עוד קצת על מטבוליזם ותזונה- מחקר
מחקר נוסף, ההולך עם המידע החדש בנושא תזונה ומטבוליזם של חומצות אמינו וחברינו המתילים שעושים צרות בגלל פעילות לקויה של מערכת העיכול J Nutr. 2005 Jul;135(7):1609-12. Related Articles, Links Nutritional and functional importance of intestinal sulfur amino Acid metabolism. Shoveller AK, Stoll B, Ball RO, Burrin DG. Department of Animal and Poultry Science, University of Guelph, Guelph, ON, Canada N1G 2W1; The metabolism of sulfur amino acids, methionine and cysteine, has been linked to several key aspects of human health and cellular function. In addition, the metabolism of dietary amino acids by the gastrointestinal tract is nutritionally important for normal function. In the case of sulfur amino acids (SAAs), in vivo, stable isotope studies in adults suggest that the splanchnic tissues utilize as much as 30-44% of the dietary methionine and cysteine. Similarly, the dietary methionine requirement is 30% lower in total parenteral nutrition (TPN)-fed piglets, a condition in which dietary nutrients largely bypass intestinal metabolism. These data suggest that intestinal metabolism of methionine is substantial, yet the intestinal metabolic fate of dietary methionine is largely unknown. Dietary cysteine likely plays a key role in intestinal epithelial antioxidant function as a precursor for glutathione. Moreover, cysteine and glutathione may also regulate epithelial cell proliferation via modulation of redox status. Recent evidence indicates that transformed colonic epithelial cells are capable of methionine transmethylation and transsulfuration. This review discusses the evidence of intestinal SAA metabolism and how this affects nutrient requirements and epithelial function. והיישום בעצם קיים כיום בגישה של DAN! או לפחות העיקרון קיים. מעניין המחקר הזה- המדבר על הקשר שבין ציטוקינים, שהם פרואינפלמטוריים, ונמצאו לא מעט, אצל ילדי הספקטרום, בעלי הדלקות החוזרות, בדרכי הנשימה (הילדון שלי, לצערי) לבין המנגנון של המתילציה הפגומה, בכבד כפי שמוסר המאמר הזה: Curr Med Chem Cardiovasc Hematol Agents. 2005 Jul;3(3):267-81. Related Articles, Links Influence of impaired liver methionine metabolism on the development of vascular disease and inflammation. Avila MA, Berasain C, Prieto J, Mato JM, Garcia-Trevijano ER, Corrales FJ. Division of Hepatology and Gene Therapy, CIMA University of Navarra, Pamplona, Spain. [email protected] Methionine (Met) metabolism involves the sequential formation of S-adenosylmethionine (SAM, the main biological methyl donor), S-adenosylhomocysteine (SAH) and homocysteine (Hcy). Hcy can be remethylated to Met or catabolized through the trans-sulfuration pathway. In mammals, as much as 48% of Met metabolism and up to 85% of all transmethylation reactions occur in the liver. These figures underscore the central role played by this organ in Met metabolism. Maintaining the homeostasis of this metabolic cycle has proved to be essential for the preservation of liver function up to the point of preventing its neoplastic transformation. However, an adequate hepatic metabolism of Met is not only important for the liver parenchymal cell. Evidence has accumulated over the past few years supporting the involvement of Met-derived metabolites in the triggering or attenuation of pathological processes with systemic implications. This is best illustrated by the fact that a deteriorated liver function has emerged as a major factor in the development of hyperhomocysteinemia. Elevated plasma levels of Hcy have been related to several disorders including cardiovascular and cerebrovascular diseases. On the other end, liver damage also leads to deficient SAM synthesis. Among the consequences of impaired SAM synthesis in liver tissue are the enhanced production of pro-inflammatory cytokines and mediators. In this review, we will address the mechanisms and consequences of abnormal Met metabolism in liver injury, the systemic implications of such impairment and finally the potential therapeutic interventions.
