Impaired glucose tolerance, a consequence of excessive carbohydrate consumption.

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Case Reports1 April 1955IMPAIRED GLUCOSE TOLERANCE, A CONSEQUENCE OF EXCESSIVE CARBOHYDRATE CONSUMPTIONSAMUEL ALPERT, M.D.SAMUEL ALPERT, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-42-4-927 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDespite intensive investigative work, diabetes mellitus remains a disorder of unknown etiology whose clinical manifestations constitute a symptom complex composed of impaired glucose tolerance, neuropathy, nephropathy, retinopathy and accelerated atherosclerosis. The site of the anatomic defect remains obscure. There is no indication that the primary basic pathology is wholly confined to the pancreas, nor is there evidence that excessive carbohydrate consumption is in any way related to the development of the disorder. On the other hand, any primary affliction of the pancreas may give rise to carbohydrate disturbances indistinguishable from that seen in true diabetes mellitus by reason of diminished...Bibliography1. Del GrecoScapellato FL: Transient diabetes with coma following short term excessive consumption of carbohydrate, Diabetes 2: 457-461 (Nov.-Dec.) 1953. CrossrefMedlineGoogle Scholar2. Homans J: Degeneration of the island of Langerhans associated with experimental diabetes in the cat, J. M. Research 30: 49-68 (Jan.) 1914. MedlineGoogle Scholar3. JacobsColwell HRAR: Lesions in the pancreas and in the anterior hypophysis, with fatal acidosis following prolonged intravenous administration of glucose (in dogs), Am. J. Physiol. 116: 194-200 (June) 1936. CrossrefGoogle Scholar4. Woerner CA: Effects of continuous intravenous injection of dextrose in increasing amounts of blood sugar level, pancreatic islands and liver of guinea pigs, Anat. Rec. 75: 91-105 (Sept.) 1939. CrossrefGoogle Scholar5. DohanLukens FCFD: Experimental diabetes produced by the administration of glucose, Endocrinology 42: 244-262 (Apr.) 1948. CrossrefMedlineGoogle Scholar6. Peterson GA: Degranulation of beta cells of rat's pancreas by glucose correlated with alterations in glucose tolerance, Proc. Soc. Exper. Biol. and Med. 70: 352-355 (Feb.) 1949. CrossrefMedlineGoogle Scholar7. BarronState SSD: Effect of prolonged administration of dextrose on beta cells on islets of Langerhans, Arch. Path. 48: 297-304 (Oct.) 1949. Google Scholar8. LukensDohan FDFC: Pituitary diabetes in cat; recovery following insulin or dietary treatment, Endocrinology 30: 175-202 (Feb.) 1942. CrossrefGoogle Scholar9. LukensDolanWolcott FDFCMW: Pituitary diabetes in cat; recovery following phlorizin treatment, Endocrinology 32: 475-487 (June) 1943. CrossrefGoogle Scholar10. AndersonLong EJA: The effect of hyperglycemia in insulin secretion as determined with isolated rat pancreas, Endocrinology 40: 92, 1947. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, N. Y.*Received for publication April 29, 1954.From the Veterans Administration, New York Regional Office. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRemission in DiabetesAFTERNOON GLUCOSE TOLERANCE TESTING: A KEY TO THE PATHOGENESIS, EARLY DIAGNOSIS AND PROGNOSIS OF DIABETOGENIC HYPERINSULINISMDie Grundstoffe der Nahrung 1 April 1955Volume 42, Issue 4Page: 927-931KeywordsAnatomical pathologyAtherosclerosisCarbohydratesDiabetes mellitusEtiologyGlucose intoleranceNeuropathyPancreasRetinopathy ePublished: 1 December 2008 Issue Published: 1 April 1955 PDF downloadLoading ...