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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity is a growing worldwide public health issue and is associated with a range of comorbidities, including cognitive deficits. The present study investigated synaptic changes in the hippocampus during the development of obesity. The treatment of newborn mice with monosodium-L-glutamate (MSG, 2 mg/g) induced obesity and recognition memory deficits in the novel object recognition (NOR) test at 16-17 weeks, but not at 8-9 weeks. Hippocampal synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD), and excitatory synaptic transmission at Schaffer collateral-CA1 (SC-CA1) synapses were compared between MSG-treated mice and age-matched control mice. LTP and fiber volley amplitudes were enhanced in MSG-treated mice at 16-17 weeks, but not at 8-9 weeks. Furthermore, the strength of paired-pulse facilitation (PPF) changed in MSG-treated mice at 16-17 weeks, but not at 8-9 weeks. These results suggest that enhanced LTP in the SC-CA1 synapses of MSG-induced obese mice involves presynaptic rather than postsynaptic mechanisms.
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PMID:Cognitive and hippocampal synaptic profiles in monosodium glutamate-induced obese mice. 3294 68

Aggravation of the chronic obstructive pulmonary disease (COPD) often leads to a slew of complications, but the correlation between COPD aggravation and the complications on the basis of molecular level remains unclear. In this study, gene expression profiles of COPD in patients at early and aggravation stages were collected and differentially-expressed genes were selected. Meanwhile, gene expression data implicated in COPD complications were analyzed to establish a regulatory network of COPD aggravation and COPD related complications. In addition, the gene enrichment function of DAVID6.7 was utilized to evaluate the similarities between COPD aggravation and COPD complications in term of biological process. By analyzing the genes of COPD aggravation and the COPD complications, we found 18 genes highly related to COPD aggravation, among which haptoglobin (HP) was correlated with 14 complications, followed by ADRB2, LCK and CA1, which were related to 13, 11 and 11 complications, respectively. As far as the complications concerned, obesity was regulated by 17 of the 18 genes, which indicated that there was a close correlation between COPD aggravation and obesity. Meanwhile, lung cancer, diabetes and heart failure were regulated by 15, 15 and 14 genes, respectively, among the 18 selected genes. This study suggested the driver genes of COPD aggravation were capable of extensively regulating COPD complications, which would provide a theoretical basis for development of cures for COPD and its complications.
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PMID:Correlation in gene expression between the aggravation of chronic obstructive pulmonary disease and the occurrence of complications. 3310 41

Obesity is a chronic condition associated with adverse memory and emotional outcomes in humans and animal models. We have recently demonstrated that post-weaning (i.e., periadolescent) high-fat diet (HFD)-induced obesity has opposite effect on hippocampal and amygdala-dependent memory in rodents: while HFD consumption impairs spatial and relational memory, it enhances cue-dependent emotional memory. However, it is still not clear whether this bidirectional HFD effect on memory is related to bidirectional alterations of hippocampal and amygdala synaptic plasticity and if it is influenced by the duration of diet intake. In the current study, we compared in male rats the impact of 2-3 and 6-7 months of HFD intake starting at weaning, thus covering adolescence, on in vivo long-term potentiation (LTP) recorded simultaneously in the hippocampal area CA1 and the basolateral amygdala (BLA). As expected, 6-7 months of HFD intake abolished LTP in the CA1 and enhanced LTP in the BLA. However, 2-3 months of of HFD exposure enhanced LTP in both CA1 and BLA suggesting a transient compensatory mechanism in hippocampus. These results indicate that post-weaning HFD intake progressively leads to bidirectional modulation of hippocampal and amygdala synaptic plasticity, as we previously demonstrated for related memory processes, yet with a different temporal dynamic.
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PMID:Bidirectional modulation of hippocampal and amygdala synaptic plasticity by post-weaning obesogenic diet intake in male rats: Influence of the duration of diet exposure. 3314 58


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