 1/2, P‐p90RSK, and both P‐(Ser 235/236) and P‐(Ser 240/244) RPS6 were increased in the EHC group (vs. CON, P<0.05).
Main limitations
The primary limitations of this study are the small number of animals per group in the DCM study, and the fact that many animals did not develop laminitis as that was not the endpoint of either study.
Conclusions
These results support further investigation of mTORC1/RPS6 signalling as a potential therapeutic target(s) in EMSAL.
The Summary is available in Chinese – see Supporting Information.</description><identifier>ISSN: 0425-1644</identifier><identifier>EISSN: 2042-3306</identifier><identifier>DOI: 10.1111/evj.12663</identifier><identifier>PMID: 28078757</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Animals ; blood serum ; body condition ; Carbohydrates ; Cattle ; Design factors ; Diet ; equine metabolic syndrome ; equine metabolic syndrome‐associated laminitis ; Exposure ; Foot Diseases - metabolism ; Foot Diseases - veterinary ; forage ; Gene Expression Regulation ; glucose ; growth factor signalling ; Hoof and Claw ; horse ; Horse Diseases - metabolism ; Horses ; Immunoblotting ; Inflammation ; Insulin ; Insulin-like growth factor I ; insulin-like growth factor I receptor ; Insulin-like growth factors ; Lamellae ; laminitis ; mitogen-activated protein kinase ; Obesity ; Phosphatidylinositol 3-Kinases ; protein content ; Proteins ; Receptor, IGF Type 1 - metabolism ; ribosomal protein S6 ; Risk factors ; Signal transduction ; Somatomedins ; Standardbred</subject><ispartof>Equine veterinary journal, 2017-09, Vol.49 (5), p.643-654</ispartof><rights>2017 EVJ Ltd</rights><rights>2017 EVJ Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3863-b9be0e021dad51080119a23120583c6ee74360ac201abc6c8bbbfe4dec132f703</citedby><cites>FETCH-LOGICAL-c3863-b9be0e021dad51080119a23120583c6ee74360ac201abc6c8bbbfe4dec132f703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fevj.12663$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fevj.12663$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28078757$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lane, H. E.</creatorcontrib><creatorcontrib>Burns, T. A.</creatorcontrib><creatorcontrib>Hegedus, O. C.</creatorcontrib><creatorcontrib>Watts, M. R.</creatorcontrib><creatorcontrib>Weber, P. S.</creatorcontrib><creatorcontrib>Woltman, K. A.</creatorcontrib><creatorcontrib>Geor, R. J.</creatorcontrib><creatorcontrib>McCutcheon, L. J.</creatorcontrib><creatorcontrib>Eades, S. C.</creatorcontrib><creatorcontrib>Mathes, L. E.</creatorcontrib><creatorcontrib>Belknap, J. K.</creatorcontrib><title>Lamellar events related to insulin‐like growth factor‐1 receptor signalling in two models relevant to endocrinopathic laminitis</title><title>Equine veterinary journal</title><addtitle>Equine Vet J</addtitle><description>Summary
Background
Insulin dysregulation, obesity, and exposure to high‐nonstructural carbohydrate (NSC) forage are risk factors for equine metabolic syndrome‐associated laminitis (EMSAL); high systemic insulin concentrations in EMSAL are proposed to induce cellular dysregulation in the digital lamellae through activation of the insulin‐like growth factor‐1 receptor.
Objectives
To use a dietary challenge model (DCM) and a euglycaemic–hyperinsulinaemic clamp (EHC) model to assess lamellar growth factor‐related signalling.
Study design
Lamellar phospho (P)‐protein concentrations of signalling proteins important in growth factor‐related signalling were assessed in 2 models: 1) lean and obese ponies on a low‐ or high‐NSC diet; and 2) EHC model using Standardbred horses.
