Eating behaviors and emotional distress are predicted by treatment and adverse outcome in patients with type 2 diabetes

Depression and anxiety are hightly prevalent among patients with Type 2 Diabetes (T2D), however not commonly related to outcomes, treatment and comorbidities. Eating behaviors could also have an implication. To evaluate the relation between mood and eating behaviors with demographic, physical, treatment, biochemical profiles and chronic comorbidities in T2D we conducted this exploratory cross sectional study in a population from Mexico. Hospital Anxiety and Depression Scale and the Three Factor Eating Questionnaire Revised 21 (TFEQ-R21) were correlated with age, gender, blood pressure, treatment and comorbidities (nephropathy, neuropathy, retinopathy and cardiopathy). Multi-linear regression models and 2^k factorial analyses were conducted. Sixty-one patients (31 male) 55 years old (SD 13) with at least 5 years of T2D were included. Anxiety correlated with depression (r = 0.25, p < 0.05). Gender (women) (std B 0.026, p < 0.001), insulin therapy (std B 0.3, p = 0.11), systolic blood pressure (std B 0.263, p = 0.02) and cardiovascular disease (std B 0.232, p = 0.035) predicted depression. Insulin therapy had a positive effect in cognitive restraint. (std B 0.32, p = 0.001). Age (std B 0.37, p = 0.003) and systolic blood pressure (std B 0.237, p = 0.048) predicted positively emotional eating (not previously published). 2^k factorial analyses proved additive interaction between complications and insulin therapy with depression. This study supports the relation between mood disorders and eating behaviors with demographic, physical, treatment, biochemical profiles and chronic comorbidities in T2D and the additive interaction between factors and mood disorders.     

Amygdala or hippocampus inactivation after retrieval induces temporary memory deficit

The hypothesis that memory is stored through a single stage of consolidation that results in a stable and lasting long-term memory has been challenged by the proposition that reactivation of a memory induces reconsolidation of the memory. The reconsolidation hypothesis is supported by evidence that, under some conditions, post-retrieval treatments affecting amygdala and hippocampus functioning impair subsequent retention performance. We now report that repeated retention testing attenuates the performance impairment induced by post-retrieval reversible inactivation of the amygdala and hippocampus of rats induced by tetrodotoxin. These findings challenge the reconsolidation hypothesis and suggest that the post-retrieval retention performance impairment is best explained as due to temporary retrieval failure.     

Enhanced inhibitory avoidance learning prevents the long-term memory-impairing effects of cycloheximide,a protein synthesis inhibitor

Interference with activity of numerous cerebral structures produces memory deficiencies; in many instances, however, when animals are over-trained such interference becomes innocuous. Systemic administration of protein synthesis inhibitors impairs long-term retention; this effect has been interpreted to mean that protein synthesis is required for memory consolidation, though little is known about the effect of protein synthesis inhibitors on memory of enhanced learning in the rat. To further analyze the protective effect of enhanced learning against amnesic treatments, groups of Wistar rats were trained in a one-trial step-through inhibitory avoidance task, using different intensities of foot-shock during training. Cycloheximide (CXM; 2.8 mg/kg), an inhibitor of protein synthesis, was injected either 30 min before training or immediately after training. Twenty-four hours after training retention latencies were recorded. Our data showed that both pre- and post-training administration of CXM produced amnesia in those groups that had been trained with relatively low foot-shock intensities, but no impairment in retention was observed when relatively high intensities of foot-shock were administered. These and similar results lead us to conclude that protein synthesis inhibitors may interfere with memory consolidation, but their effect disappears when animals are submitted to an enhanced learning experience, calling into question the idea that protein synthesis is required for memory consolidation.