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The effect of chronic uremia on activities of cerebral dihydropteridine reductase (DHPR) and tyrosine hydroxylase (TH) and content of norepinephrine and dopamine was investigated in the male Sprague-Dawley rats. The uremic animals were fed diets containing either 8% or 18% casein ad libitum, and
Recently, based on a study in rats with chronic renal failure (CRF), it has been suggested that IGF-I resistance in uremia may be caused in part by defective IGF-I receptor autophosphorylation and tyrosine kinase activity. Thus if such a defect were to develop in prolonged acute renal failure (ARF),
The occurrence of low tyrosine tissue levels in uremic subjects, possibly due to impaired phenylalanine hydroxylation, suggests that tyrosine may be an essential amino acid in uremia. Additional dietary tyrosine may thus re-dress the deficiency. This study examined growth and tyrosine/phenylalanine
Several lines of evidence suggest that tyrosine formation is impaired in renal failure. The concentration of tyrosine is decreased and the phenylalanine/tyrosine ratio is increased in plasma and in skeletal muscle cells. After an oral or intravenous load, the rise of plasma phenylalanine is
Growth in length, weight gain and gain of body nitrogen were compared in rats with stable long-term uremia (U) resulting from subtotal two-stage nephrectomy with irradiation of residual parenchyma, in sham-operated pair-fed control rats (PFC) and in ad libitum fed control rats (LC). Growth in length
OBJECTIVE
Uraemia often provokes various neurological disorders, such as mental changes, malperception, confusion, seizures and coma. Since changes in neurotransmissions induce neurological symptoms, we investigated changes in the monoamine metabolism and motor activity in uraemic
We evaluated the possibility that impaired insulin-receptor kinase activity contributes to insulin resistance by examining in vitro receptor tyrosine kinase activity and in situ receptor phosphorylation in four models of insulin resistance. Adipocytes from streptozocin-induced nonketotic diabetic
Three mixtures containing varying proportions of threonine, tyrosine, and the ornithine, lysine, and histidine salts of branched-chain keto acids have been tested as dietary supplements to a 20- to 25-g mixed-quality protein diet in patients with severe chronic uremia. Two of the three supplements
A nephrectomized rat model was developed to examine PRL resistance to dopaminergic suppression, which is frequently present in humans with renal insufficiency. The MCR and the response of PRL to a dopamine (DA) infusion (0.4 microgram/kg . min) were measured in 24-h totally nephrectomized (TN) and
The effects of exercise training on muscle protein catabolism in uremia were studied in female rats. Rats made uremic by 3/4 nephrectomy were compared with sham-operated control female rats under conditions of exercise training by swimming or no exercise. The release of amino acids from
Peripheral arterial disease occurs more frequently and has a worse prognosis in patients with chronic kidney disease (CKD). The receptor for advanced glycation end products (RAGE) is involved in multiple aspects of uremia-associated vasculopathy. Previous data suggest that the RAGE pathway may
Untreated uremic patients show grossly abnormal amino acid patterns with low concentrations of threonine, valine, tyrosine and lysine in muscle and plasma and low plasma concentrations of isoleucine, leucine and phenylalanine. Patients who had been treated for more than 10 weeks with a low protein
15 patients with severe uremia (mean serum creatinine concentration 965, range 568-1383 mumoles/l) were treated with an unselected protein restricted (16-20 g protein/day) diet and a new amino acid preparation, containing the essential amino acids in proportions which differed from those recommended
Chronic kidney disease (CKD) is defined as the progressive loss of renal function often involving glomerular, tubulo-interstitial and vascular pathology. CKD is associated with vascular calcification; the extent of which predicts morbidity and mortality. However, the molecular regulation of these