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首页> 外文期刊>Life sciences >In vitro and in vivo alterations of enzymatic glycosylation in diabetes.
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In vitro and in vivo alterations of enzymatic glycosylation in diabetes.

机译：糖尿病中酶促糖基化的体外和体内变化。

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Carbohydrate composition changes of glycoconjugates constituting the glycocalix of microvascular cells could be involved in the alterations of cell-cell interactions observed in diabetic retinopathy. In this field, we have recently reported that advanced glycation end products (AGEs) modify galactose, fucose and sialic acid contents of specific cellular glycoproteins. To better understand the mechanisms involved in glycoprotein modifications in diabetes, we now investigate whether glucose and AGEs could affect the activities of enzymes involved in galactose, fucose and sialic acid metabolism : glycosyltransferases (synthesis) and glycosidases (catabolism). For this, bovine retinal endothelial cells (BREC) and pericytes (BRP) were cultured in the presence of high glucose concentration or AGEs, and cell glycosidase and glycosyltransferase activities were measured. The same enzymatic activities were studied in the whole retina from streptozotocin-treated rats. The results show that high glucose concentration did not affect glycosidases and glycosyltransferases neither in BRP nor in BREC except for galactosyltransferase activities in BREC. Concerning BRP, only galactosyltransferase activities were altered by AGEs. In contrast, in BREC, AGEs increased beta-D galactosidase, alpha-L fucosidase and neuraminidase activities (+37%, +56%, 36% respectively) whereas galactosyltransferase, fucosyltransferase and sialyltransferase activities were decreased (-11%, -24% and -23% respectively). In the retina from diabetic rats, beta-D galactosidase, alpha-L fucosidase and neuraminidase activities increased (+70%, +57%, +78% respectively) whereas fucosyl and sialyltransferase decreased (-7% and -15% respectively). The possible consequence of these enzymatic activity changes could be a defect in the carbohydrate content of some glycoproteins that might participate in the endothelial cell dysfunctions in diabetic microangiopathy.
机译：构成微血管细胞糖杯的糖缀合物的碳水化合物组成变化可能与糖尿病性视网膜病中观察到的细胞-细胞相互作用的改变有关。在该领域，我们最近报道了高级糖基化终产物（AGEs）修饰特定细胞糖蛋白的半乳糖，岩藻糖和唾液酸含量。为了更好地了解糖尿病中糖蛋白修饰的机制，我们现在调查葡萄糖和AGEs是否会影响参与半乳糖，岩藻糖和唾液酸代谢的酶的活性：糖基转移酶（合成）和糖苷酶（分解代谢）。为此，在高葡萄糖浓度或AGEs的条件下培养牛视网膜内皮细胞（BREC）和周细胞（BRP），并测量细胞糖苷酶和糖基转移酶的活性。在链脲佐菌素处理的大鼠的整个视网膜中研究了相同的酶活性。结果表明，除了BREC中的半乳糖基转移酶活性外，高浓度的葡萄糖对BRP和BREC中的糖苷酶和糖基转移酶均无影响。关于BRP，AGEs仅改变了半乳糖基转移酶的活性。相反，在BREC中，AGEs增加了β-D半乳糖苷酶，α-L岩藻糖苷酶和神经氨酸酶的活性（分别为+37％，+ 56％，36％），而半乳糖基转移酶，岩藻糖基转移酶和唾液酸转移酶的活性却降低了（-11％，-24％）和-23％）。在糖尿病大鼠的视网膜中，β-D半乳糖苷酶，α-L岩藻糖苷酶和神经氨酸酶活性增加（分别为+70％，+ 57％，+ 78％），而岩藻糖基和唾液酸转移酶则降低（分别为-7％和-15％）。这些酶活性变化的可能结果可能是某些糖蛋白的碳水化合物含量存在缺陷，这些糖蛋白可能参与了糖尿病微血管病中的内皮细胞功能障碍。

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