Brain metabolic alterations in patients with type 1 diabetes-hyperglycemia-induced injury
Microangiopathic end-organ injury is common in type 1 diabetes. However, the pathophysiology of diabetic encephalopathy is poorly understood. The authors studied 10 normotensive patients with type 1 diabetes with retinopathy, autonomic neuropathy, but without nephropathy, and 10 healthy subjects. Pr...
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Veröffentlicht in: | Journal of cerebral blood flow and metabolism 2004-12, Vol.24 (12), p.1393-1399 |
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creator | MÄKIMATTILA, Sari MALMBERG-CEDER, Kirsi ROINE, Risto O HÄKKINEN, Anna-Maija VUORI, Kim SALONEN, Oili SUMMANEN, Paula YKI-JÄRVINEN, Hannele KASTE, Markku HEIKKINEN, Sami LUNDBOM, Nina |
description | Microangiopathic end-organ injury is common in type 1 diabetes. However, the pathophysiology of diabetic encephalopathy is poorly understood. The authors studied 10 normotensive patients with type 1 diabetes with retinopathy, autonomic neuropathy, but without nephropathy, and 10 healthy subjects. Proton magnetic resonance spectroscopy was performed at 1.5 T in the frontal cortex, thalamus, and posterior frontal white matter. There was no change in N-acetyl-containing compounds (NA), but choline-containing compounds (Cho) were increased in the white matter and in the thalamus; myo-inositol was increased in the white matter, glucose excess was found in all brain, and water intensity was increased in the cortical voxel in the patients. Calculated lifetime glycemic exposure correlated inversely with Cho and NA in white matter and with Cho in thalamus. Concentrations of soluble intercellular adhesion molecules and vascular cell adhesion molecules were increased in the patients. In conclusion, in patients with type 1 diabetes, the increase in adhesion molecules and an association between altered brain metabolites and glycemic exposure suggest the presence of a vascularly mediated, progressive metabolic disturbance in the brain. |
doi_str_mv | 10.1097/00004647-200412000-00008 |
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However, the pathophysiology of diabetic encephalopathy is poorly understood. The authors studied 10 normotensive patients with type 1 diabetes with retinopathy, autonomic neuropathy, but without nephropathy, and 10 healthy subjects. Proton magnetic resonance spectroscopy was performed at 1.5 T in the frontal cortex, thalamus, and posterior frontal white matter. There was no change in N-acetyl-containing compounds (NA), but choline-containing compounds (Cho) were increased in the white matter and in the thalamus; myo-inositol was increased in the white matter, glucose excess was found in all brain, and water intensity was increased in the cortical voxel in the patients. Calculated lifetime glycemic exposure correlated inversely with Cho and NA in white matter and with Cho in thalamus. Concentrations of soluble intercellular adhesion molecules and vascular cell adhesion molecules were increased in the patients. In conclusion, in patients with type 1 diabetes, the increase in adhesion molecules and an association between altered brain metabolites and glycemic exposure suggest the presence of a vascularly mediated, progressive metabolic disturbance in the brain.</description><identifier>ISSN: 0271-678X</identifier><identifier>EISSN: 1559-7016</identifier><identifier>DOI: 10.1097/00004647-200412000-00008</identifier><identifier>PMID: 15625413</identifier><identifier>CODEN: JCBMDN</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Adult ; Biological and medical sciences ; Brain Injuries - etiology ; Brain Injuries - metabolism ; Brain Injuries - pathology ; Diabetes Mellitus, Type 1 - complications ; Diabetes Mellitus, Type 1 - metabolism ; Female ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Humans ; Hyperglycemia - complications ; Hyperglycemia - metabolism ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Magnetic Resonance Imaging ; Male ; Medical sciences ; Nervous system (semeiology, syndromes) ; Neurology ; Traumas. Diseases due to physical agents ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Journal of cerebral blood flow and metabolism, 2004-12, Vol.24 (12), p.1393-1399</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c258t-ac4e2d92546b0a51aa1dc90d3d295c01a5c40a3a4813bb58ed0be70c0c9d6a3c3</citedby><cites>FETCH-LOGICAL-c258t-ac4e2d92546b0a51aa1dc90d3d295c01a5c40a3a4813bb58ed0be70c0c9d6a3c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16333638$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15625413$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MÄKIMATTILA, Sari</creatorcontrib><creatorcontrib>MALMBERG-CEDER, Kirsi</creatorcontrib><creatorcontrib>ROINE, Risto O</creatorcontrib><creatorcontrib>HÄKKINEN, Anna-Maija</creatorcontrib><creatorcontrib>VUORI, Kim</creatorcontrib><creatorcontrib>SALONEN, Oili</creatorcontrib><creatorcontrib>SUMMANEN, Paula</creatorcontrib><creatorcontrib>YKI-JÄRVINEN, Hannele</creatorcontrib><creatorcontrib>KASTE, Markku</creatorcontrib><creatorcontrib>HEIKKINEN, Sami</creatorcontrib><creatorcontrib>LUNDBOM, Nina</creatorcontrib><title>Brain metabolic alterations in patients with type 1 diabetes-hyperglycemia-induced injury</title><title>Journal of cerebral blood flow and metabolism</title><addtitle>J Cereb Blood Flow Metab</addtitle><description>Microangiopathic end-organ injury is common in type 1 diabetes. However, the pathophysiology of diabetic encephalopathy is poorly understood. The authors studied 10 normotensive patients with type 1 diabetes with retinopathy, autonomic neuropathy, but without nephropathy, and 10 healthy