The peri-ovulatory time period in humans is associated with increased taste sensitivity to glucose but not calorie-free sweeteners.

Recent research has shown that KATP channels in mouse taste bud cells enhance glucose taste signaling by depolarizing the cell when ATP is present. Relatedly, estradiol has been shown to enhance glucose sensing in human pancreatic β cells via closure of KATP channels. Since taste tissue has estradiol receptors, we linked these 2 observations and tested whether elevated estradiol may also enhance taste sensitivity and liking for glucose in humans. We hypothesized that around the time of ovulation, when estrogen peaks during the menstrual cycle in female participants, oral taste detection thresholds for glucose (metabolizable monosaccharide) would decrease but would not for sucralose or the glucose analog methyl-D-glucopyranoside (MDG) (both nonmetabolizable sweeteners that do not close KATP channels). Fifteen healthy eumenorrheic females were asked to track their urinary estrogen metabolite estrone-3-glucuronide (E3G) via a fertility monitor. The participants were tested using oral detection thresholds for glucose, sucralose and MDG during the E3G nadir at menstruation and E3G peak (>100 ng/mL) at peri-ovulation. Seven male participants were also tested for glucose detection thresholds over the same 2-wk interval. Female participants were also asked to rate their liking for glucose solutions at mildly sweet (450 mM) and moderately sweet (900 mM) concentrations. Detection thresholds for glucose, but not sucralose or MDG, decreased peri-ovulation during estrogen peak (P < 0.05), indicating enhanced sensitivity to glucose specifically. Males showed no change in glucose threshold over the 2 wk. Liking ratings for 900 mM glucose tended to increase during ovulation (P = 0.06). These observations are consistent with the idea that estrogen and/or other co-modulating hormones, such as luteinizing hormone and progesterone, enhance a metabolic signaling pathway during the peri-ovulatory phase.