Effects of acetyl- and proprionyl- l-carnitine on peripheral nerve function and vascular supply in experimental diabetes
l-Carnitine metabolism is abnormal in diabetes mellitus, and treatment with acetyl- l-carnitine (ALC) improves the function of cardiac muscle, retina, and peripheral nerve in experimental models. The aim was to compare the effects of ALC and proprionyl- l-carnitine (PLC) on motor and sensory nerve c...
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| Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 1995-09, Vol.44 (9), p.1209-1214 |
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| container_title | Metabolism, clinical and experimental |
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| creator | Cotter, M.A. Cameron, N.E. Keegan, A. Dines, K.C. |
| description | l-Carnitine metabolism is abnormal in diabetes mellitus, and treatment with acetyl-
l-carnitine (ALC) improves the function of cardiac muscle, retina, and peripheral nerve in experimental models. The aim was to compare the effects of ALC and proprionyl-
l-carnitine (PLC) on motor and sensory nerve conduction in streptozotocin-diabetic rats and to ascertain whether their action could be mediated by a vascular mechanism. ALC and PLC treatment for 2 months after diabetes induction attenuated the development of sciatic motor nerve conduction velocity (NCV) deficits by 59.4% ± 4.4% and 46.9% ± 3.2%, respectively. There was a similar level of protection for sensory saphenous NCV (42.9% ± 6.6% and 47.8% ± 6.0%, respectively). Neither ALC nor PLC prevented the development of resistance to hypoxic conduction failure (RHCF) in sciatic nerve from diabetic rats. A 46.5% ± 3.4% deficit in sciatic endoneurial blood flow, measured by microelectrode polarography and hydrogen clearance, in diabetic rats was partially prevented by both ALC (48.7% ± 6.4%) and PLC (69.4% ± 10.1%). ALC had no significant effect on blood flow in nondiabetic rats. Thus, the data show that these
l-carnitine derivatives have a similar efficacy in preventing nerve dysfunction, which depends on a neurovascular action. |
| doi_str_mv | 10.1016/0026-0495(95)90018-7 |
| format | Article |
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l-carnitine (ALC) improves the function of cardiac muscle, retina, and peripheral nerve in experimental models. The aim was to compare the effects of ALC and proprionyl-
l-carnitine (PLC) on motor and sensory nerve conduction in streptozotocin-diabetic rats and to ascertain whether their action could be mediated by a vascular mechanism. ALC and PLC treatment for 2 months after diabetes induction attenuated the development of sciatic motor nerve conduction velocity (NCV) deficits by 59.4% ± 4.4% and 46.9% ± 3.2%, respectively. There was a similar level of protection for sensory saphenous NCV (42.9% ± 6.6% and 47.8% ± 6.0%, respectively). Neither ALC nor PLC prevented the development of resistance to hypoxic conduction failure (RHCF) in sciatic nerve from diabetic rats. A 46.5% ± 3.4% deficit in sciatic endoneurial blood flow, measured by microelectrode polarography and hydrogen clearance, in diabetic rats was partially prevented by both ALC (48.7% ± 6.4%) and PLC (69.4% ± 10.1%). ALC had no significant effect on blood flow in nondiabetic rats. Thus, the data show that these
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l-carnitine (ALC) improves the function of cardiac muscle, retina, and peripheral nerve in experimental models. The aim was to compare the effects of ALC and proprionyl-
l-carnitine (PLC) on motor and sensory nerve conduction in streptozotocin-diabetic rats and to ascertain whether their action could be mediated by a vascular mechanism. ALC and PLC treatment for 2 months after diabetes induction attenuated the development of sciatic motor nerve conduction velocity (NCV) deficits by 59.4% ± 4.4% and 46.9% ± 3.2%, respectively. There was a similar level of protection for sensory saphenous NCV (42.9% ± 6.6% and 47.8% ± 6.0%, respectively). Neither ALC nor PLC prevented the development of resistance to hypoxic conduction failure (RHCF) in sciatic nerve from diabetic rats. A 46.5% ± 3.4% deficit in sciatic endoneurial blood flow, measured by microelectrode polarography and hydrogen clearance, in diabetic rats was partially prevented by both ALC (48.7% ± 6.4%) and PLC (69.4% ± 10.1%). ALC had no significant effect on blood flow in nondiabetic rats. Thus, the data show that these
l-carnitine derivatives have a similar efficacy in preventing nerve dysfunction, which depends on a neurovascular action.</description><subject>Acetylcarnitine - pharmacology</subject><subject>Acetylcarnitine - therapeutic use</subject><subject>Action Potentials</subject><subject>Animals</subject><subject>Associated diseases and complications</subject><subject>Biological and medical sciences</subject><subject>Blood Flow Velocity</subject><subject>Blood Glucose - metabolism</subject><subject>Body Weight</subject><subject>Carnitine - analogs & derivatives</subject><subject>Carnitine - pharmacology</subject><subject>Carnitine - therapeutic use</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Kinetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neural Conduction - drug effects</subject><subject>Peripheral Nerves - blood supply</subject><subject>Peripheral Nerves - drug effects</subject><subject>Peripheral Nerves - physiopathology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sciatic Nerve - blood supply</subject><subject>Sciatic Nerve - physiopathology</subject><issn>0026-0495</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcGKFDEQhoMo67j6Bgo5iOihtZLuTjoXQZbdVVjwoueQTioYyaTbpHvYeXvTzjBHIVCE-v4i-YqQ1ww-MmDiEwAXDXSqf6_6DwqADY18Qnasb3kzCICnZHdBnpMXpfwGACkHcUWupBBCKrkjj7feo10KnTw1FpdjbKhJjs55mnOY0naPjTU5hSUkpFOiM-Yw_8JsIk2YD0j9muxS2X_Bgyl2jSbTss5zPNKQKD5ukT2mpUZcMCMuWF6SZ97Egq_O9Zr8vLv9cfO1efh-_-3my0NjW2BLw52zzHrHhOKWO9WObSf7oXfOCME6OTrRDaqDkYsBLHBpxYiMG694O3Rctdfk3Wlu_dGfFcui96FYjNEknNaipeyh7eUGdifQ5qmUjF5XAXuTj5qB3oTrzabebOrtbMK1rLE35_nruEd3CZ0N1_7bc7-KMdFnk2woF6wVqlWcV-zzCcPq4hAw62IDJosu5Lof7abw_3f8BeNDnYY</recordid><startdate>199509</startdate><enddate>199509</enddate><creator>Cotter, M.A.