Efecto del consumo de mate sobre el perfil lipídico en pacientes hipercolesterolémicos

El consumo diario de mate, en dosis de 50g o 100g, produce un descenso en CT y CLDL, mejorando el índice aterogénico en individuos hipercolesterolémicos

Obesity and addiction: can a complication of surgery help us understand the connection?

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/137403/1/obr12542_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/137403/2/obr12542.pd

Estudio del impacto de las dietas hiperlipémicas en células mononucleares en sangre periférica: resultados preliminares

Los trastornos metabólicos asociados con la dieta tienen un gran impacto en la salud, debido a su relación con enfermedades crónicas no transmisibles. Las células mononucleares de sangre periférica (PBMC) tienen un papel importante como biomarcadores tempranos en el estudio del impacto de las dietas ricas en grasas en el metabolismo de los lípidos. Estos permiten profundizar el conocimiento de la patogénesis por métodos no invasivos. Por lo tanto, el objetivo es estudiar PBMC como una herramienta de investigación para la expresión génica en las alteraciones del metabolismo de los lípidos. Se obtuvieron muestras de diez conejos neozelandeses, divididos en el grupo control (n=5) alimentado con alimento balanceado (C), y el grupo de casos (n=5) alimentado con el mismo alimento suplementado con un 17% de grasa bovina (G). Los grupos de grasa no reciben sobrecarga de fructosa, manteniendo constante la concentración de carbohidratos y proteínas, típica de los alimentos básicos equilibrados. Se realizaron pruebas bioquímicas para determinar los niveles de glucosa en sangre (Gl), triglicéridos (TG), colesterol total (CT) y lipoproteínas de alta densidad (HDL). En PBMC, se realizaron pruebas inmunohistoquímicas para SREBP1c y SERBP2 (unión de proteínas a elementos reguladores estériles). Valores similares de Gl (C: 140 ± 28.4 mg / dL vs G: 118.3 ± 12.0 mg / dL) y TG (C: 144.1 ± 15.5 mg / dL vs.G: 135.6 ± 8.3 mg / dL) pueden observarse en estudios bioquímicos preliminares de ambos grupos, mientras que el grupo G muestra un aumento en CT (42.8 ± 21.6 mg / dL) en comparación con el grupo C (27.1 ± 4.5 mg / dl). Los valores de HDL fueron menor en el grupo C (9,3 ±4,76 vs 11,8 ± 3,45 mg/dl), y se calculó el índice aterogénico, con un valor mayor en grupo G (3,64 vs 2,91). Sin embargo, algunos animales del grupo G tienen valores similares al grupo C para CT (21.7 ± 2.4 mg / dl), HDL (9,9 ± 3,8) e IA (2,2), grupo de normocolesterolemia (NC). Por lo tanto, estos animales no muestran cambios bioquímicos a pesar de la ingesta de grasas como ocurre con otros. Los estudios de tejido hepático mostraron esteatosis (tinción con aceite rojo O), así como la presencia de SREBP1c (relación perinuclear / nuclear: C: 2.0, F: 0.71, NG: 1.81) y SERBP2 (relación perinuclear / nuclear: C: 3.29, F: 0.85, NG: 0.57) en PBMC. En conclusión, estos resultados indicarían una activación de la regulación génica sin cambios a nivel bioquímico en grupo NC. Estos resultados indican que es posible estudiar la expresión génica en PBMC, porque se puede observar la presencia de moléculas específicas relacionadas con el metabolismo de los lípidos.Fil: Avena, M. V.. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina. Universidad "Juan Agustín Maza"; ArgentinaFil: Elias, María. Universidad "Juan Agustín Maza"; ArgentinaFil: Heredia, Rocío. Universidad "Juan Agustín Maza"; ArgentinaFil: Mussi Stoizik, Jessica Anabella. Universidad "Juan Agustín Maza"; ArgentinaFil: Colombo, Regina Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Funes, Abi Karenina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Fornes, Miguel Walter. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Saez Lancellotti, Tania Emilce Estefania. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Boarelli, Paola Vanina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina. Universidad "Juan Agustín Maza"; ArgentinaIV Reunión Conjunta de Sociedades de Biología de la República Argentina: “Nuevas Evidencias y Cambios de Paradigmas en Ciencias Biológicas”MendozaArgentinaSociedad de Biología de CuyoSociedad de Biología de CórdobaAsociación de Biología de Tucumá