מחקר נוסף, ההולך עם המידע החדש בנושא תזונה ומטבוליזם של חומצות אמינו וחברינו המתילים שעושים צרות בגלל פעילות לקויה של מערכת העיכול J Nutr. 2005 Jul;135(7):1609-12. Related Articles, Links Nutritional and functional importance of intestinal sulfur amino Acid metabolism. Shoveller AK, Stoll B, Ball RO, Burrin DG. Department of Animal and Poultry Science, University of Guelph, Guelph, ON, Canada N1G 2W1; The metabolism of sulfur amino acids, methionine and cysteine, has been linked to several key aspects of human health and cellular function. In addition, the metabolism of dietary amino acids by the gastrointestinal tract is nutritionally important for normal function. In the case of sulfur amino acids (SAAs), in vivo, stable isotope studies in adults suggest that the splanchnic tissues utilize as much as 30-44% of the dietary methionine and cysteine. Similarly, the dietary methionine requirement is 30% lower in total parenteral nutrition (TPN)-fed piglets, a condition in which dietary nutrients largely bypass intestinal metabolism. These data suggest that intestinal metabolism of methionine is substantial, yet the intestinal metabolic fate of dietary methionine is largely unknown. Dietary cysteine likely plays a key role in intestinal epithelial antioxidant function as a precursor for glutathione. Moreover, cysteine and glutathione may also regulate epithelial cell proliferation via modulation of redox status. Recent evidence indicates that transformed colonic epithelial cells are capable of methionine transmethylation and transsulfuration. This review discusses the evidence of intestinal SAA metabolism and how this affects nutrient requirements and epithelial function. והיישום בעצם קיים כיום בגישה של DAN! או לפחות העיקרון קיים. מעניין המחקר הזה- המדבר על הקשר שבין ציטוקינים, שהם פרואינפלמטוריים, ונמצאו לא מעט, אצל ילדי הספקטרום, בעלי הדלקות החוזרות, בדרכי הנשימה (הילדון שלי, לצערי) לבין המנגנון של המתילציה הפגומה, בכבד כפי שמוסר המאמר הזה: Curr Med Chem Cardiovasc Hematol Agents. 2005 Jul;3(3):267-81. Related Articles, Links Influence of impaired liver methionine metabolism on the development of vascular disease and inflammation. Avila MA, Berasain C, Prieto J, Mato JM, Garcia-Trevijano ER, Corrales FJ. Division of Hepatology and Gene Therapy, CIMA University of Navarra, Pamplona, Spain. [email protected] Methionine (Met) metabolism involves the sequential formation of S-adenosylmethionine (SAM, the main biological methyl donor), S-adenosylhomocysteine (SAH) and homocysteine (Hcy). Hcy can be remethylated to Met or catabolized through the trans-sulfuration pathway. In mammals, as much as 48% of Met metabolism and up to 85% of all transmethylation reactions occur in the liver. These figures underscore the central role played by this organ in Met metabolism. Maintaining the homeostasis of this metabolic cycle has proved to be essential for the preservation of liver function up to the point of preventing its neoplastic transformation. However, an adequate hepatic metabolism of Met is not only important for the liver parenchymal cell. Evidence has accumulated over the past few years supporting the involvement of Met-derived metabolites in the triggering or attenuation of pathological processes with systemic implications. This is best illustrated by the fact that a deteriorated liver function has emerged as a major factor in the development of hyperhomocysteinemia. Elevated plasma levels of Hcy have been related to several disorders including cardiovascular and cerebrovascular diseases. On the other end, liver damage also leads to deficient SAM synthesis. Among the consequences of impaired SAM synthesis in liver tissue are the enhanced production of pro-inflammatory cytokines and mediators. In this review, we will address the mechanisms and consequences of abnormal Met metabolism in liver injury, the systemic implications of such impairment and finally the potential therapeutic interventions.