</creator><creator>Cameron, N.E.</creator><creator>Keegan, A.</creator><creator>Dines, K.C.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>199509</creationdate><title>Effects of acetyl- and proprionyl- l-carnitine on peripheral nerve function and vascular supply in experimental diabetes</title><author>Cotter, M.A. ; Cameron, N.E. ; Keegan, A. ; Dines, K.C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c301t-2ddc1cfd1692c2d93b347585dda66147bd648940b2680c027c6be12af92384293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Acetylcarnitine - pharmacology</topic><topic>Acetylcarnitine - therapeutic use</topic><topic>Action Potentials</topic><topic>Animals</topic><topic>Associated diseases and complications</topic><topic>Biological and medical sciences</topic><topic>Blood Flow Velocity</topic><topic>Blood Glucose - metabolism</topic><topic>Body Weight</topic><topic>Carnitine - analogs & derivatives</topic><topic>Carnitine - pharmacology</topic><topic>Carnitine - therapeutic use</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetes Mellitus, Experimental - physiopathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Kinetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neural Conduction - drug effects</topic><topic>Peripheral Nerves - blood supply</topic><topic>Peripheral Nerves - drug effects</topic><topic>Peripheral Nerves - physiopathology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sciatic Nerve - blood supply</topic><topic>Sciatic Nerve - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cotter, M.A.</creatorcontrib><creatorcontrib>Cameron, N.E.</creatorcontrib><creatorcontrib>Keegan, A.</creatorcontrib><creatorcontrib>Dines, K.C.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Metabolism, clinical and experimental</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cotter, M.A.</au><au>Cameron, N.E.</au><au>Keegan, A.</au><au>Dines, K.C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of acetyl- and proprionyl- l-carnitine on peripheral nerve function and vascular supply in experimental diabetes</atitle><jtitle>Metabolism, clinical and experimental</jtitle><addtitle>Metabolism</addtitle><date>1995-09</date><risdate>1995</risdate><volume>44</volume><issue>9</issue><spage>1209</spage><epage>1214</epage><pages>1209-1214</pages><issn>0026-0495</issn><eissn>1532-8600</eissn><abstract>l-Carnitine metabolism is abnormal in diabetes mellitus, and treatment with acetyl-
l-carnitine (ALC) improves the function of cardiac muscle, retina, and peripheral nerve in experimental models. The aim was to compare the effects of ALC and proprionyl-
l-carnitine (PLC) on motor and sensory nerve conduction in streptozotocin-diabetic rats and to ascertain whether their action could be mediated by a vascular mechanism. ALC and PLC treatment for 2 months after diabetes induction attenuated the development of sciatic motor nerve conduction velocity (NCV) deficits by 59.4% ± 4.4% and 46.9% ± 3.2%, respectively. There was a similar level of protection for sensory saphenous NCV (42.9% ± 6.6% and 47.8% ± 6.0%, respectively). Neither ALC nor PLC prevented the development of resistance to hypoxic conduction failure (RHCF) in sciatic nerve from diabetic rats. A 46.5% ± 3.4% deficit in sciatic endoneurial blood flow, measured by microelectrode polarography and hydrogen clearance, in diabetic rats was partially prevented by both ALC (48.7% ± 6.4%) and PLC (69.4% ± 10.1%). ALC had no significant effect on blood flow in nondiabetic rats. Thus, the data show that these
l-carnitine derivatives have a similar efficacy in preventing nerve dysfunction, which depends on a neurovascular action.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>7666797</pmid><doi>10.1016/0026-0495(95)90018-7</doi><tpages>6</tpages></addata></record> |
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| subjects | Acetylcarnitine - pharmacology Acetylcarnitine - therapeutic use Action Potentials Animals Associated diseases and complications Biological and medical sciences Blood Flow Velocity Blood Glucose - metabolism Body Weight Carnitine - analogs & derivatives Carnitine - pharmacology Carnitine - therapeutic use Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - physiopathology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Kinetics Male Medical sciences Neural Conduction - drug effects Peripheral Nerves - blood supply Peripheral Nerves - drug effects Peripheral Nerves - physiopathology Rats Rats, Sprague-Dawley Sciatic Nerve - blood supply Sciatic Nerve - physiopathology |
| title | Effects of acetyl- and proprionyl- l-carnitine on peripheral nerve function and vascular supply in experimental diabetes |
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