Sialic acid transferase activities of normal and diabetic (db/db) mice kidne

Bardos, P.; Lacord-Bonneau, M.; Rakotoarivony, J; Müh, J.P.; Weill, J

doi:10.1016/0020-711x(80)90138-x

Cited by 9 publications

(1 citation statement)

References 12 publications

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“…Sialyltransferase is responsible for the attachment of sialic acid to the membrane and has been reported to be depressed in renal tissue from diabetic mice (34) and heart muscle from cardiomyopathic hamsters (28). It is possible that the defect in diabetic cardiomyopathy may lie elsewhere along the pathway of ultimate attachment of the sialic acid to the proper position on the glycoprotein (35) rather than at the level of sialyltransferase.…”

Section: Resultsmentioning

confidence: 99%

Alterations in Ca2+ binding by and composition of the cardiac sarcolemmal membrane in chronic diabetes.

Pierce¹,

Kutryk²,

Dhalla³

1983

Proc. Natl. Acad. Sci. U.S.A.

117

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Chronic streptozotocin-induced diabetes in rats was associated with a significant loss in the ability of isolated cardiac sarcolemmal membranes to bind Ca2+. Administration of insulin to the diabetic rats normalized the sarcolemmal Ca2+ binding capacity. The content of sialic acid residues, which are considered to represent a superficial Ca2+ pool in sarcolemma, was decreased in preparations from diabetic rats, and this change also was reversible upon insulin treatment of the diabetic rats.Treatment of sarcolemma with neuraminidase decreased Ca2+ binding by 37% in control preparations but had no effect on diabetic preparations. Diphosphatidylglycerol content was decreased but other acidic phospholipids such as phosphatidylinositol and phosphatidylserine, which also bind Ca2', were not altered during diabetes. An increase in lysophosphatidylcholine and a decrease in phosphatidylethanolamine contents were observed in membranes isolated from diabetic rats. These results suggest that some alterations occur in Ca2+ binding and composition of heart sarcolemma in chronically diabetic rats and may provide further insight into the pathogenesis of diabetic cardiomyopathy.Chronic diabetes mellitus has been associated with primary defects in the contractile function of the heart (1-3). The precise subcellular mechanism responsible for this diabetic cardiomyopathy is unknown; however, it has been suggested (4) that alterations in Ca2+ metabolism in the heart occur. Depressed Ca2' uptake by the sarcoplasmic reticulum as well as alterations in Ca2+-activated ATPase have been demonstrated for sarcoplasmic reticular and myofibrillar fractions from diabetic rat hearts (5, 6). In view of the importance of the movement of extracellular Ca2+ across the myocardial membrane in modulating the contractile performance of the heart (7, 8), it is possible that alterations in trans-sarcolemmal Ca2`flux may participate in this cardiomyopathy. This hypothesis has been indirectly supported by a preliminary study in which an abnormal response of isolated heart preparations from diabetic animals to extracellular Ca2' was found (9). In addition, the presence of a general cardiac sarcolemmal membrane lesion has been supported by data documenting altered tissue Na+,K+ and Ca2O contents (3, 10, 11).The present study was undertaken to examine sarcolemmal characteristics in an experimental model of chronic diabetes. By virtue of its content of acidic phospholipids and sialic acid residues, heart sarcolemma is known to have a remarkable ability to bind Ca2' and so is considered to serve as a superficial Ca2+ pool for the generation of contractile activity (7,8,12).Thus, identification of changes in the sarcolemmal composition and Ca2' binding activity could extend our knowledge concerning the molecular mechanisms associated with defective cardiac muscle function in diabetic cardiomyopathy. METHODSMale Sprague-Dawley rats weighing 200-250 g were used in this study. Animals were randomly separated into control and experimental groups. Experiment...

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Section: Resultsmentioning

confidence: 99%