Diurnal Variation of Human Sweet Taste Recognition Thresholds Is Correlated With Plasma Leptin Levels

Abstract

OBJECTIVE-It has recently been proposed that the peripheral taste organ is one of the targets for leptin. In lean mice, leptin selectively suppresses gustatory neural and behavioral responses to sweet compounds without affecting responses to other taste stimuli, whereas obese diabetic db/db mice with defects in leptin receptor lack this leptin suppression on sweet taste. Here, we further examined potential links between leptin and sweet taste in humans. RESEARCH DESIGN AND METHODS-A total of 91 nonobese subjects were used to determine recognition thresholds using a standard stair-case methodology for various taste stimuli. Plasma leptin levels were determined by an enzyme-linked immunosorbent assay at several timepoints during the day under normal and restricted-meal conditions. RESULTS-The recognition thresholds for sweet compounds exhibited a diurnal variation from 0800 to 2200 h that parallels variation for leptin levels, with the lowest thresholds in the morning and the highest thresholds at night. This diurnal variation is sweet-taste selective-it was not observed in thresholds for other taste stimuli (NaCl, citric acid, quinine, and monosodium glutamate). The diurnal variation for sweet thresholds in the normal feeding condition (three meals) was independent of meal timing and thereby blood glucose levels. Furthermore, when leptin levels were phase-shifted following imposition of one or two meals per day, the diurnal variation of thresholds for sweet taste shifted in parallel.CONCLUSIONS-This synchronization of diurnal variation in leptin levels and sweet taste recognition thresholds suggests a mechanistic connection between these two variables in humans.

Taste perception, associated hormonal modulation, and nutrient intake

“…In human studies, the recognition thresholds for sweet compounds exhibited a diurnal variation from 8:00 am to 10:00 pm that parallels variation for leptin levels, with the lowest thresholds in the morning and the highest thresholds at night. 60 Together, these data confirm that leptin activation of taste cells inhibits gustatory response to sweet compounds.…”

“…Hormones that bind to receptors on taste cells alter the palatability of food and, therefore, intake. Current knowledge of the hormonal modulation of taste function is summarized in Table 1 [60][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75][76][77] and described in greater detail below.…”

Modulation of sweet taste sensitivity by orexigenic and anorexigenic factors

“…The hormone directly acts on taste receptor cells via Ob-Rb expressed in these cells and it specifically inhibits peripheral variations in sweetener thresholds were significantly different among 3 meal conditions. This diurnal variation is sweet-taste selective: it was not observed in thresholds for other taste stimuli (NaCl, citric acid, quinine and mono-sodium glutamate) [14]. By contrast, the diurnal variations for sweet recognition thresholds disappeared in the over-weight and obese subjects (BMI > 25: Shigemura et al, unpublished observation).…”

“…To examine this possibility, we measured recognition thresholds of non-obese subjects (BMI < 25) for various taste stimuli and plasma leptin levels at several time-points during the day under normal meal conditions with 3 meals, and restricted meal conditions with 1 or 2 meals per day [14]. In the normal feeding condition, leptin concentrations started rising before cannabinoids also oppose the action of leptin and enhance sweet taste responses in mice [18].…”

“…Leptin, an anorexigenic mediator that reduces food intake by acting on hypothalamic receptors [11], selectively suppresses sweet taste responses and these effects may be mediated by leptin receptor, Ob-Rb, expressed in sweet-sensitive receptor cells [12][13][14]. Glucagon-like peptide-1 (GLP-1), an incretin that influences glucose transport, metabolism and homeostasis [15], normally acts to maintain or enhance sweet taste sensitivity by its paracrine activity [16].…”