Pub Date : 1986-04-10DOI: 10.11213/TONYOBYO1958.29.SPPL2_121
信夫 坂本
{"title":"第29回日本糖尿病学会総会記録 ワークショップ X 糖尿病と糖・ケトン体代謝","authors":"信夫 坂本","doi":"10.11213/TONYOBYO1958.29.SPPL2_121","DOIUrl":"https://doi.org/10.11213/TONYOBYO1958.29.SPPL2_121","url":null,"abstract":"","PeriodicalId":53409,"journal":{"name":"Journal of the Japan Diabetes Society","volume":"29 1","pages":"121-124"},"PeriodicalIF":0.0,"publicationDate":"1986-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63537924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-04-05DOI: 10.11213/TONYOBYO1958.29.SPPL1_41
D. Stribling, D. Tomlinson
{"title":"Effects of ICI 128, 436 on Animal Models of Neuropathy","authors":"D. Stribling, D. Tomlinson","doi":"10.11213/TONYOBYO1958.29.SPPL1_41","DOIUrl":"https://doi.org/10.11213/TONYOBYO1958.29.SPPL1_41","url":null,"abstract":"","PeriodicalId":53409,"journal":{"name":"Journal of the Japan Diabetes Society","volume":"29 1","pages":"41-41"},"PeriodicalIF":0.0,"publicationDate":"1986-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63535752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-04-05DOI: 10.11213/TONYOBYO1958.29.SPPL1_34
D. Yue
The pathogenesis of diabetic neuropathy is incompletely understood. The accumulation of sorbitol has been postulated to be an important cause of the neuropthy. However, deficiency of myoinositol in diabetic peripheral nerves has also been documented and suggested as a cause of the neuropathy. The relative importance of sorbitol accumulation and myoinositol deficiency is not known and these two processes have usually been regarded as independent phenomena. In Streptozotocin diabetic rats, the centrations con of these two metabolites can be normalized by treatment with Sorbinil (5mg/kg body weight). These results suggest that the two processes are inter-related. The deficiency of nerve myoinositol can also be demonstrated in galactosaemic rats and again this can be normalized by aldose reductase inhibition. These results suggest that sorbitol or galactitol accumulations are primary events which lead to myoinositol deficiency. The finding of a relationship between sorbitol and myoinositol metabolism provide a unified concept relating the two abnormalities of diabetic nerve in the pathogenesis of diabetic neuropathy.
{"title":"Polyols Accumulation and Effect of Aldose Reductase Inhibitor in STZ-Diabetic Rats","authors":"D. Yue","doi":"10.11213/TONYOBYO1958.29.SPPL1_34","DOIUrl":"https://doi.org/10.11213/TONYOBYO1958.29.SPPL1_34","url":null,"abstract":"The pathogenesis of diabetic neuropathy is incompletely understood. The accumulation of sorbitol has been postulated to be an important cause of the neuropthy. However, deficiency of myoinositol in diabetic peripheral nerves has also been documented and suggested as a cause of the neuropathy. The relative importance of sorbitol accumulation and myoinositol deficiency is not known and these two processes have usually been regarded as independent phenomena. In Streptozotocin diabetic rats, the centrations con of these two metabolites can be normalized by treatment with Sorbinil (5mg/kg body weight). These results suggest that the two processes are inter-related. The deficiency of nerve myoinositol can also be demonstrated in galactosaemic rats and again this can be normalized by aldose reductase inhibition. These results suggest that sorbitol or galactitol accumulations are primary events which lead to myoinositol deficiency. The finding of a relationship between sorbitol and myoinositol metabolism provide a unified concept relating the two abnormalities of diabetic nerve in the pathogenesis of diabetic neuropathy.","PeriodicalId":53409,"journal":{"name":"Journal of the Japan Diabetes Society","volume":"29 1","pages":"34-34"},"PeriodicalIF":0.0,"publicationDate":"1986-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63536019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-04-05DOI: 10.11213/TONYOBYO1958.29.SPPL1_7
P. Dyck