Methods
Ponies stratified for body condition (lean [LN, n = 11] and obese [OB, n = 11]) were exposed to a low‐NSC diet (LO, n = 5 per group for LN LO and OB LO) or a high NSC diet (HI, n = 6 per group for LN HI and OB HI groups) for 7 days. For the EHC model, horses were administered insulin (constant rate infusion [6 mIU/kg bwt/min] combined with 50% dextrose, EHC group, n = 8)] or saline (0.57 mL/kg bwt/h, CON group, n = 8) for 48 h. Immunoblotting was employed to assess concentrations of activated/phosphorylated and total protein for members of the PI3K/Akt/mTORC1 and Ras/ERK pathways in lamellar samples from both models.
Results
In the DCM, lamellar P‐(Ser 240/244) RPS6 was increased in OB HI ponies (vs. OB LO, P<0.05); positive correlations existed (P<0.05; r>0.5) between Day 7 basal serum insulin concentrations and lamellar concentrations of P‐p70S6K and P‐(Ser 240/244) RPS6. In the EHC model, lamellar concentrations of P‐Akt, P‐p70S6K, P‐ERK 1/2, P‐p90RSK, and both P‐(Ser 235/236) and P‐(Ser 240/244) RPS6 were increased in the EHC group (vs. CON, P<0.05).
Main limitations
The primary limitations of this study are the small number of animals per group in the DCM study, and the fact that many animals did not develop laminitis as that was not the endpoint of either study.
Conclusions
These results support further investigation of mTORC1/RPS6 signalling as a potential therapeutic target(s) in EMSAL.
The Summary is available in Chinese – see Supporting Information.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Animals</subject><subject>blood serum</subject><subject>body condition</subject><subject>Carbohydrates</subject><subject>Cattle</subject><subject>Design factors</subject><subject>Diet</subject><subject>equine metabolic syndrome</subject><subject>equine metabolic syndrome‐associated laminitis</subject><subject>Exposure</subject><subject>Foot Diseases - metabolism</subject><subject>Foot Diseases - veterinary</subject><subject>forage</subject><subject>Gene Expression Regulation</subject><subject>glucose</subject><subject>growth factor signalling</subject><subject>Hoof and Claw</subject><subject>horse</subject><subject>Horse Diseases - metabolism</subject><subject>Horses</subject><subject>Immunoblotting</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Insulin-like growth factor I</subject><subject>insulin-like growth factor I receptor</subject><subject>Insulin-like growth factors</subject><subject>Lamellae</subject><subject>laminitis</subject><subject>mitogen-activated protein kinase</subject><subject>Obesity</subject><subject>Phosphatidylinositol 3-Kinases</subject><subject>protein content</subject><subject>Proteins</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>ribosomal protein S6</subject><subject>Risk factors</subject><subject>Signal transduction</subject><subject>Somatomedins</subject><subject>Standardbred</subject><issn>0425-1644</issn><issn>2042-3306</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0U1rFDEYB_AgFrutHvwCEvBiD9M-SeYlc5RSq7LQi3odMplntlkzyZpkdulN8Av0M_pJzHarB0HMJS_88ofkT8hLBucsjwvcrs8Zr2vxhCw4lLwQAuqnZJGXVcHqsjwmJzGuAYTgJX9GjrmERjZVsyA_lmpCa1WguEWXIg1oVcKBJk-Ni7M17uf3e2u-Il0Fv0u3dFQ6-ZAPWbYaN3lDo1k5ZbNd5Us07Tyd_ID2IQ23yqV9HLrB62Cc36h0azS1ajLOJBOfk6NR2YgvHudT8vnd1afL98Xy5vrD5dtloYWsRdG3PQICZ4MaKgYSGGsVF4xDJYWuEZtS1KA0B6Z6XWvZ9_2I5YCaCT42IE7Jm0PuJvhvM8bUTSbq_esd-jl2HAAqYLKt_kuZrCQDwdsm09d_0bWfQ_6OrFoucy1tKbI6OygdfIwBx24TzKTCXceg25fY5RK7hxKzffWYOPcTDn_k79YyuDiAnbF49--k7urLx0PkL2keqYM</recordid><startdate>201709</startdate><enddate>201709</enddate><creator>Lane, H. E.</creator><creator>Burns, T. A.</creator><creator>Hegedus, O. C.</creator><creator>Watts, M. R.</creator><creator>Weber, P. S.</creator><creator>Woltman, K. A.</creator><creator>Geor, R. J.