Antioxidant Food Supplements and Obesity-Related Inflammation
H. Mangge, K. Summers, G. Almer, R. Prassl, D. Weghuber, W. Schnedl and D. Fuchs
Affiliation: Research Unit on Lifestyle and Inflammation-associated Risk Biomarkers, Clinical Institute of Medical and Chemical Laboratory Diagnosis, Medical University of Graz, Auenbruggerplatz 30, 8036 Graz, Austria.
Keywords: Antioxidants, obesity, inflammation, oxidative stress, food supplements, leptin, Th1, tryptophan, serotonin, melatonin.
The obesity prevalence is growing worldwide and largely responsible for the increased incidence of cardiovascular
disease, the most common cause of death in the western world. Excessive food intake along with insufficient physical
exercise is the basic impetus for this development. The obese state is commonly associated with an increase in leptin
levels and chronic immune-mediated inflammation. Despite high leptin levels, the leptin response, normally associated
with satiety and satiation, seems to be impaired and individuals continue to consume calorie-rich food. Antioxidant food
additives such as sodium sulphite, sodium benzoate and curcumin were shown to suppress the leptin release in lipopolysaccharide-
treated murine adipocytes. Based on this, we hypothesize that the insufficient leptin release, caused by excessive
consumption of food additives, may lead to a reduced exposure of the central nervous system to leptin and ultimately
propagate obesity. On the other hand, leptin has been shown to favor Th1-type activity, which ultimately decreases tryptophan
levels. Tryptophan derivatives, serotonin and melatonin, induce satiety/satiation through several mechanisms. In
this context, the antioxidant suppression of leptin release and Th1-type activity is beneficial to increase serotonin and
melatonin levels. The molecules in the mechanism described in this review are highly integrated in the reward system, and
have been implicated in the addiction behavior of obesity. Based on these facts, the involvement of antioxidant food supplements
in the mechanisms of the reward-deficiency syndrome which perpetuates obesity will be discussed.
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