Although the relation between PUFA and cardiovascular disease has been widely demonstrated [1, 9, 10], limited information is available for histological changes.
Data on various aortic layers are essential for understanding various diseases (such hypertension or diabetes) that may remodel the tissue geometry and biomechanical properties of the vascular wall differentially .
Only two previous studies have investigated the effect of marine fatty acids on aorta histopathology. Park S. and Park Y. results suggested that the hypolipidemic action of fish oil had protective effects on aorta histopathology in male Wistar rats . And Engler, et al., who show how DHA-fed spontaneously hypertensive rats significantly reduced blood pressure and vascular wall thicknesses in the coronary, thoracic, and abdominal aorta compared with controls .
In our study, despite the thickness of the aorta was not affected by any of the treatments, the ratio EPA:DHA 1:1 shown the highest value. And the highest value of wrinkling too. This indicates a healthier condition. A lower density of elastic layers and less wrinkling indicates increased stiffness of the aorta which has been associated with greater vascular damage [11, 14].
That’s the reason why the ratio EPA:DHA 1:1 is the best at maintaining or improving the aorta’s structure, and hence its function. We should emphasize that the portion of the aorta was taken from the same zone, therefore the results of the other variables can be attributed to diet or strain and not to the location of the tissue sampling. All treatments had a similar fat and energy content and, hence, the observed differences can be attributed to the different EPA:DHA ratios.
According to the literature, omega 3 supplementation prevents the inflammation of the adipose tissue in obese and diabetic mice  and diminishes hypertrophy and hyperplasia in that tissue . Our results seem to be contrary to the literature; in adipose tissue we observed hypertrophy of tissue when the abdominal fat weight/body weight ratio in SHROB rats (6.7-7.8%) was higher than in Wistar rats (3.6-4.3%). There were significant differences in all treatment groups. Treatments did not affect this ratio in either Wistar or SHROB rats. This may be because SHROB rats were too severely affected by the diseases or because the weekly recommended dosage was too low.
The greater presence of differently-sized adipocytes could be explained by the relation between PUFA, and peroxisome-proliferator-activated receptor γ (PPARγ), which plays a critical role in the regulation of adipocyte differentiation. PUFA are potential ligands for this nuclear receptor, which may be the reason why rats fed PUFA have more adipocytes of different sizes . The PPAR family can also inhibit NF-кß factor transcription, which is also related to inflammation . This may explain why PUFA prevents inflammation.
However, the effect of different types of PUFA on body adiposity is still controversial. Omega-3 PUFA treatments, as our results show, improve inflammation in this tissue, especially in SHROB rats. Even being a very affected model, after the EPA:DHA treatment SHROB rats showed a slight inflammation or non- existent inflammation in all cases.
The effects of omega-3 PUFA on liver are the most controversial, showing contradictory results [17, 18]. In our study Wistar rats showed better results in all the parameters determined in liver, specifically EPA:DHA 1:1 treatment, which showed the best results, leading to a total absence of any inflammatory process.
Various studies have shown that both the excess and the total absence of omega 3 PUFA in experimental animals have given rise to hepatic steatosis [19, 20]. This could be explained by the nature of the PUFA n-3, which is fat. It is therefore of the utmost importance to establish the correct dosage range for these fatty acids.
In our study, in healthy rats - Wistar rats- , the best treatment is EPA:DHA 1:1 implying a preventative role in the liver. However in the group of rats affected -SHROB rats- EPA:DHA 1:1 ratio also provides the less harmful location of steatosis.
Finally, epidemiological studies suggest that omega-3 PUFA slow down the progression of renal dysfunction in patients [21, 22] and experimental models of diabetes [23, 24].
In our results, unlike SHROB rats, Wistar rats showed no renal dysfunction. A comparison of the treatments in SHROB rats shows that EPA:DHA 1:1 did not cause renal atrophy.
Considering the greater effect in Wistar rats than in SHROB rats, treatments of marine fish-oil seem to be more preventative than restorative in kidney tissue. As in liver tissue.
All this suggests that within the protective role of PUFA, the most appropriate ratio of its components is EPA:DHA 1:1 ratio as has been already described in the article of Lluis, et al. carried on by our group. But also improves histological parameters in Obese rats with Metabolic Syndrome, as demonstrated in this work.
The SHROB strain, also known as the Koletsky rat, is considered to be a good model for MS. It has monogenetic obesity superimposed on a hypertensive genetic background. The obesity mutation is a recessive trait, designated fak, which is a nonsense mutation of the leptin receptor gene. This mutation renders the SHROB incapable of central and peripheral responses to leptin. Animals can be identified as genetically obese at about five weeks of age and they also develop premature vascular disease, particularly of the abdominal arteries, although, microscopically, the lesions that occur in these vessels simulate those of human atherosclerosis . The SHROB rats also develop severe glomerulosclerosis and renal failure . SHROB strain has been used in many pharmacological studies with antihypertensive and antidiabetic drugs but our results indicate that it is probably not such a useful model for distinguishing subtle changes caused by diets.