Drosophila melanogaster: A model to study obesity effects on genes expression and developmental changes on descendants.

Maternal obesity and metabolic diseases are two of the most important potential dangers to offspring, given that impaired offspring may cause deficiencies that impair the adult life and health. This study evaluated the oxidative damage, the enzymatic antioxidant defenses, and the enzymes of fatty acid metabolism, such as Acyl-CoA Synthetase and Acetyl-CoA Synthetase (mRNA expression levels), as well as the modulation of cell stress signaling pathway, as Hsp83, and gene expression and insulin-like peptide DILP6 in Drosophila melanogaster models that received a high fat diet (HFD) (10% and 20% of coconut oil) throughout their development period. After 7 days, the progenitor flies were removed and, the remaining eggs were monitored daily, until the eclosion. The descendants were then exposed to a regular diet (RD). The results revealed that the HFD caused a decrease in the proportion of eclosion, lifespan, MTT reduction in mitochondrial enriched fractions, AceCS1 levels, mRNA expression levels (SOD and CAT), and in catalase activity a decrease was only observed in the group that received the highest concentration of coconut oil. In parallel, it was demonstrated an increase in the upregulation of HSP83 mRNA levels, but only when 10% of coconut oil was added, and an increase in glucose and triglyceride levels, as well as in DILP6 mRNA levels in larger concentration of coconut oil tested (20%). In conclusion, flies that have progenitors fed with HFD can develop metabolic dysfunctions, causing oxidative insults, which are involved in the shortening of lifespan.

Hypolipidemic action of chrysin on Triton WR-1339-induced hyperlipidemia in female C57BL/6 mice.

Chrysin (5,7-dihydroxyflavone) is a flavonoid, natural component of traditional medicinal herbs, present in honey, propolis and many plant extracts. The objective of this study was to investigate the hypolipidemic properties of chrysin on Triton WR-1339-induced hyperlipidemia in female C57BL/6 mice. Triton WR-1339 was administered intraperitoneally (400 mg/kg) to overnight-fasted mice to develop acute hyperlipidemia. Chrysin was administered orally (10 mg/kg) 30 min before Triton WR-1339. At 24 h after Triton WR-1339 injection, blood samples were collected to measure plasma lipid levels. The hepatic thiobarbituric acid reactive substances (TBARS), carbonyl content, non-protein sulfhydryl (NPSH) and ascorbic acid (AA) levels, as well as catalase (CAT) and superoxide dismutase (SOD) activity were recorded. Chrysin administration significantly decreased total cholesterol levels. In addition, it partially decreased non-high density lipoprotein-cholesterol and triglycerides levels in plasma of hyperlipidaemic mice. In addition chrysin administration prevented the increase on TBARS levels and prevented the decrease in SOD activity induced by Triton WR-1339. These findings indicated that chrysin was able to decrease plasma lipids concentration and that its antioxidant properties was, at least in part, involved in the hypolipidaemic action of chrysin.

Pentylenetetrazol-induced seizures are associated with Na⁺,K⁺-ATPase activity decrease and alpha subunit phosphorylation state in the mice cerebral cortex.

The present study aimed to investigate whether Na(+),K(+)-ATPase activity and phosphorylation state of the catalytic α subunit are altered by pentylenetetrazol (PTZ)-induced seizures. PTZ (30, 45 or 60 g/kg, i.p.) was administered to adult male Swiss mice, and Na(+),K(+)-ATPase activity and phosphorylation state were measured in the cerebral cortex 15 min after PTZ administration. Na(+),K(+)-ATPase activity significantly decreased after PTZ-induced seizures (60 mg/kg). Immunoreactivity of phosphorylated Ser943 at α subunit was increased after PTZ-induced seizures. A significant positive correlation between Na(+),K(+)-ATPase activity and latency to myoclonic jerks and generalized seizures was found. Conversely, a strong negative correlation between Ser943 phosphorylation and latency to generalized seizures was detected. Given the role of Na(+),K(+)-ATPase as a major regulator of brain excitability, Ser943 at Na(+),K(+)-ATPase α subunit may represent a potentially valuable new target for drug development for seizure disorders.