subjects. Proton magnetic resonance spectroscopy was performed at 1.5 T in the frontal cortex, thalamus, and posterior frontal white matter. There was no change in N-acetyl-containing compounds (NA), but choline-containing compounds (Cho) were increased in the white matter and in the thalamus; myo-inositol was increased in the white matter, glucose excess was found in all brain, and water intensity was increased in the cortical voxel in the patients. Calculated lifetime glycemic exposure correlated inversely with Cho and NA in white matter and with Cho in thalamus. Concentrations of soluble intercellular adhesion molecules and vascular cell adhesion molecules were increased in the patients. In conclusion, in patients with type 1 diabetes, the increase in adhesion molecules and an association between altered brain metabolites and glycemic exposure suggest the presence of a vascularly mediated, progressive metabolic disturbance in the brain.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Brain Injuries - etiology</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - pathology</subject><subject>Diabetes Mellitus, Type 1 - complications</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Female</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Humans</subject><subject>Hyperglycemia - complications</subject><subject>Hyperglycemia - metabolism</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Traumas. Diseases due to physical agents</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0271-678X</issn><issn>1559-7016</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMlOxDAMhiMEYoblFVAvcAtkadL2CIhNGokLSHCq3MQDGXUZklSob08GBvAhduzvd6KfkIyzc86q4oKlyHVeUJEyTwejm1a5Q-ZcqYoWjOtdMmei4FQX5cuMHISw2hBSqX0y40oLlXM5J69XHlyfdRihGVpnMmgjeohu6EOWButUYh9D9uniexanNWY8sw4ajBjoe7r7t3Yy2DmgrrejQZtkq9FPR2RvCW3A420-JM-3N0_X93TxePdwfbmgRqgyUjA5Clul7-iGgeIA3JqKWWlFpQzjoEzOQEJectk0qkTLGiyYYaayGqSRh-TsZ-_aDx8jhlh3LhhsW-hxGEOtCyGEFjqB5Q9o_BCCx2W99q4DP9Wc1Rtb619b6z9bv1tlkp5s3xibDu2_cOtjAk63AAQD7dJDb1z457SUUstSfgEFsYEY</recordid><startdate>200412</startdate><enddate>200412</enddate><creator>MÄKIMATTILA, Sari</creator><creator>MALMBERG-CEDER, Kirsi</creator><creator>ROINE, Risto O</creator><creator>HÄKKINEN, Anna-Maija</creator><creator>VUORI, Kim</creator><creator>SALONEN, Oili</creator><creator>SUMMANEN, Paula</creator><creator>YKI-JÄRVINEN, Hannele</creator><creator>KASTE, Markku</creator><creator>HEIKKINEN, Sami</creator><creator>LUNDBOM, Nina</creator><general>Lippincott Williams & Wilkins</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>200412</creationdate><title>Brain metabolic alterations in patients with type 1 diabetes-hyperglycemia-induced injury</title><author>MÄKIMATTILA, Sari ; MALMBERG-CEDER, Kirsi ; ROINE, Risto O ; HÄKKINEN, Anna-Maija ; VUORI, Kim ; SALONEN, Oili ; SUMMANEN, Paula ; YKI-JÄRVINEN, Hannele ; KASTE, Markku ; HEIKKINEN, Sami ; LUNDBOM, Nina</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c258t-ac4e2d92546b0a51aa1dc90d3d295c01a5c40a3a4813bb58ed0be70c0c9d6a3c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Brain Injuries - etiology</topic><topic>Brain Injuries - metabolism</topic><topic>Brain Injuries - pathology</topic><topic>Diabetes Mellitus, Type 1 - complications</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Female</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Humans</topic><topic>Hyperglycemia - complications</topic><topic>Hyperglycemia - metabolism</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Traumas. 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However, the pathophysiology of diabetic encephalopathy is poorly understood. The authors studied 10 normotensive patients with type 1 diabetes with retinopathy, autonomic neuropathy, but without nephropathy, and 10 healthy subjects. Proton magnetic resonance spectroscopy was performed at 1.5 T in the frontal cortex, thalamus, and posterior frontal white matter. There was no change in N-acetyl-containing compounds (NA), but choline-containing compounds (Cho) were increased in the white matter and in the thalamus; myo-inositol was increased in the white matter, glucose excess was found in all brain, and water intensity was increased in the cortical voxel in the patients. Calculated lifetime glycemic exposure correlated inversely with Cho and NA in white matter and with Cho in thalamus. Concentrations of soluble intercellular adhesion molecules and vascular cell adhesion molecules were increased in the patients. In conclusion, in patients with type 1 diabetes, the increase in adhesion molecules and an association between altered brain metabolites and glycemic exposure suggest the presence of a vascularly mediated, progressive metabolic disturbance in the brain.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>15625413</pmid><doi>10.1097/00004647-200412000-00008</doi><tpages>7</tpages></addata></record> |
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subjects | Adult Biological and medical sciences Brain Injuries - etiology Brain Injuries - metabolism Brain Injuries - pathology Diabetes Mellitus, Type 1 - complications Diabetes Mellitus, Type 1 - metabolism Female Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Humans Hyperglycemia - complications Hyperglycemia - metabolism Injuries of the nervous system and the skull. Diseases due to physical agents Magnetic Resonance Imaging Male Medical sciences Nervous system (semeiology, syndromes) Neurology Traumas. Diseases due to physical agents Vascular diseases and vascular malformations of the nervous system |
title | Brain metabolic alterations in patients with type 1 diabetes-hyperglycemia-induced injury |
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