Research reportLifelong consumption of trans fatty acids promotes striatal impairments on Na+/K+ ATPase activity and BDNF mRNA expression in an animal model of mania

- TFA can facilitate damage in amphetamine-administered rats of the second generation.
- Brain incorporation of TFA reduced Na+/K+ ATPase activity in striatum.
- TFA was related to increase in oxidative damage and BDNF mRNA expression after AMPH.

PurposeTo evaluate the toxicity of chronic consumption of processed foods that are rich in trans fat on the lipid composition of brain membranes, as well as its functional repercussions.MethodsA second generation of male rats born from mothers and grandmothers supplemented with soybean oil (SOC, an isocaloric control group) or hydrogenated vegetable fat (HVF, rich in TFA) (3 g/kg; p.o.) were kept under oral treatment until 90 days of age, when they were exposed to an AMPH-induced model of mania.ResultsThe HVF group presented 0.38% of TFA incorporation in the striatum, affecting Na+/K+ ATPase activity, which was decreased per se and following AMPH-exposure. The HVF group also showed increased protein carbonyl (PC) and brain-derived neurotrophic factor (BDNF) mRNA levels after AMPH administration, while these oxidative and molecular changes were not observed in the other experimental groups. Additionally, a negative correlation between striatal Na+/K+ ATPase activity and PC levels (r2 = 0.49) was observed.ConclusionThe prolonged consumption of trans fat allows TFA incorporation and increases striatal oxidative status, thus impairing the functionality of Na+/K+-ATPase and affecting molecular targets as BDNF mRNA. We hypothesized that the chronic intake of processed foods (rich in TFA) facilitates the development of neuropsychiatric diseases, particularly bipolar disorder.