Alpha-glucosidase inhibition prevents increased collagen fluorescence in experimental diabetes

Effects of long-term treatment with α-glucosidase inhibitor on the peripheral nerve function and structure in Goto-Kakizaki rats: a genetic model for Type 2 diabetes

“…In fact, endoneurial vessels of old GK rats have luminal narrowing and thickened walls, suggesting the importance of vascular factors in the development of the neuropathic change26. α‐Glucosidase inhibitors are known to inhibit the thickening of the basement membrane of the retina10, glycation of the basement membrane and interstitial collagen28, 29. The improvement of neuropathy in Vg‐treated GK rats may therefore be in part accounted for by inhibition of the development of endoneurial microangiopathy.…”

Pharmacology of Glucosidase Inhibitors

“…As could be expected from single-dose studies, elevated blood glucose concentrations and/or the urinary volume and glucose excretion and, last but not least, basal or prandial hyperinsulinaemia in diabetic rats and mice were dose dependently and markedly reduced by administration of acarbose (AXEN and SCLAFANI 1990;AXEN 1993;COHEN 1993;FOELLMER et al 1993;FRIEDMAN et al 1991;GRAY and OLEFSKY 1982;HAMADA et al 1989a;KATOVICH et al 1991;MAROT and LEMARCHAND-BRUSTEL 1988;PETERSON et al 1988;PETERSON 1991;PETERSON et al 1993;TULP et al 1988a;TuLP et al 1988b;TULP et al 1993;VASSELLI et al 1982;YAMASHITA et al 1984). Combined treatment of streptozotocin (STZ)-diabetic rats with insulin and acarbose was more effective than treatment with low-dosed insulin alone (HAMADA et al 1989b;KATOVICH and MELDRUM 1993a), as is indicated by ameliorated hyperglycaemia, polydipsia, urinary glucose excretion and glycated haemoglobin (GHb).…”

“…Basal glucose concentrations of hyperinsulinaemic rats, diabetic rats and mice were significantly ameliorated by acarbose (FOELLMER et al 1993;FRIEDMAN et al 1991;PETERSON et al 1993;. No effect of acarbose on basal blood glucose was reported by other authors (COHEN 1993;FRIED et al 1993;MAGGIO et al 1993;RUSSEL et al 1993a;VASSELLI et al 1993). In the latter experiments, blood sampies were collected from rats after a very short time period of food withdrawal (3 h only) or with the an im als under halothane anaesthesia.…”

“…These studies have generally shown that acarbose has a consistent body weight-lowering action, which was generally dose dependent and did not appear to be associated with any consistent change in food intake, although food intake was frequently increased. However, genetically or STZ-induced diabetic rats or mice exhibited no reduction of body weight or even an increased body weight gain during long-term administration of acarbosc in comparison to diabetic control animals (ABDOLLAHI et al 1993;COHEN 1993;FAILLA and SEIDEL 1993;FOELLMER et al 1993;KATOVICH anel MELDRUM 1993a;KOEVARY 1993;LEE 1982;MAGGIO et al 1993;PETERSON ct al. 1993;TULP et al 1993;Y AMASHITA et al 1984).…”

“…GHb, a long-term indicator of glycaemic control, was attenuated or normalized after administration of acarbose COHEN 1993;FOELLMER et al 1993;HAMADA et al 1989a;KATOVICH and MELDRUM 1993a;MAGGIO et al 1993;PETERSON 1991;PETERSON et al 1988PETERSON et al ,1993TuLP et al 1988b;TULP et al 1993;VASSELLI et al 1993), miglitol (DEBouNo et al 1989 and voglibose . In insulin-dependent BB/Wor rats the GHb was not significantly reduced by acarbose (KOEVARY 1993).…”