-II signaling reduces food intake by suppressing the hypothalamic expression of neuropeptide Y and orexins via AMPK dephosphorylation [ 48 ] .
Ras, Estrogen, and LipoxinA4
In this context, it is noteworthy that ovariectomized (OVX) female rats treated with estradiol benzoate (EB) had a 30–40% reduction in the levels of AT-I receptor mRNA in pituitary and HTS (hypothalamic-thalamic-septa) tissue samples as compared to OVX, control animals. In the pituitary, the mRNA levels for angiotensinogen (AGT) were increased by 45% following estrogen administration. In addition
presence of EPA and DHA in the cell membrane (because of their supplementation) can enhance the formation of anti-inflammatory resolvins, protectins and maresins. Even though AA forms the precursor to the anti-inflammatory lipoxinA4 (LXA4), the presence of angiotensin-II, a pro-inflammatory molecule [ 11 - 13 ] perhaps may drive the generation of pro-inflammatory metabolites from AA instead of anti-inflammatory LXA4. In a previous study, [ 14 ] we showed that PUFAs inhibit the activity of angiotensin converting enzyme (ACE) that is needed for the formation of Ang
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40°C/min to 160°C (0 min), then increased at the rate of 30°C/min to 190°C (0.5 min) and finally increased at the rate of 30°C/min to 230°C for 2.6 min, where it was maintained for 4.9 min. The total analysis lasted approximately 8 min and the gas flow rate was 0.8 ml/min with hydrogen as the carrier gas. Fatty acids were identified by comparing their retention times with those of commercially available standards.
Isolation and analyses of fatty acid derivatives
5(S),6(R)-LipoxinA4 , 5(S),6(R), 15(R)- LipoxinA4 , 5(S)-HETE, 5(S)-oxoETE, 12(S)-HETE, 15(S