Effect of alpha-glucosidase inhibition on the nonenzymatic glycation of glomerular basement membrane

Cohen, Morrel H.; Klepser, Henry; Wu, Van-Yu

doi:10.1016/0306-3623(91)90016-y

Cited by 15 publications

(4 citation statements)

References 36 publications

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“…In accordance with the reduced glycation of glomerular basement membrane by a-glucosidase inhibition in streptozotocin-diabetic rats [25], acarbose (40 mg 100 g-' diet) completely prevented the diabetic renal hypertrophy in these rats that was increased by 35% in the untreated rats ( Fig. 10).…”

Section: Nephroparhysupporting

confidence: 62%

“…Improved blood glucose control in diabetic animals under acarbose treatment does not only lead to lower glycated haemoglobin concentrations but also to a prevention of the glycation process of glomerular basement membranes in streptozotocin-diabetic rats as was shown by Cohen et ul. [25]. Furthermore, in an equivalent study it was shown that the development of advanced glycation endproducts (AGEs) in the connective tissue was reduced concerning the skin collagen and prevented concerning the tendon collagen compared with the untreated diabetic group [26].…”

Section: Effects On Hyperglycaemia and Non-enzymatic Glycation In Diamentioning

confidence: 99%

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Pharmacology of α‐glucosidase inhibition

Bischoff¹

1994

Eur J Clin Investigation

173

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The development of α‐amylase and brush‐border α‐glucosidase inhibitors is reviewed. The mode of action as well as pharmacological and pharmacodynamic properties of selected inhibitors with special regard to the most thoroughly investigated α‐glucosidase inhibitor acarbose are discussed. Inhibition of intestinal α‐glucosidases delays the digestion of starch and sucrose, flattens the postprandial blood glucose excursions, and thus mimics the effects of dieting on hyperglycaemia, hyperinsulinaemia and hypertriglyceridaemia. Therefore, the mechanism of α‐glucosidase inhibition represents the pharmacological optimization of the dietary principle of delayed carbohydrate absorption. In pre‐clinical studies using diabetic animals the oral administration of acarbose improved the metabolic state and reduced the blood glucose area under the curve. As a consequence, the process of non‐enzymatic glycation of proteins was retarded as indicated by reduced glycated haemoglobin, glomerular basement membranes or advanced glycation end‐products (AGEs) in collagen. These improved biochemical parameters correlated with beneficial effects against the development of diabetic nephropathy and neuropathy. Thus, the treatment of diabetic animals with acarbose does not only improve the metabolic state but has also the potential to delay, or possibly prevent, the development of diabetic complications.

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Section: Nephroparhysupporting

confidence: 62%

Section: Effects On Hyperglycaemia and Non-enzymatic Glycation In Diamentioning

confidence: 99%

Pharmacology of α‐glucosidase inhibition

Bischoff¹

1994

Eur J Clin Investigation

173

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

Wada

Koyama

Mizukami

et al. 1999

Diabetes Metab. Res. Rev.

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Background Continuous hyperglycemia is implicated in the pathogenesis of chronic diabetic complications. It is not well known, however, how and to what extent the development of neuropathy is inhibited by blood glucose control in subjects with Type 2 diabetes. We investigated therefore the effects of an α‐glucosidase inhibitor (voglibose; Vg) on neuropathic changes in diabetic Goto‐Kakizaki (GK) rats, a genetic model for Type 2 diabetes. Methods Twelve week‐old male GK rats were given a diet containing Vg (50 ppm) for 24 weeks and monitored for blood glucose, glycated hemoglobin, motor nerve conduction velocity (MNCV). At the end of the administration period (Na+, K+)‐ATPase activity and the structure of the peripheral nerves were examined. Age‐ and sex‐matched normal Wistar rats were treated similarly and served as controls. Results GK rats showed fasting hyperglycemia after 8 weeks of age, and Vg treatment significantly lowered levels of blood glucose and glycated hemoglobin. Slowing of MNCV to 80% of normal control levels was detected in GK rats. Vg treatment inhibited this delay by 24% at 24 weeks and 57% at 36 weeks of age. Nerve (Na+, K+)‐ATPase activity was reduced to 80% of normal control levels in GK rats and was restored by Vg treatment. Teased fiber studies revealed a higher incidence of fibers with paranodal, segmental demyelination and axonal degeneration in GK rats. Vg treatment significantly inhibited the development of these nerve‐fiber abnormalities. Conclusions Lowering of high blood glucose levels achieved by the use of Vg in GK rats improved MNCV and demyelinative nerve changes with restoration of (Na+, K+)‐ATPase activity. Copyright © 1999 John Wiley & Sons, Ltd.

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“… 58 Similarly, in 1990, a comparable research study conducted using Cohen and Rosenmann 59 diabetic rats demonstrated significantly less incidence and severity of glomerulosclerosis in study animals as compared to controls, with 3 months (p<0.05), 5 and 7 months (p<0.01) of acarbose therapy. Further research by Cohen et al , 60 using streptozocin diabetic rats, concluded that 8 weeks of acarbose therapy reduced glomerular basement membrane (GBM) glycation and retarded the nephropathogenic process in experimentally induced diabetes mellitus. Macedo et al 61 later made similar conclusions demonstrating that combination therapy with acarbose and insulin in alloxan-diabetic rats prevented GBM thickening, and the existing thickening was equivalent to that expected for normal rats of the same age.…”

Section: Surrogate End Pointsmentioning

confidence: 99%

Acarbose: safe and effective for lowering postprandial hyperglycaemia and improving cardiovascular outcomes

2015

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α-Glucosidase inhibitors (AGIs) are a class of oral glucose-lowering drugs used exclusively for treatment or prevention of type 2 diabetes mellitus. AGIs act by altering the intestinal absorption of carbohydrates through inhibition of their conversion into simple sugars (monosaccharides) and thus decrease the bioavailability of carbohydrates in the body, significantly lowering blood glucose levels. The three AGIs used in clinical practice are acarbose, voglibose and miglitol. This review will focus on the cardiovascular properties of acarbose. The current available data suggest that AGIs (particularly acarbose) may be safe and effective for the treatment of prediabetes and diabetes.

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Effect of alpha-glucosidase inhibition on the nonenzymatic glycation of glomerular basement membrane

Cited by 15 publications

References 36 publications

Pharmacology of α‐glucosidase inhibition

Pharmacology of α‐glucosidase inhibition

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

Acarbose: safe and effective for lowering postprandial hyperglycaemia and improving cardiovascular outcomes

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