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Protein toxicity is the effect of the buildup of protein metabolic waste compounds, like urea, uric acid, ammonia, and creatinine. Protein toxicity has many causes, including urea cycle disorders, genetic mutations, excessive protein intake, and insufficient kidney function, such as chronic kidney disease and acute kidney injury .
As a result of FAH deficiency, the substrate fumarylacetoacetate can accumulate in proximal renal tubular cells and hepatocytes, resulting in damage to the kidney and liver, respectively. [3] Type II tyrosinemia results from a mutation in the TAT gene, which encodes the enzyme tyrosine aminotransferase. [4]
All plasma proteins except Gamma-globulins are synthesised in the liver. [1] Human serum albumin, osmolyte and carrier protein; α-fetoprotein, the fetal counterpart of serum albumin; Soluble plasma fibronectin, forming a blood clot that stops bleeding; C-reactive protein, opsonin on microbes, [2] acute phase protein; Various other globulins
The primary effects are progressive liver and kidney dysfunction. The liver disease causes cirrhosis, conjugated hyperbilirubinemia, elevated AFP, hypoglycemia and coagulation abnormalities. This can lead to jaundice, ascites and hemorrhage. There is also an increased risk of hepatocellular carcinoma.
Aflatoxins were not found in liver samples of individuals with marasmus. [25] It has been known that the liver organ is the main target of aflatoxins and chronic toxicity can result in immunosuppressive and carcinogenic effects. [25] However, there is currently conflicting evidence to pinpoint a connection between kwashiorkor and aflatoxins.
Outside the range of pH that is compatible with life, proteins are denatured and digested, enzymes lose their ability to function, and the body is unable to sustain itself. The kidneys maintain acid-base homeostasis by regulating the pH of the blood plasma. Gains and losses of acid and base must be balanced.
Genes coding for the enzyme are primarily expressed in the liver, in the kidney cortex and (to a lesser extent) in the β-cells of the pancreatic islets and intestinal mucosa (especially during times of starvation). [7] Glucose 6-phosphatase is present in a wide variety of muscles across the animal kingdom, albeit at very low concentrations. [10]
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]