Regulation of amino acid catabolism in rats fed diets with different protein content

[eng] Current lifestyle with high-energy diets and characterized by sedentary is triggering an alarming growth in obesity. Obesity along with metabolic syndrome- related co-morbidities (i.e. insulin resistance, atherosclerosis, sleep apnea, depression, asthma, hypertension and the alteration of blood lipid transport) are the most apparent consequence of the excess energy. Under conditions of excess dietary energy, the body cannot easily dispose of the excess amino-N against the evolutively-adapted schemes that prevent its wastage; thus ammonia and glutamine formation and urea excretion are decreased. High lipid and energy availability limit the utilization of glucose, and high glucose spares the production of ammonium from amino acids, decreasing the synthesis of glutamine and its utilization by the intestine and kidney. In contrast, high protein diets enhance protein synthesis and growth, and the synthesis of non-protein-N-containing compounds. But these outlets are not enough; consequently, less- conventional mechanisms are activated, such as increased synthesis of NO? followed by higher nitrite (and nitrate) excretion and changes in the microbiota. In this study we studied how the initial phase of development of metabolic syndrome can affects the function of liver as main site of amino-N metabolism, and to determine whether doubling the protein content in the diet induced significant changes in enzyme of amino acids metabolism along intestine and on liver. The common result obtained by these studies is that, both in case of hyperlipidic or hyperproteic diets, elimination of excess N is necessary but cannot be easily carried out through the metabolic pathways/tissues we evaluated, although possible alternative pathways have been taken into consideration. [cat] L’estil de vida actual amb les dietes d'alt contingut energetic, i caracteritzat pel sedentarisme, esta provocant un creixement alarmant de l'obesitat. L'obesitat, juntament amb les comorbiditats relacionades amb la sindrome metabolica (es a dir, resistencia a la insulina, aterosclerosi, apnea del son, depressio, asma, la hipertensio i l'alteracio del transport de lipids en la sang) son la consequencia mes evident de l'exces d’energia. En condicions d'exces d'energia de la dieta, el cos no pot eliminar rapidament l'exces d'amino-N contra els esquemes adaptats evolutivament i que impedeixin el seu deteriorament; aixi, la formacio d'amoniac i de glutamina i l'excrecio d'urea disminueixen. Els elevats nivells de lipids i de la disponibilitat d'energia limiten la utilitzacio de la glucosa, i nivells elevats de glucosa estalvia la produccio d'amoni a partir dels aminoacids, disminuint la sintesi de glutamina i la seva utilitzacio per l'intesti i el ronyo. En contrast, les dietes d’elevat contingut en proteines incrementen la sintesi de proteines i el creixement, i la sintesi de compostos que contenen N i no son proteines. Pero aquests mecanismes no son suficients i en consequencia, s'activen mecanismes menys convencionals, com ara augment de la sintesi de NO ? seguides per l’augment del nitrit (i nitrat) i la seva excrecio, juntament amb canvis en la microbiota. En aquest treball es va estudiar com la fase inicial de desenvolupament de la sindrome metabolica pot afectar la funcio del fetge com lloc principal del metabolisme d'amino-N, i per determinar si la duplicacio del contingut de proteines en la dieta induia canvis significatius en els enzims del metabolisme d'aminoacids al llarg intesti i al fetge. El resultat generic obtingut per aquests estudis es que, tant en el cas de que la dieta sigui hiperlipidica o hiperproteica, l'eliminacio de l'exces de N es necessaria, pero no es pot dur a terme facilment a traves de les vies metaboliques / teixits que avaluem, tot i les possibles vies alternatives s'han tingut en consideracio.