Vitamin E deficiency is rare in humans and depletion of vitamin E can take some considerable time, perhaps months. There is no single tissue that stores vitamin E, but rather all tissues contain vitamin E in relation to their fat content. Adipose tissue therefore has large reserves of vitamin E as it is the tissue with the highest content of fat, with typical adipose tissue perhaps containing 200 to 700 nmol/g. Plasma also contains a reasonably large reservoir of vitamin E in the lipoproteins that transport them as well as erythrocytes. The composition of vitamin E in tissue tends to reflect the isomers present in the food ingested, with α-tocopherol and γ-tocopherol tending to be the most common isomers in supplements and Western diets, respectively. Adipose tissue is often used to assess vitamin E status in individuals and studies have used adipose tissue to assess supplementation with vitamin E capsules.
Deficiency of vitamin E causes peripheral neuropathy because the larger sensory neurones die possibly due to lack of protection from membrane bound vitamin E. Adipose tissue concentrations of vitamin E are predictive of neuronal concentrations which makes them useful clinically. Peripheral neuropathy is also associated with severe burns, possibly because the massive free radical generation causes depletion of vitamin E. Researchers1 have investigated vitamin E status following severe burns in paediatric patients by using biopsies of adipose tissue to assess vitamin E levels. Adipose tissue concentrations of α-tocopherol remained within the normal range for the first week (199 nmol/g), but started to drop significantly in weeks 2 (133 nmol/g) and 3 (109 nmol/g). Individual vitamin E levels dropped at around 6.1 nmol/g/d, and the decrease in α-tocopherol was likely due to the increased free radicals generated by the injury. However, levels did recover after week 3 indicating improved health.
RdB
