Showing papers on "Fibromyalgia published in 1963"
TL;DR: It is suggested that severe diabetes presenting with loss of weight and ketosis is predominantly a disease in which insulin secretion is either deficient or becoming deficient.
Abstract: severe insulin deficiency of an absolute type, as Bornstein and Lawrence (1951) have suggested. While others possess levels of insulin which are not very different from those of normal subjects in the post-absorptive state, this does not imply that the pancreatic islet tissue is normal in patients of this type. The islet tissue in this type of patient is in any case secreting insulin under the stimulus of a raised blood sugar, probably to a maximal extent. Indeed, such patients appear to be unable to respond to an additional glucose load by secreting additional insulin (Seltzer and Smith, 1959). Failure of blood pyruvate to rise after glucose ingestion in this class of diabetic patients (Smith and Taylor, 1956) may also be related to their inability to secrete insulin. It may be, therefore, that most patients in this group are suffering from some degree of impairment of islet-cell function. This group ultimately seems to suffer a complete exhaustion of the islet cells, since insulin is not detectable in their pancreases at necropsy (Wrenshall et al., 1952), nor does endogenous insulin (assayed by immunological methods) appear to be present in their serum some time after the beginning of insulin treatment (Yalow and Berson, 1961). Insulin is also present at very low levels in the protein fractions of serum from these patients when the blood is taken many hours after insulin injections (Taylor, 1963, unpublished). This type of diabetes, associated at the time of onset with relatively high blood-insulin levels, shows some analogies with that induced in animals by growth-hormone administration (Randle and Young, 1956). Nevertheless, in this form of human diabetes (as opposed to that of the obese) growthhormone levels do not seem to be raised (Erlich and Randle, 1961). It is uncertain, therefore, if growth hormone has any direct role in the genesis of this type of diabetes, though its presence might be necessary for the diabetes to develop. In conclusion, it is suggested that severe diabetes presenting with loss of weight and ketosis is predominantly a disease in which insulin secretion is either deficient or becoming deficient. The high blood-insulin levels sometimes encountered in the early stages of this condition may reflect a stage of overstimulation of beta cells preceding final exhaustion. It is possible that in at least some of these patients the insulin antagonism is a consequence and not the cause of the insulin deficiency. Summary Serum from 22 cases of untreated diabetes presenting with ketosis has been examined for insulin activity. Insulin was found in serum or protein fractions of many of these cases, though it was not detectable in a minority of cases with high blood sugars or in diabetic coma. Effects of this insulin in whole serum often appeared to be masked by insulin antagonists. One such antagonist, with its possible relation to diabetic ketosis, is discussed.
72 citations