{"title":"Quantitation of Neurologic Deficits in Diabetic Neuropathy","authors":"P. Dyck","doi":"10.11213/TONYOBYO1958.29.SPPL1_7","DOIUrl":"https://doi.org/10.11213/TONYOBYO1958.29.SPPL1_7","url":null,"abstract":"","PeriodicalId":53409,"journal":{"name":"Journal of the Japan Diabetes Society","volume":"29 1","pages":"7-11"},"PeriodicalIF":0.0,"publicationDate":"1986-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63537821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-04-05DOI: 10.11213/tonyobyo1958.29.sppl1_69
A. Douglas
{"title":"Assessment Design of Neuropathy in Diabetes Control and Complications Trial (DCCT) in the U.S.A.","authors":"A. Douglas","doi":"10.11213/tonyobyo1958.29.sppl1_69","DOIUrl":"https://doi.org/10.11213/tonyobyo1958.29.sppl1_69","url":null,"abstract":"","PeriodicalId":53409,"journal":{"name":"Journal of the Japan Diabetes Society","volume":"29 1","pages":"69-69"},"PeriodicalIF":0.0,"publicationDate":"1986-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63537710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-04-05DOI: 10.11213/TONYOBYO1958.29.SPPL1_49
D. Ewing
{"title":"Heart Rate Variability for the Assessment of Autonomic Neuropathy","authors":"D. Ewing","doi":"10.11213/TONYOBYO1958.29.SPPL1_49","DOIUrl":"https://doi.org/10.11213/TONYOBYO1958.29.SPPL1_49","url":null,"abstract":"","PeriodicalId":53409,"journal":{"name":"Journal of the Japan Diabetes Society","volume":"29 1","pages":"49-49"},"PeriodicalIF":0.0,"publicationDate":"1986-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63536054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-04-05DOI: 10.11213/TONYOBYO1958.29.SPPL1_100
R. Yates, C. Perkins, J. Kemp
{"title":"Clinical Evaluation of “Statil”. Pharmacokinetics and Biochemistry","authors":"R. Yates, C. Perkins, J. Kemp","doi":"10.11213/TONYOBYO1958.29.SPPL1_100","DOIUrl":"https://doi.org/10.11213/TONYOBYO1958.29.SPPL1_100","url":null,"abstract":"","PeriodicalId":53409,"journal":{"name":"Journal of the Japan Diabetes Society","volume":"29 1","pages":"100-100"},"PeriodicalIF":0.0,"publicationDate":"1986-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63535731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-04-05DOI: 10.11213/TONYOBYO1958.29.SPPL1_42
A. Sima
{"title":"The Effects of Early and Late Insulin Treatment on the Neuropathy in the BB-rat","authors":"A. Sima","doi":"10.11213/TONYOBYO1958.29.SPPL1_42","DOIUrl":"https://doi.org/10.11213/TONYOBYO1958.29.SPPL1_42","url":null,"abstract":"","PeriodicalId":53409,"journal":{"name":"Journal of the Japan Diabetes Society","volume":"29 1","pages":"42-42"},"PeriodicalIF":0.0,"publicationDate":"1986-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63535813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-01-01DOI: 10.11213/TONYOBYO1958.29.SPPL1_26
P. Low
We propounded the hypoxic hypothesis of diabetic neuropathy to reconcile morphologic descriptions of microangiopathy and descriptions of diffuse metabolic abnormalities in human (HDN) and experimental diabetic neuropathy (EDN). We have provided the following evidence for endoneurial hypoxia. 1) Indirect evidence of endoneurial hypoxia (reduced creatine phosphate; increased lactate)1) in acute and chronic experimental diabetic neuropathy.2)2) Reduced nerve blood flow (NBF) in chronic EDN2). 3) Direct evidence of endoneurial hypoxia based on microelectrode recordings of endoneurial oxygen tensions (PnO2) in chronic EDN. Sixty percent of oxygen tension values fell below the critical oxygen tension.2)3) 4) Oxygen supplementation partially prevented both the electrophysiologic and biochemical abnormalities in experimental diabetic neuropathy.3)5) To examine the role of sugar alcohol accumulation, PnO2 measurements were made in chronic experimental galactose neuropathy. Pn02 reduction occurred in proportion to the increase in intercapillary distance.4 6) To examine the role of hypoxia alone, rats were reared in a hypoxic (10% oxygen) environment for up to ten weeks. These animals developed nerve conduction slowing and RICB in the absence of sugar alcohol accumulation or myoinositol reduction. 7) Computer simulation studies are in good agreement with experimental data.
