Abstract
The satiety inducing hormone leptin acts not only at central nervous system but also at peripheral level. Leptin receptors are found in several sense related organs, including the mouth. A role of leptin in sweet taste response has been suggested but, until now, studies have been based on in vitro experiments, or in assessing the levels of the hormone in circulation. The present study investigated whether the levels of leptin in saliva are related to taste perception in children and whether Body Mass Index (BMI) affects such relationship. Sweet and bitter taste sensitivity was assessed for 121 children aged 9-10 years and unstimulated whole saliva was collected for leptin quantification, using ELISA technique. Children females with lower sweet taste sensitivity presented higher salivary leptin levels, but this is only in the normal weight ones. For bitter taste, association between salivary leptin and caffeine threshold detection was observed only in preobese boys, with higher levels of salivary hormone in low sensitive individuals. This study is the first presenting evidences of a relationship between salivary leptin levels and taste perception, which is sex and BMI dependent. The mode of action of salivary leptin at taste receptor level should be elucidated in future studies.
Highlights
Leptin is a hormone primarily produced by white adipose tissue that regulates energy homeostasis by inducing satiety and energy expenditure [1]
No major differences in salivary leptin levels were observed between sexes (10.41±0.76 versus 9.28± 0.63 (P = 0.255), boys and girls, resp.)
Taking into consideration the individual salivary flow rate, the amount of leptin secreted per unit of time is positively correlated with ‰ Body Mass Index (BMI), despite the correlation being weak (R = 0.226; P = 0.018), with a tendency for higher salivary leptin levels in obese children, comparatively to normal weight ones (Figure 1)
Summary
Leptin is a hormone primarily produced by white adipose tissue that regulates energy homeostasis by inducing satiety and energy expenditure [1]. This 16 kDa protein is encoded by the obese (ob) gene and, since its discovery by Friedman, it has been linked to obesity [2]. Despite the action of leptin in energy homeostasis being known to be mainly a long-term control, by modulating the hypothalamic circuits that regulate feeding and energy expenditure [3], a short-term mediation of the neuroendocrine response to fasting has been evidenced [4]. Elevation in plasma leptin concentration has been reported to alter olfactory-mediated responses to food odours, but there is debate on whether it increases [8] or decreases [9,10,11] responsiveness.
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