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Protein Metabolism clinical trials

View clinical trials related to Protein Metabolism.

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NCT ID: NCT01461603 Active, not recruiting - Critical Illness Clinical Trials

Local Effects of Amino Acids and 3-hydroxybutyrate in the Bilaterally Perfused Human Leg

Start date: September 2011
Phase: N/A
Study type: Interventional

Introduction: Protein loss during critical illness is an important problem and is shown to predict overall survival. In animal studies, infusion of leucine is shown to increase the synthesis of muscle protein by 30-40% and decrease protein degradation by 30%. Objectives: Compared to saline, an amino acid or 3hydroxybutyrate infusion in the femoral artery will promote protein synthesis and inhibit breakdown assessed with local a/v phenylalanine and tyrosine tracer kinetics in healthy volunteers. These effects will include distinct alterations in muscle signal events, in particular mTOR. Methods: n = 10 healthy male subjects are equipped with catheters in aa. femorals and vv. femorals bilaterally under local anaesthetics. Each study comprises a 3-hour basal period and a 3-hour period with hyperinsulinaemic-euglycaemic clamp. During the test, samples of arterial and venous blood and 4 muscle biopsies are obtained. The intervention contain continues saline infusion compared to either amino acids (Vamin) or 3hydroxybutyrate solution FFa-3OHB. Perspectives: This study elucidates the direct effect of aminoacids and ketone bodies on muscle protein metabolism in humans and contribute to further development of nutritional therapy in human catabolic states.

NCT ID: NCT00497380 Active, not recruiting - Protein Metabolism Clinical Trials

Arginine Feeding: a Novel Strategy to Improve Protein Metabolism in Cancer and the Response to Surgery

Start date: April 2009
Phase: N/A
Study type: Interventional

Muscle catabolism is a major problem in cancer patients undergoing surgery as it negatively affects post-operative recovery. Recent evidence exists that protein metabolic changes are already apparent in cancer before muscle wasting is being present. In line, patients with breast cancer, generally characterized by a normal nutritional status, were recently found to be arginine deficient. Arginine deficiency in cancer can be explained by: 1) Reduced arginine availability, due to exhaustion of endogenous (muscle) sources of arginine 2) Enhanced arginine catabolism, due to conversion of arginine by arginase, which is abundant in tumors. Protein is the most important endogenous source of arginine. Arginine deficiency will lead to a negative feedback loop in cachexia by promoting protein breakdown in an attempt to restore plasma arginine levels. We hypothesize that pre-operative arginine supplementation in breast cancer patients diminishes the occurrence of muscle wasting after surgery by 1) normalizing arginine availability pre-operatively, resulting in conservation of protein, 2) diminishing the catabolic effects of surgery by supplying exogenous arginine for the post-operative response, 3) enhancing the anabolic capacity to feeding through supplying substrate for protein synthesis.