uremia/carbohydrate

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Lipid and carbohydrate metabolism in uraemia.

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Lipid and carbohydrate metabolism variables were studied in twenty-eight patients with chronic renal failure (mean GFR 7.7 +/- 2.5 ml/min) and uraemic symptoms. 71% of the patients had hypertriglyceridaemia (greater than or equal to 2.2 mmol/l). Total serum cholesterol was normal while VLDL

Lipid and carbohydrate metabolism in uremia. Influence of treatment with protein-reduced diet and essential amino acids.

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The effects of low protein diet on lipid and carbohydrate metabolism in uremia were investigated in 22 patients treated during a period of 3--18 months (mean 9.5 months). Before treatment, the patients showed elevated serum triglycerides, low alpha-lipoprotein cholesterol and reduced glucose

Acute uremia following dietary potassium depletion. II. Effect on tissue carbohydrate composition.

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In order to evaluate the potential role of hyperkalemia and metabolic acidosis on the disturbances of carbohydrate metabolism normally seen in uremia, a specific model of acute uremia devoid of hyperkalemia and severe metabolic acidosis was chosen. Therefore, rats were deprived of potassium prior to

Carbohydrate metabolism in uraemia.

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OBJECTIVE Most uraemic patients are insulin resistant. This review focuses on the occurrence, mechanisms and consequences of this insulin resistance. Hypoglycaemia is also possible in a minority of uraemic patients; its causes are discussed at the end of the review. RESULTS Insulin resistance is

Carbohydrate metabolism and uraemia-mechanisms for glycogenolysis and gluconeogenesis.

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Disturbances of carbohydrate metabolism during acute uraemia are characterized by the degradation of liver and muscle glycogen with a simultaneous activation of hepatic gluconeogenesis. After binephrectomy, the substitution of essential amino acids and keto analogues stimulate liver, but not

Uremia-induced disturbances in hepatic carbohydrate metabolism: enhancement by sucrose feeding.

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A high-sucrose (S) diet accentuates anorexia and stunts growth in uremic (U) rats, and an oral S load induces a greater hyperfructosemia in U rats than in control (C) rats. Four studies were performed to determine the roles of S feeding and an acute S load on liver carbohydrate (CHO) metabolism in U

Studies on the role of the liver and splanchnic tissues in the production of carbohydrate intolerance in uremia.

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The potential contribution of the splanchnic tissues to the carbohydrate intolerance of uremia was studied in fasted, partially nephrectomized rats. The livers of sham operated (C) and partially nephrectomized (Nx) rats were perfused with physiologic concentrations of potential gluconeogenic

Acute uremia following dietary potassium depletion. I. Effect on blood parameters related to carbohydrate metabolism.

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The effect of an acute uremic state with normokalemia and only mild metabolic acidosis on blood metabolic intermediates related to carbohydrate metabolism was investigated in rats. Therefore animals were deprived of potassium by feeding a low-potassium diet for 4 weeks prior to induction of

Autoxidation products of both carbohydrates and lipids are increased in uremic plasma: is there oxidative stress in uremia?

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BACKGROUND Advanced glycation end products (AGEs), formed by non-enzymatic glycation and oxidation (glycoxidation) reactions, have been implicated in the pathogenesis of several diseases, including normoglycemic uremia. AGE research in uremia has focused on the accumulation of carbohydrate-derived

Oxidative protein damage with carbohydrates and lipids in uremia: 'Carbonyl stress'.

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Chronic uremia appears to be in a state of an increased oxidative stress. Under oxidative stress, proteins are modified directly by reactive oxygen species with the eventual formation of oxidised amino acids. Proteins are also modified indirectly with reactive carbonyl compounds formed by the

Tumor markers in uremia: carcinoembryonic antigen, neuron-specific enolase, carbohydrate antigen CA-50 and alpha-fetoprotein.

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The incidence of the tumor markers was studied in 140 patients aged between 18 and 84 years who had been on dialysis for 4-188 months. Neuron-specific enolase increased in 81 cases, CA-50 carbohydrate antigen in 44, while alpha-fetoprotein was within the normal range. Carcinoembryonic antigen (CEA)

[Influence of long-term treatment with human recombinant erythropoietin on secretion of hormones regulating carbohydrate metabolism in hemodialyzed patients with chronic uremia].

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The study aimed to assess the influence of long-term rhuEPO treatment on secretion of pancreatic hormones (insulin, glucagon). A total of 27 haemodialyzed and 9 healthy subjects were examined. Nine patients with uraemic anaemia were treated with rhuEPO for 12 months (EPO group) while another nine

Carbohydrate metabolism in uremia.

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Abnormalities of insulin and glucose metabolism, namely glucose intolerance, inhibition of insulin secretion and insulin resistance, are present in children with chronic renal failure. Insulin resistance is universal among children with end-stage renal disease and may be caused by uremic toxins

Disorders of carbohydrate and lipid metabolism in uremia.

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Glucose intolerance and hypertriglyceridemia appear to be frequent metabolic concomitants of chronic uremia. Both these abnormalities are ameliorated but not eliminated by intensive hemodialysis and aggressive treatment of the uremic state. The plasma lipid alteration appears to result principally

Carbohydrate metabolism in uremia.

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