Regulation of the Na+/K+- ATPase by insulin: Why and how?

Identification of differentially expressed genes in skeletal muscle of non-diabetic insulin-resistant and insulin-sensitive Pima Indians by differential display PCR

“…The skeletal muscle mRNA expression of ATP1A2 could respond similarly to hypoinsulinaemic and insulin-resistant states. Furthermore, α2 subunit mRNA expression was increased by long-term insulin treatment of 3T3-L1 cells [22,25]; the treatment presumably induced insulin resistance [26,27]. Thus, the increased skeletal muscle mRNA expression of ATP1A2 in insulin-resistant subjects of this study might be a secondary effect of insulin resistance.…”

“…The ATP1A2 gene encodes the α2 subunit of Na + /K + -ATPase, which is specifically expressed in skeletal muscle, heart and fat tissues [21]. Several isoforms of Na + /K + -ATPase exist from different combinations of the α and β subunits [22]. In the streptozotocin (STZ) rat model of diabetes, increased muscle α2 subunit mRNA [23] and protein concentrations [24] with no change or decrease of enzyme activity were observed in skeletal muscle.…”

Effect of selenium nanoparticles with different sizes in primary cultured intestinal epithelial cells of crucian carp, Carassius auratus gibelio

“…As for the Na + /K + -ATPase, its activity provided the driving force for a secondary active transport of solutes, such as amino acids, phosphate, vitamins and, in epithelial cells, glucose. 36 According to previous studies, intestinal digestion products, such as glucose and amino acids, are dependent on the Na + /K + -ATPase; thus, its activity could reflect the level of cell metabolism at a certain extent. 37 The results of the Na + /K + -ATPase activities obtained in the present study were consistent with the determined LDH activities and protein contents.…”

Antihypertensive Treatment in Type 2 Diabetic Patients

“…Altered cation transport is another of several mechanisms by which insulin resistance might raise blood pressure. Both sodium/potassium-ATPase (Ewart & Klip, 1995;Sweeney & Klip, 1998) and calcium-ATPase pumps (Levy et al, 1989;Zemel et al, 1993) are insulin sensitive; thus, when insulin resistance is present, the activity of these pumps in the smooth muscle of the arterial wall might be reduced. This would lead to an intracellular accumulation of sodium and calcium, thereby sensitizing the vascular wall to pressor substances (Resnick, 1993).…”