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1.
Mol Neurobiol ; 58(9): 4639-4651, 2021 Sep.
Article in English | MEDLINE | ID: mdl-34155583

ABSTRACT

The effects of the consumption of high-fat diets (HFD) have been studied to unravel the molecular pathways they are altering in order to understand the link between increased caloric intake, metabolic diseases, and the risk of cognitive dysfunction. The saturated fatty acid, palmitic acid (PA), is the main component of HFD and it has been found increased in the circulation of obese and diabetic people. In the central nervous system, PA has been associated with inflammatory responses in astrocytes, but the effects on neurons exposed to it have not been largely investigated. Given that PA affects a variety of metabolic pathways, we aimed to analyze the transcriptomic profile activated by this fatty acid to shed light on the mechanisms of neuronal dysfunction. In the current study, we profiled the transcriptome response after PA exposition at non-toxic doses in primary hippocampal neurons. Gene ontology and Reactome pathway analysis revealed a pattern of gene expression which is associated with inflammatory pathways, and importantly, with the activation of lipid metabolism that is considered not very active in neurons. Validation by quantitative RT-PCR (qRT-PCR) of Hmgcs2, Angptl4, Ugt8, and Rnf145 support the results obtained by RNAseq. Overall, these findings suggest that neurons are able to respond to saturated fatty acids changing the expression pattern of genes associated with inflammatory response and lipid utilization that may be involved in the neuronal damage associated with metabolic diseases.


Subject(s)
Hippocampus/drug effects , Inflammation/genetics , Lipid Metabolism/drug effects , Neurons/drug effects , Palmitic Acid/pharmacology , Animals , Hippocampus/metabolism , Inflammation/metabolism , Neurons/metabolism , Rats , Rats, Wistar , Signal Transduction/drug effects , Transcriptome
2.
Mycoses ; 44(3-4): 95-7, 2001 May.
Article in English | MEDLINE | ID: mdl-11413930

ABSTRACT

In this study, the coats of 20 cats with no dermatophytosis lesions were sampled for colonization by Microsporum canis, which was isolated in 45% of cases. All cats were treated with oral terbinafine for 3 weeks. The drug was administered orally at a daily dosage 8.25 mg kg-1. Mycologic status was assessed at the end of the treatment; and after follow-up at 2 days, and 4 and 9 weeks. The final evaluation revealed a complete mycologic cure of all cats by obtaining negative cultures, thereby demonstrating that terbinafine is an effective method of eradication of dermatophyte colonization.


Subject(s)
Antifungal Agents/therapeutic use , Dermatomycoses/drug therapy , Microsporum , Naphthalenes/therapeutic use , Administration, Oral , Animals , Cats , Dermatomycoses/microbiology , Dermatomycoses/transmission , Disease Models, Animal , Female , Follow-Up Studies , Male , Terbinafine
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