https://repositorio.uca.edu.ar/handle/123456789/14267 2026-04-06T12:59:40Z https://repositorio.uca.edu.ar/handle/123456789/14320 Título: Effects of prenatal stress and postnatal high fat diet feeding on BALB/c mice metabolism Autor: Quiroga, Sofia; Juárez, Yamila R.; Tellechea, Mariana L.; Genaro, Ana María; Burgueño, Adriana Laura Resumen: Resumen: In-utero exposure to maternal stress increases short and long term risk of suffering metabolic diseases. Exposure to stressful events leads to an increase in glucocorticoids release by activation of the HPA axis, therefore early programming of the HPA axis has emerged as a key underlying mechanism of stress-related disorders. Evidence suggests that a stressful prenatal environment seems to favour adverse metabolic conditions. To test this hypothesis in BALB/c mice, a strain susceptible to stress but resistant to metabolic effects of a high fat diet (HFD), we exposed female pregnant mice to restraint stress during the last week of pregnancy (2 h/day). Offspring were fed with HFD between weeks 4 and 28 of age. Prenatally stressed (PS) females and males fed with HFD showed higher body weight (females: p<0.001, n= 8; males: p<0.01, n= 8) and adipose tissue content (adipose tissue weight/body weight, both sexes: p<0.001, n= 8). Females were hyperinsulinemic (p<0.001, n= 5), with decreased expression of Foxo1 (Forkhead box protein O1) a transcription factor that plays important roles in regulation of gluconeogenesis and glycogenolysis by insulin signaling (p<0.05, n= 5) and Adiponectin (p<0.05, n= 5) in adipose tissue. On the other hand, PS males (fed with standard or HFD) had hypertriglyceridemia (p<0.001, n= 8) and hypercholesterolemia (p<0.001, n= 8). PS per se, in males, decreased the expression of Adiponectin (p<0.01, n= 5). PS animals showed a great susceptibility to develop obesity. We conclude that PS may give rise to some adverse effects, and abnormal phenotype may be provoked by or exacerbated in a later life nutritional challenge. We intend to continue our research by evaluating whether epigenetic alterations are responsible for the observed gene expression alterations. 2019-01-01T00:00:00Z https://repositorio.uca.edu.ar/handle/123456789/14272 Título: Circadian biomarkers in asymptomatic offspring of patients with late-onset Alzheimer's disease and their relationship with cognitive performance Autor: Abulafia, Carolina Andrea; Duarte-Abritta, Bárbara; Sánchez, Stella M.; Villarreal, Mirta F.; Ladrón de Guevara, María Soledad; Sevlever, Gustavo; Fiorentini, Leticia; Guinjoan, Salvador M.; Vigo, Alejandro G. Resumen: Abstract: Introduction: Early neuropathological changes characteristic of late-onset Alzheimer's disease (LOAD) impact structures that regulate circadian rhythms and particularly sleep. Indeed, sleep pattern is emerging as a potential biomarker, mechanistic pathway and treatment target in LOAD. We hypothesized that circadian rhythm anomalies would already be present in asymptomatic, middle-aged offspring of patients with LOAD (O-LOAD) prior to cognitive decline. Materials and methods: We tested 35 subjects with at least one parent with LOAD (O-LOAD) and 31 healthy individuals without family history of Alzheimer's disease (control subjects, CS) with a series of cognitive tests, as well as actigraphy measures of sleep-wake rhythm, cardiac autonomic function via heart rate variability (HRV), and bodily temperature. Results: O-LOAD displayed subtle yet significant deficits in verbal episodic memory (RAVLT learning 48.32 ± 1.59 vs. 44.12 ± 1.21, p = 0.005; delayed recall 10.55 ± 0.38 vs. 8.68 ± 0.52, p = 0.005) and language (Vocabulary 50.5 ± 1.06 vs. 45.06 ± 1.48, p= 0.004) compared to CS. O-LOAD showed a more extended sleep duration (439.26 min ± 9.41 vs. 473.66 min ± 10.57, p = .018) and reduced sleep efficiency (97.07 % ± .41 vs. 95.75 % ± .48, p = .042). No significant differences were found for body temperature or HRV variables. Correlations between increased sleep duration and poorer cognition were found in CS but not in O-LOAD. Improved cognitive performance was associated to indicators of greater sympathetic activity. Conclusions: Our results support the hypothesis that sleep pattern disturbances are already present very early on in relatively young asymptomatic subjects. The unexpected reduced cognitive results found in O-LOAD suggest that cognitive decline could start earlier than anticipated in the form of subtle cognitive changes within the clinically normal range. It is widely accepted that sleep pattern disturbances would result in cognitive alterations. Taken these information together with the correlations between sleep duration and cognition present in CS but absent in O-LOAD suggest some impairment in the mechanisms underlying the sleep-cognitive relationship. Sleep pattern deserves further study as a potential biomarker in LOAD, even in healthy middle-aged individuals. 2019-01-01T00:00:00Z