Feeding High Oleic Acid Canola Oil or Olive Oil Alters Inflammation, Insulin Resistance and Lipid Metabolism in a Rodent Model of Diet Induced Obesity

It is recommended that the majority of dietary fat be from monounsaturated fatty acids (MUFA) as their consumption has been shown to improve risk factors involved in the development of type 2 diabetes (T2D). Studies of the health benefits of MUFA have been performed almost exclusively using olive oil. The effects of consuming different sources of MUFA on immunological and metabolic health are unknown. A new cultivar of Canola is available that contains the same proportion of oleic acid as olive oil, however the positional distribution of fatty acids on triglyceride molecules likely differ. The aim of this study was to determine the efficacy of feeding MUFA using Canola oil on risk factors for T2D in an animal model of diet induced obesity (DIO). To determine this, DIO rats were fed either a low fat diet (LF; 12% w/w fat, 12% MUFA) high fat diet low in MUFA (HF; 20% w/w, 12% MUFA), a high fat diet containing olive oil (OO; 20% w/w, 30% MUFA), or a high fat diet containing high oleic acid Canola oil (HCO; 20 w/w, 30% MUFA) and the effect on immune function, insulin sensitivity and the fatty acid composition of structural and stored lipids were measured. Feeding LF led to greater inflammatory cytokine production and plasma glucose concentration following an OGTT with changes in phospholipid fatty acid composition compared to HF (p<0.05). Increasing MUFA in the diet resulted in a lower production of the inflammatory cytokines IL-6 and TNF-α by stimulated splenocytes (p<0.05); however OO resulted in a lower TNF-α production compared to HCO. Feeding OO resulted in a higher proportion of T-helper cells (CD4+) expressing activation markers (CD152, CD71) compared to feeding HF or HCO (p<0.05). Feeding different sources of MUFA did not alter glucose metabolism; however, increasing the amount of MUFA in the diet from Canola oil resulted in a significantly greater plasma insulin and glucose concentration compared to rodents fed the HF diet (p<0.05). Feeding different sources of MUFA did not affect the fatty acid composition in the sn-2 position of triglycerides in the liver or perirenal adipose tissue. However, in spleen phospholipids, feeding OO led to significantly greater proportions of oleic acid and linoleic acid, compared to those fed HCO. Feeding HF resulted in a higher proportion of linoleic acid and lower oleic acid in spleen phospholipids compared to high MUFA diets. This suggests that both the source of MUFA (triglyceride species) as well as the overall content of MUFA and fat in the diet alters lipid metabolism and thereby could alter other physiological processes. In summary, feeding high MUFA diets lowered the pro-inflammatory response compared to a low MUFA diet; however, different sources of MUFA are not equivalent. Feeding MUFA from OO was more effective in dampening a pro-inflammatory response compared to HCO, despite having the same fatty acid composition. Future research will determine if this is due to changes in the fatty acid composition of phospholipids and triglycerides.