The present study shows that CO has a beneficial effect against the DM-associated dyslipidemia, oxidative stress and glucose intolerance, thereby exhibiting a trend toward anti-atherosclerotic profile. On the contrary, PO has a trend toward pro-atherosclerotic profile. It has been reported in the literature that CO possesses many of the health benefits, viz. hypocholesterolemic, hypolipemic, antiplaque, antioxidant[3
] and antidiabetic[12
] properties. One of the reasons could be the difference in chain lengths that are metabolized differently. The major FA content of CO is medium-chain lauric acid (48%).[3
] Lauric acid (C 12:0) gets converted into monolaurins – the best fat similar to mother’s milk.[3
] The short- and medium-chain SFAs are easily digested, absorbed and utilized by the body and contribute less fat deposition when compared to long-chain fatty acids (LCFAs).[14
] LCFAs, however, are transported via chylomicrons into the lymphatic system, allowing for extensive uptake into the adipose tissue, as evident in our study, by the hypolipedemic activity of CO in D rats.
The present study has also observed aggravated D-associated dyslipidemia  and oxidative stress  in the PO-fed group. PO, an SFA dietary oil, contains 40% of palmitic acid (C16:0) and only 0.2% lauric acid.[2
] Palmitic acid is suspected to possess a hypercholesterolemic effect.[16
] It increases the cholesterol ester transport protein activity, which is responsible for the transfer of cholesterol from HDL to LDL. This, in turn, is responsible for the decrease in the HDL-C concentration combined with an increase in LDL-C.[17
] Moreover, palmitic acid is metabolized to palmitoleic acid, which, in turn, reduces HDL-C.[18
] We also observed an increase in the non-HDL-C levels and AI in the PO-treated D group, which further confirms the harmful effects of palmitic acid-rich PO on health. The increase in the non-HDL-C level and oxidative stress in the PO-fed group may result in the formation of more oxidized LDL-C, which is known to accelerate the atherosclerosis process. The beneficial effects of CO and the deleterious effects of PO were also observed in our earlier study involving N and stressed rats.[2
] Hence, it can be suggested that the deleterious effects observed by the SFA-rich oil is dependent on the type of FAs present.
Results of OGTT have shown better glucose tolerance with CO whereas PO has impaired glucose tolerance. The observed difference in insulin sensitivity between two SFA-containing oils studied may be related to the TG level. There are reports on the association of elevated serum TGs with insulin resistance. As per Storlien et al
., one of the mechanisms for the fat-induced insulin resistance could be attributed to an increased accumulation of TG in the skeletal muscle.[19
] Besides, several other studies involving animals and humans have shown that the FA composition of muscle membrane phospholipid is closely associated with insulin action, altering fluidity and receptor activity.[20
] The difference in insulin sensitivity between two SFA-containing oils studied may also be due to the change in the composition of FA in the membrane phospholipids. It has been reported earlier that CO, due to the increased content of lauric acid, improves insulin sensitivity and reduces the incidence of DM.[13
] But, peripheral insulin sensitivity was significantly and negatively correlated with the proportion of palmitic and palmitoleic acids.[21
] Amelsvoort et al
. have also reported that PO feeding resulted in a lower rate of insulin-stimulated glucose uptake and insulin binding to the cells (lower number of low-affinity binding sites) than feeding sunflower oil.[22
] Therefore, based on our results, we can state that the insulin insensitivity due to the higher intake of saturated fat may be relevant to palmitic acid-rich oil but may not be due to lauric acid-rich CO.
The present study claims the protective role of lauric acid-rich CO against oxidative stress, dyslipidemia and glucose intolerance. PO due to low content of lauric acid and high content of palmitic acid was found to manifest deleterious effects of SFA. Hence, consumption of high amount of lauric acid- and less amount of palmitic acid-containing oils is likely to provide marked improvement in many aspects of the metabolic syndrome via a range of direct and indirect effects on glucose/lipid metabolism in the body against DM and DM-associated complications. It can be concluded that it is not just SFA but also the type of FA (lauric acid) present in the dietary oil used that is important.