Evidence on n-3 Fatty Acids and Oleic Acid Role in Retinal Inflammation and Microvascular Integrity: Insight from a Hyperlipidemic Rat Model.

Loss of retinal function due to manifestation of chronic inflammation and oxidative stress in hyperglycemia is well addressed. However, the effect of hyperlipidemia on retinal inflammation and microvascular integrity, and the modulatory effects of oxidation-stable oleic acid and long-chain n-3 fatty acids have never been addressed. The objective of this investigation was to assess the retinoprotective effect of oxidation stable oleic acid and oxidation-susceptible EPA + DHA on retinal inflammation and microvascular integrity, under hyperlipidemic conditions. Male Wistar rats were fed with control (7.0% lard), high-fat (35.0% lard), high-fat with fish oil (17.5% fish oil + 17.5% lard), high-fat with olive oil (17.5% olive oil + 17.5% lard), and high-fat with fish oil and olive oil (11.66% fish oil + 11.66% of olive oil + 11.66% of lard) diet for 90 days. Systemic and retinal inflammation, as measured by eicosanoids and cytokines, retinal expression of NF-kB, capillary degeneration, and pericyte loss, were assessed. Hyperlipidemia significantly (p < 0.05) increased the markers of inflammation (PGE2, LTB4, LTC4, IL-1ß, MCP-1, and TNF-α) in serum and retina. Besides, the retinal NF-kB-p65 expression, capillary degeneration, and pericyte loss were significantly (p < 0.05) increased under hyperlipidemic conditions. Dietary incorporation of oleic acid and EPA + DHA significantly (p < 0.05) suppressed hyperlipidemia-induced effects in the retina. In conclusion, hyperlipidemia causes retinal aberrations by compromising the balance in the inflammatory response and microvascular integrity. Dietary incorporation of oleic acid and long-chain n-3 fatty acids prevents hyperlipidemia-induced aberrations in the retina.

Dietary omega-3 but not omega-6 fatty acids down-regulate maternal dyslipidemia induced oxidative stress: A three generation study in rats.

BACKGROUND: Maternal nutrition modulates fetal metabolic programming and development later. Maternal dyslipidemia effects on oxidative stress (OS) in offsprings and its modulation by dietary fatty acids over generations remains to be elucidated. The objective of present study was to assess the long-term (three generations) effect of omega-3 fatty acids on OS under dyslipidemia. METHODS: Weanling female Wistar rats were fed with control diet (7% lard), high fat diet (35% lard, HFL), high fat with fish oil (21% fish oil + 14% lard, HFF), high fat with canola oil (21% canola oil + 14% lard, HFC) and high fat with sunflower oil (21% sunflower oil + 14% lard, HFS). Following 60 days feeding, the female rats were mated with sexually matured males (fed normal chow diet) and continued with the above diet regimen during pregnancy and lactation. The pups after lactation were continued with their maternal diet for 60 days and subjected to mating and feeding trial as above for two generations. Serum lipid profiles, OS markers (lipid peroxidation, nitric oxide release and protein carbonyl) and antioxidant defence enzymes (catalase, SOD, glutathione peroxidase and glutathione transferase) were assessed in serum, liver and uterus of rats fed on experimental and control diets for three generations. RESULTS: Feeding HFL diet increased blood lipids, OS and lowered the antioxidant enzymes activity in serum, liver and uterus (p < 0.05). The reduction in the antioxidant enzymes in HFL group were higher in third followed by second generation compared to first generation (p < 0.05). Omega-3 fatty acids prevented the dyslipidemia induced loss of antioxidant enzyme activities in serum, liver and uterus. CONCLUSIONS: Our data show for the first time that offsprings born to dyslipidemic mothers' exhibit diminished enzymatic antioxidant defence and its progressive reduction in future generation, and dietary omega-3 fatty acids restore the enzymatic antioxidant defence in offsprings and suppress the markers of OS.