</creator><creator>McCutcheon, L. J.</creator><creator>Eades, S. C.</creator><creator>Mathes, L. E.</creator><creator>Belknap, J. K.</creator><general>Wiley Subscription Services, Inc</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>K9.</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope></search><sort><creationdate>201709</creationdate><title>Lamellar events related to insulin‐like growth factor‐1 receptor signalling in two models relevant to endocrinopathic laminitis</title><author>Lane, H. E. ; Burns, T. A. ; Hegedus, O. C. ; Watts, M. R. ; Weber, P. S. ; Woltman, K. A. ; Geor, R. J. ; McCutcheon, L. J. ; Eades, S. C. ; Mathes, L. E. ; Belknap, J. K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3863-b9be0e021dad51080119a23120583c6ee74360ac201abc6c8bbbfe4dec132f703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Animals</topic><topic>blood serum</topic><topic>body condition</topic><topic>Carbohydrates</topic><topic>Cattle</topic><topic>Design factors</topic><topic>Diet</topic><topic>equine metabolic syndrome</topic><topic>equine metabolic syndrome‐associated laminitis</topic><topic>Exposure</topic><topic>Foot Diseases - metabolism</topic><topic>Foot Diseases - veterinary</topic><topic>forage</topic><topic>Gene Expression Regulation</topic><topic>glucose</topic><topic>growth factor signalling</topic><topic>Hoof and Claw</topic><topic>horse</topic><topic>Horse Diseases - metabolism</topic><topic>Horses</topic><topic>Immunoblotting</topic><topic>Inflammation</topic><topic>Insulin</topic><topic>Insulin-like growth factor I</topic><topic>insulin-like growth factor I receptor</topic><topic>Insulin-like growth factors</topic><topic>Lamellae</topic><topic>laminitis</topic><topic>mitogen-activated protein kinase</topic><topic>Obesity</topic><topic>Phosphatidylinositol 3-Kinases</topic><topic>protein content</topic><topic>Proteins</topic><topic>Receptor, IGF Type 1 - metabolism</topic><topic>ribosomal protein S6</topic><topic>Risk factors</topic><topic>Signal transduction</topic><topic>Somatomedins</topic><topic>Standardbred</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lane, H. E.</creatorcontrib><creatorcontrib>Burns, T. A.</creatorcontrib><creatorcontrib>Hegedus, O. C.</creatorcontrib><creatorcontrib>Watts, M. R.</creatorcontrib><creatorcontrib>Weber, P. S.</creatorcontrib><creatorcontrib>Woltman, K. A.</creatorcontrib><creatorcontrib>Geor, R. J.</creatorcontrib><creatorcontrib>McCutcheon, L. J.</creatorcontrib><creatorcontrib>Eades, S. C.</creatorcontrib><creatorcontrib>Mathes, L. E.</creatorcontrib><creatorcontrib>Belknap, J. K.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Equine veterinary journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lane, H. E.</au><au>Burns, T. A.</au><au>Hegedus, O. C.</au><au>Watts, M. R.</au><au>Weber, P. S.</au><au>Woltman, K. A.</au><au>Geor, R. J.</au><au>McCutcheon, L. J.</au><au>Eades, S. C.</au><au>Mathes, L. E.</au><au>Belknap, J. K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lamellar events related to insulin‐like growth factor‐1 receptor signalling in two models relevant to endocrinopathic laminitis</atitle><jtitle>Equine veterinary journal</jtitle><addtitle>Equine Vet J</addtitle><date>2017-09</date><risdate>2017</risdate><volume>49</volume><issue>5</issue><spage>643</spage><epage>654</epage><pages>643-654</pages><issn>0425-1644</issn><eissn>2042-3306</eissn><abstract>Summary
Background
Insulin dysregulation, obesity, and exposure to high‐nonstructural carbohydrate (NSC) forage are risk factors for equine metabolic syndrome‐associated laminitis (EMSAL); high systemic insulin concentrations in EMSAL are proposed to induce cellular dysregulation in the digital lamellae through activation of the insulin‐like growth factor‐1 receptor.