{"title":"Evidence for Hypoxic Hypothesis of Diabetic Neuropathy","authors":"P. Low","doi":"10.11213/TONYOBYO1958.29.SPPL1_26","DOIUrl":"https://doi.org/10.11213/TONYOBYO1958.29.SPPL1_26","url":null,"abstract":"We propounded the hypoxic hypothesis of diabetic neuropathy to reconcile morphologic descriptions of microangiopathy and descriptions of diffuse metabolic abnormalities in human (HDN) and experimental diabetic neuropathy (EDN). We have provided the following evidence for endoneurial hypoxia. 1) Indirect evidence of endoneurial hypoxia (reduced creatine phosphate; increased lactate)1) in acute and chronic experimental diabetic neuropathy.2)2) Reduced nerve blood flow (NBF) in chronic EDN2). 3) Direct evidence of endoneurial hypoxia based on microelectrode recordings of endoneurial oxygen tensions (PnO2) in chronic EDN. Sixty percent of oxygen tension values fell below the critical oxygen tension.2)3) 4) Oxygen supplementation partially prevented both the electrophysiologic and biochemical abnormalities in experimental diabetic neuropathy.3)5) To examine the role of sugar alcohol accumulation, PnO2 measurements were made in chronic experimental galactose neuropathy. Pn02 reduction occurred in proportion to the increase in intercapillary distance.4 6) To examine the role of hypoxia alone, rats were reared in a hypoxic (10% oxygen) environment for up to ten weeks. These animals developed nerve conduction slowing and RICB in the absence of sugar alcohol accumulation or myoinositol reduction. 7) Computer simulation studies are in good agreement with experimental data.","PeriodicalId":53409,"journal":{"name":"Journal of the Japan Diabetes Society","volume":"29 1","pages":"26-26"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63535885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-01-01DOI: 10.11213/TONYOBYO1958.29.SPPL1_64
P. Low, B. Zimmerman, P. Dyck
Quantitation of cardiac vagal abnormalities can be accurately done using heart period measurements. Measurements of postganglionic sudomotor failure is now possible using the quantitative sudomotor axon reflex test (Q-SART)1). We performed Q-SART measurements on the forearm and proximal foot of 38 patients with diabetic neuropathy and 62 controls. These results were compared with HP measurements on the same patients. Responses to deep breathing (DB) and Valsalva maneuver (VM) were determined and BP was measured supine and standing. HP responses were abnormal to DB and VM in 71% and 63% of diabetics; both tests were abnormal in 58%. The Q-SART was abnormal in the foot in 66% of diabetics. Results of HP and Q-SART recordings were concordant in 66% of patients. 18% had abnormal HP but normal Q-SART recordings while 11% had abnormal Q-SART but normal HP. 31% of patients who had
{"title":"Quantitation of Postganglionic Sudomotor Function","authors":"P. Low, B. Zimmerman, P. Dyck","doi":"10.11213/TONYOBYO1958.29.SPPL1_64","DOIUrl":"https://doi.org/10.11213/TONYOBYO1958.29.SPPL1_64","url":null,"abstract":"Quantitation of cardiac vagal abnormalities can be accurately done using heart period measurements. Measurements of postganglionic sudomotor failure is now possible using the quantitative sudomotor axon reflex test (Q-SART)1). We performed Q-SART measurements on the forearm and proximal foot of 38 patients with diabetic neuropathy and 62 controls. These results were compared with HP measurements on the same patients. Responses to deep breathing (DB) and Valsalva maneuver (VM) were determined and BP was measured supine and standing. HP responses were abnormal to DB and VM in 71% and 63% of diabetics; both tests were abnormal in 58%. The Q-SART was abnormal in the foot in 66% of diabetics. Results of HP and Q-SART recordings were concordant in 66% of patients. 18% had abnormal HP but normal Q-SART recordings while 11% had abnormal Q-SART but normal HP. 31% of patients who had","PeriodicalId":53409,"journal":{"name":"Journal of the Japan Diabetes Society","volume":"29 1","pages":"64-64"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63537093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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