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Hypouricemia or hypouricaemia is a level of uric acid in blood serum that is below normal. In humans, the normal range of this blood component has a lower threshold set variously in the range of 2 mg/dL to 4 mg/dL, while the upper threshold is 530 μmol/L (6 mg/dL) for women and 619 μmol/L (7 mg/dL) for men. [1]
A low-protein diet is used as a therapy for inherited metabolic disorders, such as phenylketonuria and homocystinuria, and can also be used to treat kidney or liver disease. Low protein consumption appears to reduce the risk of bone breakage, presumably through changes in calcium homeostasis. [1]
Low carbon diet: Consuming food which has been produced, prepared and transported with a minimum of associated greenhouse gas emissions. Low-fat diet; Low glycemic index diet; Low-protein diet; Low sodium diet; Low-sulfur diet; Some common macrobiotic ingredients. Macrobiotic diet: A diet in which processed food is avoided. Common components ...
Unless high blood levels of uric acid are determined in a clinical laboratory, hyperuricemia may not cause noticeable symptoms in most people. [5] Development of gout – which is a painful, short-term disorder – is the most common consequence of hyperuricemia, which causes deposition of uric acid crystals usually in joints of the extremities, but may also induce formation of kidney stones ...
A key regulatory step is the production of 5-phospho-α-D-ribosyl 1-pyrophosphate by ribose-phosphate diphosphokinase, which is activated by inorganic phosphate and inactivated by purine ribonucleotides. It is not the committed step to purine synthesis because PRPP is also used in pyrimidine synthesis and salvage pathways.
Uric acid is a product of the metabolic breakdown of purine nucleotides, and it is a normal component of urine. [1] High blood concentrations of uric acid can lead to gout and are associated with other medical conditions, including diabetes and the formation of ammonium acid urate kidney stones .
The disorder is caused by a mutation of the purine nucleoside phosphorylase (PNP) gene, located at chromosome 14q13.1. [3] [4] This mutation was first identified by Eloise Giblett, a professor at the University of Washington, in 1975. [5] PNP is a key enzyme in the purine catabolic [6] pathway, and is required for purine degradation.
In the U.S. and Canada, the Reference Daily Intake (RDI) is used in nutrition labeling on food and dietary supplement products to indicate the daily intake level of a nutrient that is considered to be sufficient to meet the requirements of 97–98% of healthy individuals in every demographic in the United States.