Chronodisruption and Gut Microbiota: Triggering Glycemic Imbalance in People with Type 2 Diabetes.

The desynchronization of physiological and behavioral mechanisms influences the gut microbiota and eating behavior in mammals, as shown in both rodents and humans, leading to the development of pathologies such as Type 2 diabetes (T2D), obesity, and metabolic syndrome. Recent studies propose resynchronization as a key input controlling metabolic cycles and contributing to reducing the risk of suffering some chronic diseases such as diabetes, obesity, or metabolic syndrome. In this analytical review, we present an overview of how desynchronization and its implications for the gut microbiome make people vulnerable to intestinal dysbiosis and consequent chronic diseases. In particular, we explore the eubiosis-dysbiosis phenomenon and, finally, propose some topics aimed at addressing chronotherapy as a key strategy in the prevention of chronic diseases.

Lifestyle, psychological well-being, and body mass index of indigenous women

Lifestyle, psychological well-being, and body mass index of indigenous women. Introduction. Obesity is more common in women and has also been found to be present in indigenous populations. During university studies, obesity-related lifestyles are in the process of consolidation, and although this is known, research is limited to addressing physical activity and diet, ignoring other lifestyle components, such as life appreciation. Additionally, there is a need to corroborate whether psychological well-being contributes to excess weight in indigenous women. Objective. To determine whether there is an association between lifestyle, psychological well-being, and body mass index (BMI) in indigenous women. Materials and methods. A cross-sectional study was conducted among 110 female Zapotec university students in Juchitán, Oaxaca, Mexico. The Psychological Well-Being Scale, the Healthy Lifestyle Scale for University Students, and a questionnaire about personal data were used. Body weight and height were measured to calculate BMI. Results. There was a negative correlation between BMI, self-acceptance (r = -0.33; p < 0.01), and life appreciation (r = -0.22; p < 0.05). Positive correlations were found between lifestyle and psychological well-being dimensions, with the strongest correlations being observed between life appreciation and purpose in life (r = 0.55) and self-acceptance (r = 0.48). The multivariable models determined that life appreciation and self-acceptance are associated with BMI. Conclusion. Life appreciation and self-acceptance are predictors of BMI and are even more strongly associated than exercise and nutrition behaviors(AU)

La obesidad es más frecuente en mujeres, aún en poblaciones indígenas. Durante los estudios universitarios, los estilos de vida relacionados con la obesidad se encuentran en proceso de consolidación, y aunque esto es conocido, las investigaciones se limitan a abordar la actividad física y la dieta, ignorando otros componentes del estilo de vida, como la apreciación por la vida. Adicionalmente, es necesario corroborar si el bienestar psicológico contribuye al exceso de peso en mujeres indígenas. Objetivo. Determinar si existe asociación entre los estilos de vida, el bienestar psicológico y el Índice de Masa Corporal (IMC) en mujeres indígenas. Materiales y métodos. Se realizó un estudio transversal en 110 mujeres zapotecas estudiantes universitarias en Juchitán, Oaxaca, México. Se utilizó la escala de bienestar psicológico, la escala de estilos de vida saludables para estudiantes universitarias y un cuestionario sobre datos personales. Se midió el peso corporal y la estatura para calcular el IMC. Resultados. Hubo correlación negativa entre el IMC, la autoaceptación (r=-0,33; p<0,01) y la apreciación por la vida (r=-0,22; p<0,05). Se encontraron correlaciones entre las dimensiones de estilos de vida y las dimensiones de bienestar psicológico: las correlaciones más fuertes se observaron entre apreciación por la vida y propósito en la vida (r 0 0.55) y autoaceptación (r = 0.48). La apreciación por la vida y la autoaceptación son factores predictores del IMC. Conclusión. La apreciación por la vida y la autoaceptación son predictores del IMC, incluso más fuertemente asociados que el ejercicio físico y la alimentación(AU)

Oxytocinergic cells of the posterior hypothalamic paraventricular nucleus participate in the food entrained clock.

The mechanisms underlying food anticipatory activity are still poorly understood. Here we explored the role of oxytocin (OT) and the protein c-Fos in the supraoptic nucleus (SON), medial (PVNm) and posterior (PVNp) regions of the paraventricular hypothalamic nucleus. Adult rats were assigned to one of four groups: scheduled restricted feeding (RF), ad libitum (AL), fasting after restricted feeding (RF-F), to explore the possible persistence of oscillations, or ad libitum fasted (AL-F). In the SON and in the PVNm, OT cells were c-Fos positive after food intake; in contrast, OT cells in the PVNp showed c-Fos activation in anticipation to food access, which persisted in RF-F subjects. We conclude that OT and non-OT cells of the SON and PVNm may play a role as recipients of the entraining signal provided by food intake, whereas those of the PVNp which contain motor preautonomic cells that project to peripheral organs, may be involved in the hormonal and metabolic anticipatory changes in preparation for food presentation and thus, may be part of a link between central and peripheral oscillators. In addition, due to their persistent activation they may participate in the neuronal network for the clock mechanism that leads to food entrainment.

¿Los protocolos experimentales son un símil real de la diabetes humana? / Are experimental protocols an authentic simile of human diabetes?

