hypoproteinemia/carbohydrate

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11 rezilta yo

Effects of low carbohydrate diets on energy and nitrogen balance and body composition in rats depend on dietary protein-to-energy ratio.

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OBJECTIVE Truly ketogenic rodent diets are low in carbohydrates but also low in protein. The aim of this study was to differentiate effects of ketosis, low carbohydrate (LC) and/or low-protein intake on energy and nitrogen metabolism. METHODS We studied the nitrogen balance of rats fed LC diets with

Hypoproteinemia-induced mucosal albumin leakage. Influence of luminal nutrients.

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Previous studies indicate that a peptide enteral formula significantly attenuates the intestinal water and albumin loss in volume-expanded rats with acute hypoproteinemia. The purpose of this study was to determine the relative abilities of the fat, carbohydrate, and protein components of the

Chronic toxicity of propoxur on carbohydrate, protein and serum electrolyte levels in catfish, Heteropneustes fossilis.

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Alterations in the biochemical parameters of the catfish treated with low sublethal concentration (2.15 mg.L-1; 1/3 of 96 h LC50) of a carbamate pesticide-propoxur under static laboratory conditions for 10, 20 and 30 days were assayed. The fish elicited consistent hyperglycemia, concomitant with

[Risk of damage to the organ of vision in low birth weight infants].

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The authors presented their own material of years 1974-1977. During this period 8788 children were born, in it 737 (8,3%) with low birth weight (below 2500 g). Retrolental fibroplasia was diagnosed in 4 children, it was 0,5% of newborns with low birth weight, and 0,04% of the all live-borns. The

Chronic enteritis associated with the malabsorption and protein-losing enteropathy in the horse.

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Chronic granulomatous enteritis associated with weight loss and hypoproteinemia was identified in 2 horses. Both horses continued to have normally formed feces. Malabsorption of carbohydrate and lipid, with concomitant gastrointestinal protein loss was demonstrated in 1 case. One horse was treated

The effect of dietary manipulation on hepatic lipid accumulation in rats undergoing small intestinal bypass.

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Small intestinal bypass performed for morbid obesity produces hepatic fat infiltration which persists in some patients for more than 5 years. In an attempt to define causative and preventative factors of hepatic steatosis following small intestinal bypass, a rat model was developed. In this study,

Protein-losing enteropathy secondary to intestinal lymphangiectasia in a dog.

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Protein-losing enteropathy secondary to intestinal lymphangiectasia was diagnosed in a 1 1/2 -year-old female Doberman Pinscher. Poor growth rate, intermittent diarrhea, ascites, edema, hypoproteinemia, grossly dilated intestinal lymphatics, and impaired fat absorption characterized the disease.

[Indications and possibilities for parenteral nutrition (author's transl)].

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Parenteral nutrition is a basic therapy. It is necessary to have a preoperative definition of the nutritional condition and metabolism of the surgical patient. All disturbances such as catabolism and hypoproteinemia must be analyzed and treated. Patients in good general condition who need parenteral

[Pathogenesis and intensive care of infants with toxic-dystrophic syndrome].

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Eighty-two children with the toxic dystrophic syndrome coursing in the presence of acute enteric infection were examined. A number of pathogenetically significant disorders were revealed: salt-deficient exsicosis, exsication, hypopotassemia, anemia, hypoproteinemia, stable metabolic acidosis,

[Internal complications following jejunoileostomy in the treatment of extreme obesity].

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More than 250 patients with extreme obesity were treated at the Chir. Univ.-Klinik Erlangen by 30 + 20 cm jejunoileostomy. The patients lose overweight and reach nearly normal weight after 9-12 months. Carbohydrate intolerance and hypertriglyceridema disappear. Ensuing malabsorption and also the

Metabolic derangements in deficiency of citrin, a liver-type mitochondrial aspartate-glutamate carrier.

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Citrin, encoded by SLC25A13, is a liver-type mitochondrial aspartate-glutamate carrier (AGC), of which deficiency, in autosomal recessive trait, causes neonatal intrahepatic cholestasis (NICCD) and adult-onset type II citrullinemia (CTLN2). NICCD patients have jaundice, hypoproteinemia,

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