Metabolically healthy obesity: Is there a link with PUFA intake and status?

The aim of this study was to compare dietary intake and status of polyunsaturated fatty acids (PUFA) in plasma and erythrocyte phospholipids metabolically healthy-and unhealthy, obese and non-obese persons. Metabolic health status in 171 participants was defined according to criteria for metabolic syndrome. Obese and non-obese metabolically unhealthy persons (MUHO and MUHNO) had higher energy intake of n-6 PUFA (7.82±1.03 and 7.49±0.86), and lower intake of n-3 PUFA (0.60±0.12 and 0.62±0.11) compared to obese and non-obese metabolically healthy persons (MHO and MHNO) (5.92±0.63 and 5.72±0.67; 1.20±0.07 and 1.22±0.09, respectively), and higher n-6/n-3 PUFA ratio. Plasma level of n-6 PUFA was lower in MUHO and MUHNO groups (38.49±3.71 and 38.53±2.19) compared to MHNO (40.90±2.43), while n-3 PUFA status was lower in obese than in non-obese persons (3.58±0.79 and 3.50±1.02 vs 4.21± 0.80 and 4.06±1.15). MHO group had higher eicosapentaenoic/arachidonic acid ratio and estimated desaturase (SCD16, D6D) and elongase activity in plasma phospholipids compared to MHNO. Low intake of n-3 PUFA is directly associated with metabolic risk factors. These results indicated that obesity is closely associated with low levels of n-3 PUFA in plasma phospholipids, suggesting that dietary modifications including n-3 PUFA supplementation appear to be suitable therapeutic strategy in obese persons.

Polyunsaturated fatty acids in health and disease

Polyunsaturated fatty acids (PUFAs) are necessary for overall health. The two PUFAs families, n-6 and n-3 fatty acid are physiologically and metabolically distinct. Proportion of PUFAs in serum and erythrocyte phospholipids is an important determinant of both health and disease, and depends on endogenous metabolism controlled by genetic polymorphisms and dietary intake. Both n-3 and n-6 PUFAs are processed to powerful promoters of eicosanoids synthesis at the cyclooxygenase and lipoxygenase level. Evidence from observational and intervention studies suggest that n-3 PUFAs are cardioprotective, perhaps through their anti-inflammatory, anti-arrhythmic, lipid-lowering, and antihypertensive effects. In contrast, dietary n-6 PUFAs have pro-inflammatory effect. Low n-3 and elevated n-6 PUFAs levels were found in patients with cancer on different sites. The present review will focus on the current knowledge related to PUFAs intake and status in health and disease, with reference to the Serbian population.

Dietary linoleic acid elevates endogenous 2-arachidonoylglycerol and anandamide in Atlantic salmon (Salmo salarL.) and mice, and induces weight gain and inflammation in mice

Dietary intake of linoleic acid (LA) has increased dramatically during the twentieth century and is associated with a greater prevalence of obesity. Vegetable oils are recognised as suitable alternatives to fish oil (FO) in feed for Atlantic salmon (Salmo salarL.) but introduce high amounts of LA in the salmon fillet. The effect on fish consumers of such a replacement remains to be elucidated. Here, we investigate the effect of excessive dietary LA from soyabean oil (SO) on endocannabinoid levels in Atlantic salmon and mice, and study the metabolic effects in mice when SO replaces FO in feed for Atlantic salmon. Atlantic salmon were fed FO and SO for 6 months, and the salmon fillet was used to produce feed for mice. Male C57BL/6J mice were fed diets of 35 % of energy as fat based on FO- and SO-enriched salmon for 16 weeks. We found that replacing FO with SO in feed for Atlantic salmon increased LA, arachidonic acid (AA), decreased EPA and DHA, elevated the endocannabinoids 2-arachidonoylglycerol (2-AG) and anandamide (AEA), and increased TAG accumulation in the salmon liver. In mice, the SO salmon diet increased LA and AA and decreased EPA and DHA in the liver and erythrocyte phospholipids, and elevated 2-AG and AEA associated with increased feed efficiency, weight gain and adipose tissue inflammation compared with mice fed the FO salmon diet. In conclusion, excessive dietary LA elevates endocannabinoids in the liver of salmon and mice, and increases weight gain and counteracts the anti-inflammatory properties of EPA and DHA in mice.