Natural Reward Experience Alters AMPA and NMDA Receptor Distribution and Function in the Nucleus Accumbens

Natural reward and drugs of abuse converge upon the mesolimbic system which mediates motivation and reward behaviors. Drugs induce neural adaptations in this system, including transcriptional, morphological, and synaptic changes, which contribute to the development and expression of drug-related memories and addiction. Previously, it has been reported that sexual experience in male rats, a natural reward behavior, induces similar neuroplasticity in the mesolimbic system and affects natural reward and drug-related behavior. The current study determined whether sexual experience causes long-lasting changes in mating, or ionotropic glutamate receptor trafficking or function in the nucleus accumbens (NAc), following 3 different reward abstinence periods: 1 day, 1 week, or 1 month after final mating session. Male Sprague Dawley rats mated during 5 consecutive days (sexual experience) or remained sexually naïve to serve as controls. Sexually experienced males displayed facilitation of initiation and performance of mating at each time point. Next, intracellular and membrane surface expression of N-methyl-D-aspartate (NMDA: NR1 subunit) and α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA: GluA1, GluA2 subunits) receptors in the NAc was determined using a bis(sulfosuccinimidyl)suberate (BS3) protein cross-linking assay followed by Western Blot analysis. NR1 expression was increased at 1 day abstinence both at surface and intracellular, but decreased at surface at 1 week of abstinence. GluA2 was increased intracellularly at 1 week and increased at the surface after 1 month of abstinence. Finally, whole-cell patch clamp electrophysiological recordings determined reduced AMPA/NMDA ratio of synaptic currents in NAc shell neurons following stimulation of cortical afferents in sexually experienced males after all reward abstinence periods. Together, these data show that sexual experience causes long-term alterations in glutamate receptor expression and function in the NAc. Although not identical, this sex experience-induced neuroplasticity has similarities to that caused by psychostimulants, suggesting common mechanisms for reinforcement of natural and drug reward

Disorders of compulsivity: a common bias towards learning habits.

Why do we repeat choices that we know are bad for us? Decision making is characterized by the parallel engagement of two distinct systems, goal-directed and habitual, thought to arise from two computational learning mechanisms, model-based and model-free. The habitual system is a candidate source of pathological fixedness. Using a decision task that measures the contribution to learning of either mechanism, we show a bias towards model-free (habit) acquisition in disorders involving both natural (binge eating) and artificial (methamphetamine) rewards, and obsessive-compulsive disorder. This favoring of model-free learning may underlie the repetitive behaviors that ultimately dominate in these disorders. Further, we show that the habit formation bias is associated with lower gray matter volumes in caudate and medial orbitofrontal cortex. Our findings suggest that the dysfunction in a common neurocomputational mechanism may underlie diverse disorders involving compulsion.This study was funded by the WT fellowship grant for VV (093705/Z/ 10/Z) and Cambridge NIHR Biomedical Research Centre. VV and NAH are Wellcome Trust (WT) intermediate Clinical Fellows. YW is supported by the Fyssen Fondation and MRC Studentships. PD is supported by the Gatsby Charitable Foundation. JEG has received grants from the National Institute of Drug Abuse and the National Center for Responsible Gaming. TWR and BJS are supported on a WT Programme Grant (089589/Z/09/Z). The BCNI is supported by a WT and MRC grant.This is the final published version. It's also available from Molecular Psychiatry at http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201444a.html

Symmorphosis through dietary regulation: a combinatorial role for proteolysis, autophagy and protein synthesis in normalising muscle metabolism and function of hypertrophic mice after acute starvation

