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Sökning: L773:1423 016X

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1.
  • Bergstrom, J, et al. (författare)
  • Factors contributing to catabolism in end-stage renal disease patients
  • 1998
  • Ingår i: Mineral and electrolyte metabolism. - : S. Karger AG. - 0378-0392 .- 1423-016X. ; 24:1, s. 92-101
  • Tidskriftsartikel (refereegranskat)abstract
    • End-stage renal disease (ESRD) patients, whether they are treated with hemodialysis or continuous ambulatory peritoneal dialysis, frequently suffer from protein-energy malnutrition, which is associated with increased morbidity and mortality. The protein requirements in dialysis patients are increased compared to those of healthy individuals and nondialyzed patients with chronic renal failure. The intake of protein and energy is frequently reduced because of the underlying disease, comorbidity, psychosocial factors, and uremic anorexia (underdialysis). There are several factors in ESRD patients that may enhance protein catabolism and increase protein requirements, such as low energy intake, amino acid abnormalities, metabolic acidosis, endocrine abnormalities (insulin resistance, hyperglucagonemia, hyperparathyroidism, insensitivity to growth hormone and insulin-like growth factor-1, cardiac failure, infection and inflammation, anemia, and physical inactivity. The dialytic procedures per se may enhance protein catabolism due to dialytic losses of protein and amino acids and, in hemodialysis, an inflammatory response to blood-dialyzer interaction. The relative importance of the various factors which cause anorexia and stimulate protein catabolism is still not well understood.
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2.
  • Bergstrom, J (författare)
  • Regulation of appetite in chronic renal failure
  • 1999
  • Ingår i: Mineral and electrolyte metabolism. - : S. Karger AG. - 0378-0392 .- 1423-016X. ; 25:4-6, s. 291-297
  • Tidskriftsartikel (refereegranskat)abstract
    • Anorexia, nausea and vomiting in patients with severe renal failure may cause or contribute to development of protein-energy malnutrition, which is associated with increased morbidity and mortality. However, the specific mechanisms that cause appetite suppression in uremia are poorly understood. This review summarizes the general mechanisms by which appetite is regulated. Various factors are discussed that may potentially be involved in appetite suppression in chronic renal failure.
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3.
  • Flodmark, Carl-Erik, et al. (författare)
  • Red cell sodium-potassium adenosine triphosphatase sites and intracellular sodium increased in obese school children
  • 1992
  • Ingår i: Mineral and Electrolyte Metabolism. - 1423-016X. ; 18:1, s. 6-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Principally to ascertain whether mineral metabolism is involved in weight regulation, the 40 most obese of 1,774 children, aged 10-11 years, screened for obesity were compared with 46 age-matched controls. The obese children had more 3H-Ouabain erythrocyte binding sites (p = 0.04), higher intracellular sodium (p = 0.04), and lower plasma sodium (p = 0.002). After exclusion of the non-Scandinavians, the p values were p = 0.02, p = 0.03, and p = 0.03, respectively. Analysis of variance also showed the differences to be more dependent on obesity than on gender or nationality. It is concluded that obese children have more 3H-Ouabain erythrocyte binding sites indicating an increase of the sodium-potassium adenosine triphosphatase activity. The increase of intracellular sodium may increase the risk of future hypertension.
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4.
  • Stenvinkel, P (författare)
  • Leptin and its clinical implications in chronic renal failure
  • 1999
  • Ingår i: Mineral and electrolyte metabolism. - : S. Karger AG. - 0378-0392 .- 1423-016X. ; 25:4-6, s. 298-302
  • Tidskriftsartikel (refereegranskat)abstract
    • Leptin, the recently identified <i>ob</i> gene product, regulates food intake and energy expenditure in animal models. Leptin reaches the brain by a saturable transport mechanism and, via direct effects on the hypothalamus, decreases appetite and increases metabolism. Several recent studies have demonstrated markedly elevated serum leptin levels in patients with chronic renal failure (CRF) and it has been speculated that hyperleptinemia may contribute to uremic anorexia and malnutrition. Several factors may influence serum leptin levels in uremia and apart from decreased glomerular filtration rate also body fat mass and plasma insulin levels are important factors that determine serum leptin levels. The possible influence of chronic inflammation on serum leptin levels in CRF need further studies. Patients treated by peritoneal dialysis seem to have higher leptin levels compared to patients treated by hemodialysis. This could be the effect of a marked increase in body fat mass as a consequence of the continuous carbohydrate load. Leptin receptors have by now been identified in several peripheal organs which suggests that leptin besides having central effects also has a pleiotropic action. Indeed, recent findings indicate that besides regulating appetite leptin may play a role in sympathico-activation, insulin metabolism, renal sodium handing and hematopoiesis.
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