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Altered expression of adenosine receptors in heart of diabetic rat

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Diabetes results in functional, biochemical, and morphological abnormalities in the heart. Some of these changes may be attributed to altered adenosine action. This study aimed to examine the expression level of adenosine receptors (AR) in heart of streptozotocin-induced diabetic rat. Performed analyses revealed detectable levels of A1-AR, A2a-AR, A2b-AR, A3-AR mRNA and protein in whole heart and isolated cardiac myocytes. An increase in A1-AR protein content with no changes in mRNA level was observed in isolated cardiac myocytes. Diabetes resulted in an increase of A3-AR mRNA and protein levels in heart and in cardiac myocytes. The level of A2a-AR mRNA was increased in whole diabetic heart, but it decreased in cardiac myocytes with no detectable changes in protein content. We did not observe any changes in expression level of A2b-AR in diabetic heart and isolated cardiac myocytes. Administration of insulin to diabetic rat for four days resulted in returning of the ARs mRNA and protein to the levels observed in heart of normal rat. These changes in ARs genes expression, and receptors protein content correspond to some abnormalities characteristic of the diabetic heart, suggesting involvement in pathogenesis of diabetic cardiomyopathy.
Carbohydrate-deficient glycoprotein syndromes are rare, multisystemic diseases, typically with major nervous system impairment, that are caused by hypo-and unglycosylation of N-linked glycoproteins. Hence, a biochemical evidence of this abnormality, like hypoglycosylation of serum transferrin is essential for diagnosis. Clinically and biochemically, six types of the disease have been delineated. Three of them are caused by deficiencies of the enzymes that are required for a proper glycosylation of lipid - (dolichol) linked oligosaccharide (phosphomannomutase or phosphomannose isomerase or alpha-glycosyltransferase), and one results from a deficiency of Golgi resident N-acetylglucosaminyltransferase II. In addition one variant of the disease has been reported as due to a defective biosynthesis of dolichol iself. The diseases are heritable but genetics has been established for only two types. Therapy, based on administration of mannose to patients is currently under investigation. It benefits patients with deficiency of phosphomannose isomerase. Taking into account the complexity of N-linked glycosylation of proteins more of the disease variants is expected to be found.
Biochemical abnormalities observed in canine babesiosis are related to the severity of the disease. The primary biochemical abnormalities found in affected dogs are: increase of the serum activity of transaminases and alkaline phosphatase, azotemia, and hypoglycemia. The purposes of this study were: 1) to estimate biochemical abnormalities in dogs infected with large Babesia in Warsaw and 2) to evaluate statistically changes observed during canine babesiosis in dogs from Warsaw. Samples of serum were collected from dogs naturally infected with large Babesia. Among 2023 positive samples, 202 were randomly selected. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), creatinine, blood urea nitrogen (BUN), total serum protein (TSP), albumin and blood glucose concentration were determined with a clinical chemistry analyser. Elevated activity of ALT, AST and ALP was detected accordingly in: 64.9, 92.6 and 31.7% of dogs. Elevated creatinine concentration and BUN were detected accordingly in 30.7 and 62.4% of dogs. Decrease of TSP, albumin, BUN, and hypoglycemia was detected accordingly in: 19.8, 32.7, 1.5 and 18.3% of dogs. The most common biochemical abnormalities found in affected dogs were: increase of activity of transaminases and ALP, elevated creatinine concentration, hypoalbuminemia and hypoglycemia. These abnormalities resulted from hepatopathy, renal failure and fasting.
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