Animals are imbued with adaptive mechanisms spanning from the tissue/organ to the cellular scale which insure that processes of homeostasis are preserved in the landscape of size change. However we and others have postulated that the degree of adaptation is limited and that once outside the normal levels of size fluctuations, cells and tissues function in an aberant manner. In this study we examine the function of muscle in the myostatin null mouse which is an excellent model for hypertrophy beyond levels of normal growth and consequeces of acute starvation to restore mass. We show that muscle growth is sustained through protein synthesis driven by Serum/Glucocorticoid Kinase 1 (SGK1) rather than Akt1. Furthermore our metabonomic profiling of hypertrophic muscle shows that carbon from nutrient sources is being channelled for the production of biomass rather than ATP production. However the muscle displays elevated levels of autophagy and decreased levels of muscle tension. We demonstrate the myostatin null muscle is acutely sensitive to changes in diet and activates both the proteolytic and autophagy programmes and shutting down protein synthesis more extensively than is the case for wild-types. Poignantly we show that acute starvation which is detrimental to wild-type animals is beneficial in terms of metabolism and muscle function in the myostatin null mice by normalising tension production

Investigating mechanisms underpinning the detrimental impact of a high-fat diet in the developing and adult hypermuscular myostatin null mouse

Background: Obese adults are prone to develop metabolic and cardiovascular diseases. Furthermore, over-weight expectant mothers give birth to large babies who also have increased likelihood of developing metabolic and cardiovascular diseases. Fundamental advancements to better understand the pathophysiology of obesity are critical in the development of anti-obesity therapies not only for this but also future generations. Skeletal muscle plays a major role in fat metabolism and much work has focused in promoting this activity in order to control the development of obesity. Research has evaluated myostatin inhibition as a strategy to prevent the development of obesity and concluded in some cases that it offers a protective mechanism against a high-fat diet. Results: We hypothesised that myostatin inhibition should protect not only the mother but also its developing foetus from the detrimental effects of a high-fat diet. Unexpectedly, we found muscle development was attenuated in the foetus of myostatin null mice raised on a high-fat diet. We therefore re-examined the effect of the high-fat diet on adults and found myostatin null mice were more susceptible to diet-induced obesity through a mechanism involving impairment of inter-organ fat utilization. Conclusions: Loss of myostatin alters fatty acid uptake and oxidation in skeletal muscle and liver. We show that abnormally high metabolic activity of fat in myostatin null mice is decreased by a high-fat diet resulting in excessive adipose deposition and lipotoxicity. Collectively, our genetic loss-of-function studies offer an explanation of the lean phenotype displayed by a host of animals lacking myostatin signalling. Keywords: Muscle, Obesity, High-fat diet, Metabolism, Myostati

Influencia de la alimentación y el estilo de vida en el estrés oxidativo

Dado que no existen en nuestra región estudios sobre estrés oxidativo en humanos y su relación con el consumo de alimentos, comparando grupos omnívoros, ovo lacto vegetarianos y vegetarianos estrictos, se ha realizando el presente trabajo de investigación aplicada

Cocaine Is Low on the Value Ladder of Rats: Possible Evidence for Resilience to Addiction

International audienceBACKGROUND:Assessing the relative value of cocaine and how it changes with chronic drug use represents a long-standing goal in addiction research. Surprisingly, recent experiments in rats--by far the most frequently used animal model in this field--suggest that the value of cocaine is lower than previously thought.METHODOLOGY/PRINCIPAL FINDINGS:Here we report a series of choice experiments that better define the relative position of cocaine on the value ladder of rats (i.e., preference rank-ordering of different rewards). Rats were allowed to choose either taking cocaine or drinking water sweetened with saccharin--a nondrug alternative that is not biologically essential. By systematically varying the cost and concentration of sweet water, we found that cocaine is low on the value ladder of the large majority of rats, near the lowest concentrations of sweet water. In addition, a retrospective analysis of all experiments over the past 5 years revealed that no matter how heavy was past cocaine use most rats readily give up cocaine use in favor of the nondrug alternative. Only a minority, fewer than 15% at the heaviest level of past cocaine use, continued to take cocaine, even when hungry and offered a natural sugar that could relieve their need of calories.CONCLUSIONS/SIGNIFICANCE:This pattern of results (cocaine abstinence in most rats; cocaine preference in few rats) maps well onto the epidemiology of human cocaine addiction and suggests that only a minority of rats would be vulnerable to cocaine addiction while the large majority would be resilient despite extensive drug use. Resilience to drug addiction has long been suspected in humans but could not be firmly established, mostly because it is difficult to control retrospectively for differences in drug self-exposure and/or availability in human drug users. This conclusion has important implications for preclinical research on the neurobiology of cocaine addiction and for future medication development