Resumen Para el estudio de la diabetes se dispone de diversas estrategias metodológicas en modelos animales, tales como, técnicas quirúrgicas, modificaciones dietéticas, incluso manipulación genética y la administración de fármacos específicos, por su toxicidad. En animales, la diabetes experimental se logra con el uso de fármacos, como la aloxana o la estreptozotocina, los cuales producen daño irreversible en las células β-pancreáticas, aunque causan una alta mortalidad, debido a la cetosis asociada al daño agudo de estas células pancreáticas. El objetivo de este trabajo fue analizar los protocolos farmacológicos y otras estrategias disponibles, para determinar si la diabetes experimental realmente emula la diabetes humana. La diabetes es un proceso progresivo y crónico, en el que la mayor parte de las alteraciones clínicas son consecuencia, en el largo plazo, de alteraciones micro y macrovasculares. Por ello, es conveniente diferenciar entre los efectos de una hiperglucemia aguda, con aquellos que se observan cuando la hiperglucemia se prolonga a lo largo del tiempo, a fin de establecer analogías, entre el modelo experimental animal, con el síndrome diabético humano, mediante datos de laboratorio y de tipo clínico, de uso habitual en el diagnóstico y manejo de la diabetes humana.

Abstract For the study of diabetes, several methodological strategies use animal models. Such methodologies involve surgical techniques, diet modifications, some genetic manipulations and specific toxic drugs. The experimental production of diabetes in animal models use the administration of alloxan or streptozotocin and these drugs produce irreversible damage to pancreatic β-cells. However, its use is associated to a ketosis high mortality rate due to the acute damage of pancreatic cells. The aim of this review consisted in the analysis of the pharmacological diabetes production protocols as well as other available strategies, in order to elucidate which is potentially the ideal protocol that emulates human diabetes. Diabetes is a progressive and chronic process, in which most of the clinical alterations are a long-term consequence of micro and macrovascular alterations. Therefore, it is convenient to establish a difference between the effects of acute hyperglycemia, with those effects observable when hyperglycemia is present over the long-term in order to reach enough analogies between the animal experimental model with the human diabetes syndrome, through the use of laboratory and clinical indicators commonly employed for the diagnoses and management of human diabetes.

Responsivity of lateral septum-mPFC connections in alloxan-induced hyperglycemia.

The lateral septal nucleus (LSN) is related to the actions of antidepressants, and the prelimbic cortex (PL) and infralimbic cortex (IL) modulate responses to fear. However, unknown is whether experimental diabetes that is induced by alloxan alters the responsivity of these regions. We used a method in which one forebrain region (LSN) was electrically stimulated while single-unit extracellular recordings were performed in another mPFC region (PL and IL). Several experimental groups were tested: (a) animals that were subjected to long-term (42-day) alloxan-hyperglycemia and protected with insulin, (b) healthy animals that received a low dose of insulin that does not produce changes in glycemia, and (c) animals that received long-term treatment with fluoxetine. Additional healthy groups of animals received insulin or fluoxetine and underwent the forced swim test. Biological measurements indicated the induction of diabetes in alloxan-treated rats. In this group, a shift toward an inhibitory response to LSN stimulation was observed in the PL and IL compared with the control group. A low dose of insulin or fluoxetine produced similar changes in LSN-PL and LSN-IL responsivity. Long-term hyperglycemia increased inhibitory responsivity in the LSN-PL and LSN-IL, but this action was less pronounced than the action that was exerted by insulin and fluoxetine, which produced similar actions. Such similar actions were confirmed in the forced swim test, in which the antidepressant-like effects of insulin partially resembled the effects of fluoxetine. The changes that were observed in the alloxan group appeared to be related to neuronal damage, and a low dose of insulin exerted some antidepressant-like actions.

Association of polymorphisms at -174 in IL-6, and -308 and -238 in TNF-α, in the development of tuberculosis and type 2 diabetes mellitus in the Mexican population.

Polymorphisms at -176 in IL-6, and -238 and -308 in TNF-α have been described as risk factors for developing tuberculosis (TB) and type 2 diabetes mellitus (T2DM). However, it is not known how these changes influence the development of TB-T2DM comorbidity. The objective of this work was therefore to analyze the impact of these polymorphisms in the Mexican population. This is a cross-sectional study of cases and controls in which polymorphisms at -174 in IL-6, -238 and -308 in TNF-α were identified in healthy subjects, those with TB, T2DM and carriers of the comorbidity, each group consisted of 30 individuals. Descriptions of the population, frequency of genotypes and risk association were calculated, and a reduction of multifactorial dimensionality between groups (MDR) was determined. Genotype 174 G/G-of IL-6 was observed in 78% of individuals, while -308 G/G and -238 G/G of TNF-α occurred in 90% and 91% of individuals, respectively. The -174 G/G IL-6 in individuals with T2DM increased five-fold (p = .02) the risk of developing the comorbidity. The MDR analysis showed that the association of -174 G/G IL-6 and -308 G/G TNF-α in healthy individuals increased the risk of developing the comorbidity up to six-fold (p = .019), while in individuals with T2DM, this risk augmented 14-fold (p = .0002). The -174 G/G IL-6 genotype increases the risk of developing comorbidity in the T2DM population and this risk is raised when associated with -308 G/G TNF-α. These findings have implications for understanding the epidemiological dynamics of the TB-T2DM comorbidity, promoting prevention strategies and inhibiting the development of this co-morbidity.