Objectives
To use a dietary challenge model (DCM) and a euglycaemic–hyperinsulinaemic clamp (EHC) model to assess lamellar growth factor‐related signalling.
Study design
Lamellar phospho (P)‐protein concentrations of signalling proteins important in growth factor‐related signalling were assessed in 2 models: 1) lean and obese ponies on a low‐ or high‐NSC diet; and 2) EHC model using Standardbred horses.
Methods
Ponies stratified for body condition (lean [LN, n = 11] and obese [OB, n = 11]) were exposed to a low‐NSC diet (LO, n = 5 per group for LN LO and OB LO) or a high NSC diet (HI, n = 6 per group for LN HI and OB HI groups) for 7 days. For the EHC model, horses were administered insulin (constant rate infusion [6 mIU/kg bwt/min] combined with 50% dextrose, EHC group, n = 8)] or saline (0.57 mL/kg bwt/h, CON group, n = 8) for 48 h. Immunoblotting was employed to assess concentrations of activated/phosphorylated and total protein for members of the PI3K/Akt/mTORC1 and Ras/ERK pathways in lamellar samples from both models.
Results
In the DCM, lamellar P‐(Ser 240/244) RPS6 was increased in OB HI ponies (vs. OB LO, P<0.05); positive correlations existed (P<0.05; r>0.5) between Day 7 basal serum insulin concentrations and lamellar concentrations of P‐p70S6K and P‐(Ser 240/244) RPS6. In the EHC model, lamellar concentrations of P‐Akt, P‐p70S6K, P‐ERK 1/2, P‐p90RSK, and both P‐(Ser 235/236) and P‐(Ser 240/244) RPS6 were increased in the EHC group (vs. CON, P<0.05).
Main limitations
The primary limitations of this study are the small number of animals per group in the DCM study, and the fact that many animals did not develop laminitis as that was not the endpoint of either study.
Conclusions
These results support further investigation of mTORC1/RPS6 signalling as a potential therapeutic target(s) in EMSAL.
The Summary is available in Chinese – see Supporting Information.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28078757</pmid><doi>10.1111/evj.12663</doi><tpages>12</tpages></addata></record> |
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| ispartof | Equine veterinary journal, 2017-09, Vol.49 (5), p.643-654 |
| issn | 0425-1644 2042-3306 |
| language | eng |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Animals blood serum body condition Carbohydrates Cattle Design factors Diet equine metabolic syndrome equine metabolic syndrome‐associated laminitis Exposure Foot Diseases - metabolism Foot Diseases - veterinary forage Gene Expression Regulation glucose growth factor signalling Hoof and Claw horse Horse Diseases - metabolism Horses Immunoblotting Inflammation Insulin Insulin-like growth factor I insulin-like growth factor I receptor Insulin-like growth factors Lamellae laminitis mitogen-activated protein kinase Obesity Phosphatidylinositol 3-Kinases protein content Proteins Receptor, IGF Type 1 - metabolism ribosomal protein S6 Risk factors Signal transduction Somatomedins Standardbred |
| title | Lamellar events related to insulin‐like growth factor‐1 receptor signalling in two models relevant to endocrinopathic laminitis |
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