A Quantitative Immunocytochemical Study of Na⁺, K⁺-ATPase in Rat Hepatocytes After STZ-induced Diabetes and Dietary Fish Oil Supplementation

Abstract

SUMMARYBecause diabetes causes alterations in hepatic membrane fatty acid content, these changes may affect the Na ϩ ,K ϩ -ATPase. In this study we documented the effects of streptozotocin (STZ)-induced diabetes on hepatic Na ϩ ,K ϩ -ATPase catalytic ␣ 1 -subunit and evaluated whether these changes could be normalized by fish oil supplementation. Two groups of diabetic rats received fish oil or olive oil supplementation. Both groups had a respective control group. We studied the localization of catalytic ␣ 1 -subunit on bile canalicular and basolateral membranes using immunocytochemical methods and confocal laser scanning microscopy, and the Na ϩ ,K ϩ -ATPase activity, membrane fluidity, and fatty acid composition on isolated hepatic membranes. A decrease in the ␣ 1 -subunit was observed with diabetes in the bile canalicular membranes, without changes in basolateral membranes. This decrease was partially prevented by dietary fish oil. Diabetes induces significant changes as documented by enzymatic Na ϩ ,K ϩ -ATPase activity, membrane fluidity, and fatty acid content, whereas little change in these parameters was observed after a fish oil diet. In conclusion, STZ-induced diabetes appears to modify bile canalicular membrane integrity and dietary fish oil partly prevents the diabetes-induced alterations.

Blood Platelet Reactivity and its Pharmacological Modulation in (People with) Diabetes Mellitus

“…These effects of platelets on ox-LDL, as well as the activation of blood platelets by ox-LDL, contribute to the formation of the atherosclerotic lesion [24,25]. The interactions of blood platelets with atherogenic fractions of oxidised LDL can further contribute to the progression of atherogenesis through several mechanisms, including the augmented release of platelet-derived growth factor (PDGF) (a strong mitogenic and chemotactic agent) and β-thromboglobulin, enhanced synthesis of cholesterol esters in macrophages and monocytes, and increased uptake of oxidised LDL by macrophages [26]. It has been proposed that the binding of ox-LDL to the platelet surface leads to alterations in membrane fluidity, thus mediating the activating action of LDL on platelets.…”

Na/K-ATPase Activity and Ketone Body Metabolism in Long-term Diabetic Rats

“…The sequence of events however appears to be more complicated than that suggested by Kowluru et al [4]. Caution is therefore advised when Na + /K + -ATPase activity is used as marker in studies of possible pharmaceuticals against secondary complications of diabetes [7,8,13,14,27,35,47] or in other experimental situations [17,18,33].…”

“…It has been reported that in diabetic humans as well as laboratory animals the activity of Na + /K + -ATPase in erythrocytes [2][3][4][5], blood vessels [6], peripheral nerves [7][8][9], brain [10], kidney [11][12][13], liver [14,15], pancreas [16], intestine [17], muscle [18,19], retina [20] and lens [21] is reduced by a factor of up to 7 [12].…”