Abstract

Probably the first allusion to diabetes is contained in the papyrus Ebers, dated at about 1500 B .C . and the symptomatology of the disorder was described by Aretaeus in the 1 st century A.D. Prior to the late 17th century the causation of diabetes was variously ascribed to excessive food, alcohol, sex or grief or to maladies of the stomach, arteries, blood, nervous and other systems. However, in 1683 the Swiss Brunner recorded that pancreatectomised dogs displayed great thirst and polyuria before dying in coma, and in 1788 Cawley reported destruction of the pancreatic tissue in a patient dying of diabetes. These observations were largely disregarded until further evidence of a possible relationship between diabetes and the pancreas was provided by the classical experiments of von Mering and Minkowski in 1890. Twenty years earlier Langerhans, when aged 20 , had described the islets to which his name was given in 1893 by Laguesse who was the first to suggest that they might produce an internal secretion. Schafer in 1895 considered that this secretion might profoundly modify the carbohydrate metabolism of the tissues and the name “ insuline” was proposed by de Meyer in 1909.

Highlights

  • The first allusion to diabetes is contained in the papyrus Ebers, dated at about 1500 B .C . and the sym ptom atology of the dis­ order was described by Aretaeus in the 1st century A .D

  • Prior to the late 17th century the causation of diabetes was variously ascribed to excessive food, alcohol, sex or grief or to maladies of the stom ach, arteries, blood, nervous and other systems

  • In 1683 the Swiss Brunner recorded that pancreatectomised dogs displayed great thirst and polyuria before dying in com a, and in 1788 Cawley reported destruction of the pancreatic tissue in a patient dying of diabetes

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Summary

INTRODUCTION

The first allusion to diabetes is contained in the papyrus Ebers, dated at about 1500 B .C . and the sym ptom atology of the dis­ order was described by Aretaeus in the 1st century A .D. In insulin-dependent diabetics accidentally killed early in the course of the disorder, the islets were hypertrophied but some­ times contained normal or increased amounts of extractable insulin These observations suggested that the primary abnormality of idiopathic or essential diabetes lay outwith the pancreas and was not a simple failure of insulin secretion. At that time Pincus and W hite found that the prevalence of diabetes among the offspring of two parents, neither or one or both of whom was diabetic, approximated to a ratio of 1 : 2 : 4 respectively, which suggested that the disorder was inherited as a simple mendelian recessive with a penetrance of about 15-20% (i.e. that only 15-20% of those who were genetically liable to become clinically diabetic did so during their lifetime.) This hypothesis was supported by the studies of Steinberg and Hanhart others have interpreted their own investigations to show either a dominant, a sex-linked, or in the case of juvenile-onset diabetics a recessive and in older-onset diabetics a dominant-type of in­ heritance. Idiopathic or essential diabetes is undoubtedly a genetic­ ally determined disorder much more inform­ ation is required to establish the mode of its transmission. (Refs. 2. 3. 4. 5.)

GROWTH HORMONE
INSULIN ANTAGONISTS
ROLE OF THE P AN CR E AS
DIAGNOSTIC PROBLEM
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