INVESTIGADORES
GOMEZ-MEJIBA Sandra Esther
congresos y reuniones científicas
Título:
DIET-INDUCED OBESITY, INSULIN RESISTANCE AND PULMONARY INFLAMMATION
Autor/es:
DELLA-VEDOVA, MC; MUÑOZ MD,; GOMEZ MEJIBA, SE; GOMEZ N,; RAMIREZ DC
Lugar:
MENDOZA
Reunión:
Congreso; SBC; 1014
Resumen:
h: 0px; ">Obesity is a chronic inflammatory disease associated to insulinresistance and oxidative stress in a number of tissues. Ourhypothesis is that diet-induced obesity (OID) causes oxidativestress in the lung. To test this hypothesis we developed a modelof OID in which C57 mice where fed for 6, 10 and 18 weeks, acontrol low-fat diet (LFD) and a high-fat diet (HFD). Wemeasured adiposity, IR. In lung tissue we analyzed antioxidantenzyme activity (CAT, GPX and TBARS). Obese mice ate lessfood than control mice, but nevertheless the final body weighttowards the 18th weeks of diet was higher in the HFD comparedto the LFD group(LFD 27±3 g vs HFD 31.75±7g). The glucosetolerance test showed that the HFD group had more Insulinoresistant than the LFD group (18 weeks HFD 99.83±12.46 mg/dl vs LFD 122.5±19.23 mg /dl). The parameters of oxidativestress in lung were similar between the groups, however, thesetended to be different towards the 18 weeks of diet (CAT: LFD741.3± 125.8U/mg vs HFD 680± 85 U / mg; GPX: LFD 307.3±38.59 U / mg vs. HFD 272.2 ± 36.77U/mg; TBARS: LFD 4.67 ±2.19 microns / ml vs HFD 5.026 ± 2.52 mM /ml). The OIDmodel used in this study caused changes in behavior(aggressiveness) of animals, which could have causedalterations in feeding pattern and results. We conclude that thediet used in this OID model should be reformulated to reduce itseffect on animal behavior.