Alkylresorcinols are a group of phytochemical antioxidants found in cereal grains, particularly wheat, barley and rye. Oats however are not a good source of alkylresorcinols. Chemically alkylresorcinols are 1,3-dihydroxy-5-alkylbenzene homologs with alkyl side chains of 15 to 25 carbons in length. The structure of alkyrecornlkylrecorninols gives them antioxidant properties, and evidence suggests they are bioavailable in humans and animals. The alkylresorcinols make up a large proportion of the phytochemical antioxidants in cereal grains with levels of between 300 and 1500 μg per gram. Antioxidants from plants are of interest because evidence suggests they have health effects in animals when consumed regularly as part of a healthy diet. In particular, antioxidants may have insulin sensitising effects, possibly through protection of the insulin receptor from oxidative stress. Evidence suggests that insulin insensitivity caused by oxidative stress is a primary driver of weight gain and obesity.
A number of studies have investigated the insulin sensitising effects of plant antioxidants and found positive effects in both animals and humans. As interest in the alkylresorcinols has increased researchers have started to investigate their effects in animals. For example, in one study1, researchers investigated the effects of alkylresorcinols in mice fed a high sugar high fat diet (containing 29.1 % fat, 20.7 % protein, 34.0 % carbohydrates including 20.0 % sucrose) alone or with 0.4 % alkylresorcinols for 10 wk. The results showed that the alkylresorcinols inhibited the diet induced body weight gain of the control mice by 31 %. However, this inhibition was accomplished with no change to the energy intake of the mice. This adds more weight to the hypothesis that weight gain is not caused by energy intake and proves the fallacy of calorie counting diets. Instead evidence suggests that weight gain is caused by a decrease in the sensitivity of the insulin receptor.
Interestingly the alkylresorcinols improved the insulin sensitivity of the mice. This may explain the protective effects of the alkylresorcinols against body weight increase. The improvement in insulin sensitivity were reflected in a reduction in blood glucose levels in the alkylresorcinol treated mice. Analysis of tissue from the livers of the mice showed that insulin-stimulated protein kinase B phosphorylation in the hepatocytes had increased suggesting that liver insulin signalling pathways had been upregulated. There was no change to the digestion of starch or the breakdown rate of glycogen suggesting that the changes were centralised predominantly on the insulin receptor. The mice fed alkylresorcinols experienced a 40 % increase in cholesterol excretion and a 30 % reduction in cholesterol plasma levels, which may have been a result of the improvements in insulin sensitivity. Alkylresorcinols may therefore have favourable effects on the insulin system that prevent subsequent detrimental changes to body weight.
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