RESUMEN
Both obesity rates and antidepressant use have escalated in the last 20 years. Most people who start antidepressant treatment discontinue it on their own. Meanwhile, obesity rates continue to increase. To test the hypothesis that antidepressant use is a risk factor for obesity, even after long-term discontinuation, we developed a novel animal paradigm consisting of short-term exposure to stress and antidepressants, followed by long-term high-fat diet. We show here that recurrent restraint stress (RRS)-related weight loss is recovered 2 weeks after the end of stress in young growing rats receiving a high-fat diet. It is noteworthy that animals that received short-term antidepressant treatment with either imipramine or fluoxetine during 7 days of RRS showed behavioral evidence of antidepressant effects. When exposed to a high-fat diet after stress and when antidepressant treatment had ended, the animals had significant increases in caloric intake, body weight (BW) and size from 17 to 22 weeks following antidepressant discontinuation when compared with (control) RRS animals treated with saline and fed with a high-fat diet. These data are consistent with the previously described phenomenon of time-dependent sensitization, and support the notion that enduring effects of short-term antidepressant treatment become manifest on a long-term basis after antidepressant discontinuation, during conditions of high stress followed by high-fat intake. Analyses of open field and body size measurements obtained in a small subset of animals show that animals previously exposed to antidepressant had no deficits in locomotor activity and were larger. Antidepressant exposure may therefore be a covert, insidious and enduring risk factor for obesity, even after discontinuation of antidepressant treatment. Our data support the concept of persistent, long-term effects of pharmacological-environment interactions on BW regulation.
Asunto(s)
Antidepresivos/efectos adversos , Peso Corporal/efectos de los fármacos , Ambiente , Animales , Grasas de la Dieta/efectos adversos , Modelos Animales de Enfermedad , Ingestión de Alimentos/efectos de los fármacos , Ingestión de Energía/efectos de los fármacos , Modelos Lineales , Estudios Longitudinales , Masculino , Actividad Motora/efectos de los fármacos , Ratas , Ratas Sprague-Dawley , Restricción Física/efectos adversos , Estadísticas no Paramétricas , Estrés Psicológico/tratamiento farmacológico , Factores de Tiempo , Resultado del TratamientoRESUMEN
There are clinical parallels between the nature and course of depressive symptoms in major depressive disorder (MDD) and those of inflammatory disorders. However, the characterization of a possible immune system dysregulation in MDD has been challenging. Emerging data support the role of T-cell dysfunction. Here we report the association of MDD and antidepressant response to genes important in the modulation of the hypothalamic-pituitary-adrenal axis and immune functions in Mexican Americans with major depression. Specifically, single nucleotide polymorphisms (SNPs) in two genes critical for T-cell function are associated with susceptibility to MDD: PSMB4 (proteasome beta4 subunit), important for antigen processing, and TBX21 (T bet), critical for differentiation. Our analyses revealed a significant combined allele dose-effect: individuals who had one, two and three risk alleles were 2.3, 3.2 and 9.8 times more likely to have the diagnosis of MDD, respectively. We found associations of several SNPs and antidepressant response; those genes support the role of T cell (CD3E, PRKCH, PSMD9 and STAT3) and hypothalamic-pituitary-adrenal axis (UCN3) functions in treatment response. We also describe in MDD increased levels of CXCL10/IP-10, which decreased in response to antidepressants. This further suggests predominance of type 1 T-cell activity in MDD. T-cell function variations that we describe here may account for 47.8% of the attributable risk in Mexican Americans with moderate MDD. Immune function genes are highly variable; therefore, different genes might be implicated in distinct population groups.
Asunto(s)
Antidepresivos/uso terapéutico , Trastorno Depresivo Mayor/tratamiento farmacológico , Trastorno Depresivo Mayor/genética , Predisposición Genética a la Enfermedad , Inflamación/genética , Polimorfismo Genético , Linfocitos T CD4-Positivos/inmunología , Genotipo , Hispánicos o Latinos , Humanos , Inflamación/inmunología , Los Angeles , Oportunidad Relativa , Polimorfismo de Nucleótido Simple , Valores de Referencia , Resultado del TratamientoRESUMEN
30 strains of Plesiomonas shigelloides isolated from patients with acute diarrheal disease at different health centers of the country were studied. The were phenotypically characterized by conventional biochemical tests and the antimicrobial susceptibility to 11 drugs was determined by the Kirby Bauer's method. It was found that the strains of Plesiomonas shigelloides were sensitive to 7 and resistant to 6 of the investigated drugs. The presence of plasmids in 12 of the 29 analyzed strains was determined and the diversity in their plasmidic patterns was proved.
Asunto(s)
Antibacterianos/farmacología , Plásmidos/aislamiento & purificación , Plesiomonas/efectos de los fármacos , Plesiomonas/genética , Enfermedad Aguda , ADN Bacteriano/aislamiento & purificación , Diarrea/microbiología , Heces/microbiología , Humanos , Pruebas de Sensibilidad Microbiana , FenotipoRESUMEN
By means of the polymerase chain reaction (PCR) it was obtained a probe for the gen that codifies the subunit B of cholerae toxin (CTxB), which carried a Vibrio cholerae 01 reference strain. The checking of the amplified product was performed by using the hybridization techniques in colonies. This product hybridized with the gen that codifies for the subunit B of cholerae toxin isolated from Peru and Ecuador, representing the present epidemics in Latin America, but it did not so with the phylogenetically related strains.