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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Skeletal muscle contains one of the largest pools of Na,K-ATPase in the body, and therefore plays a central role in the clearance of [K(+)] from the blood during the ingestion or infusion of K(+). In the case of major hyperkalaemia (i.e. pathological increase of plasma [K(+)]), skeletal muscle can rapidly accumulate significant amounts (up to 50%) of extracellular K(+). Thus, skeletal muscle is an important temporary storage for K(+). Hyperkalaemia and impaired K(+)-tolerance frequently occurs in people who present features of the metabolic syndrome, concomitant with impaired activity of the sodium pump and decreased expression of the Na,K-ATPase subunits. These pathological conditions may lead to membrane depolarization in excitable tissues and to the development of cardiac arrhythmia or other cardiovascular complications that are a major consequence of metabolic syndrome. Thus, increasing Na,K-ATPase activity in skeletal muscle may protect from these complications.
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PMID:Regulation of the Na,K-ATPase: Special implications for cardiovascular complications of metabolic syndrome. 1797 97

The skeletal muscle sodium pump plays a major role in the removal of K(+) ions from the circulation postprandial, or after a physical activity bout, thereby preventing the development of hyperkalemia and fatigue. Insulin and muscle contractions stimulate Na(+)-K(+)-ATPase activity in skeletal muscle, at least partially via translocation of sodium pump units to the plasma membrane from intracellular stores. The molecular mechanism of this phenomenon is poorly understood. Due to the contradictory reports in the literature, the very existence of the translocation of Na(+)-K(+)-ATPase to the skeletal muscle cell surface is questionable. This review summarizes more than 30 years work on the skeletal muscle sodium pump translocation paradigm. Furthermore, the methodological caveats of major approaches to study the sodium pump translocation in skeletal muscle are discussed. An understanding of the molecular regulation of Na(+)-K(+)-ATPase in skeletal muscle will have important clinical implications for the understanding of the development of complications associated with the metabolic syndrome, such as cardiovascular diseases or increased muscle fatigue in diabetic patients.
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PMID:Frontiers: skeletal muscle sodium pump regulation: a translocation paradigm. 1877 88

Leptin, an adipose tissue hormone which regulates food intake, is also involved in the pathogenesis of arterial hypertension. Plasma leptin concentration is increased in obese individuals. Chronic leptin administration or transgenic overexpression increases blood pressure in experimental animals, and some studies indicate that plasma leptin is elevated in hypertensive subjects independently of body weight. Leptin has a dose- and time-dependent effect on urinary sodium excretion. High doses of leptin increase Na(+) excretion in the short run; partially by decreasing renal Na(+),K(+)-ATPase (sodium pump) activity. This effect is mediated by phosphatidylinositol 3-kinase (PI3K) and is impaired in animals with dietary-induced obesity. In contrast to acute, chronic elevation of plasma leptin to the level observed in patients with the metabolic syndrome impairs renal Na(+) excretion, which is associated with the increase in renal Na(+),K(+)-ATPase activity. This effect results from oxidative stress-induced deficiency of nitric oxide and/or transactivation of epidermal growth factor receptor and subsequent stimulation of extracellular signal-regulated kinases. Ameliorating "renal leptin resistance" or reducing leptin level and/or leptin signaling in states of chronic hyperleptinemia may be a novel strategy for the treatment of arterial hypertension associated with the metabolic syndrome.
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PMID:Leptin and the Regulation of Renal Sodium Handling and Renal Na-Transporting ATPases: Role in the Pathogenesis of Arterial Hypertension. 2128 76