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 bloo...
| Autor: | |
|---|---|
| Tipo de recurso: | tesis doctoral |
| Estado: | Versión publicada |
| Fecha de publicación: | 2016 |
| País: | España |
| Institución: | Universidad de Barcelona |
| Repositorio: | Dipòsit Digital de la UB |
| OAI Identifier: | oai:diposit.ub.edu:2445/106709 |
| Acceso en línea: | https://hdl.handle.net/2445/106709 http://hdl.handle.net/10803/400005 |
| Access Level: | acceso abierto |
| Palabra clave: | Aminoàcids Síndrome metabòlica Ratolins (Animals de laboratori) Amino acids Metabolic syndrome Mice (Laboratory animals) |
| Sumario: | [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. |
|---|