Interim analysis points to a direct or surrogate (not necessarily unique) role of a particular infection in the pathogenesis of parkinsonism. With eradication failure, bolus release of antigen from killed bacteria could aggravate an effect of ongoing infection.
Plasma glucose, insulin, and C peptide concentrations were determined after an oral glucose load in normal subjects and in a group of patients with non-insulin-dependent diabetes mellitus before and during a short course of treatment with chloroquine. In the control group there was a small but significant reduction in fasting blood glucose concentration but overall glucose tolerance and hormone concentrations were unaffected. In contrast, the patients with non-insulin-dependent diabetes mellitus showed a significant improvement in their glucose tolerance, which paralleled the severity of their diabetes.This response seems to reflect decreased degradation of insulin rather than increased pancreatic output. These observations suggest that treatment with chloroquine or suitable analogues may be a new approach to the management of diabetes.
IntroductionThe liver is a major target organ for insulin, removing up to half of available circulating insulin.' This hepatic uptake is mediated by receptors, and once the insulin-receptor complex has been internalised the hormone undergoes rapid degradation and clearance from the liver.2 In the rat chloroquine causes hepatic retention of insulin,3 an effect which has been ascribed to the lysosomatotropic action of chloroquine.4 We have recently shown, however, that chloroquine directly affects an insulin degrading
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