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Interference with the excretion of uric acid results in gout. Excessive excretion of uric, phosphoric, and oxalic acid salts in the urine may cause these salts to precipitate and give rise to nephrolithiasis. Uremia arises from the inadequate excretion of certain end products of protein metabolism in some kidney diseases. Certain intermediate metabolic products—lactic, pyruvic, and acetoacetic acids—accumulate in the blood and tissues in disturbances of oxidative processes and in nutritional disorders and avitaminoses. The impairment of mineral metabolism can alter the acid-base balance. A disturbance in cholesterol metabolism underlies atherosclerosis and some forms of cholelithiasis.

Several conditions are indicative of metabolic disturbances. The accumulation of metabolites can be excessive or insufficient, or the interactive qualities of the metabolites can be altered, or the transformations that the metabolites undergo can change. Intermediate metabolic products can accumulate in the body, and end products of metabolism can be insufficiently or excessively excreted. Sometimes, abnormal metabolic products are formed. For example, diabetes mellitus is a disease in which carbohydrates are not completely assimilated, and the process by which they are converted to fat is disturbed. In obesity, too large an amount of carbohydrate is converted to fat.

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At the cellular level, metabolism is the result of the regulation of the synthesis and activity of enzymes. The synthesis of each enzyme is controlled by the corresponding gene. By acting through various factors on a portion of the DNA molecule that contains information about the synthesis of a given enzyme, various intermediate metabolic products can trigger, intensify, or suppress synthesis of that enzyme. For example, the colon bacillus ceases to synthesize isoleucine in a nutrient medium when this amino acid is present in excess. An excess of isoleucine acts in two ways: (1) it inhibits the activity of the enzyme threonine dehydratase, which catalyzes the first stage of the chain reactions that end in the synthesis of isoleucine, and (2) it suppresses the synthesis of all the enzymes essential to the biosynthesis of isoleucine, including threonine dehydratase. The inhibition of threonine dehydratase is an example of the allosteric inhibition of enzymatic activity.

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