[Determination of serum semicarbazide-sensitive amine oxidase activity in diabetic retinopathy in type-2 diabetes].

Introduction: Recent data suggest that the copper-containing semicarbazide-sensitive amine oxidase enzyme (SSAO) may play a role in vascular endothelial damage through conversion of certain endogenous monoamines, like methylamine into cytotoxic aldehydes, hydrogen peroxide and ammonia. SSAO is present in various human tissues and in the serum. Elevated SSAO activities have been reported in patients with both types of diabetes mellitus.

Insulinotropic action of amino acids at their physiological concentrations: I. Experiments in incubated islets.

In order to simulate physiological conditions, the influence of a mixture of 22 amino acids together with taurine, all tested at their normal concentration in plasma, upon insulin release, D-glucose metabolism and (45)Ca net uptake was investigated in isolated rat pancreatic islets. The amino acid mixture had little effect upon insulin release at low concentrations of D-glucose but augmented, by up to 50%, the release of insulin provoked by higher concentrations of D-glucose. The effects of glibenclamide, forskolin, theophylline and cytochalasin B upon insulin release evoked by D-glucose in the absence or presence of the amino acid mixture and the changes in insulin output evoked by the omission from the amino mixture or addition to media containing only D-glucose of selected amino acid(s), as well as the influence of the amino acid mixture upon D-glucose metabolism and (45)Ca net uptake, were considered as compatible with both the role of certain amino acids as nutrients and the accumulation of other amino acids as positively charged molecules in the islet cells.

Effects of cytochalasin B and D upon insulin release and pancreatic islet cell metabolism.

Cytochalasin B is known to enhance insulin release evoked by nutrient and non-nutrient secretagogues, including D-glucose, despite inhibiting D-glucose uptake and metabolism in pancreatic islets. In the present study, cytochalasin D, which failed to affect D-glucose uptake and metabolism by isolated islets, also augmented glucose-stimulated insulin release, but unexpectedly to a lesser extent than cytochalasin B. Such was not the case, however, in islets stimulated by non-glucidic nutrients such as 2-ketoisocaproate or the association of L-leucine and L-glutamine.