Inflammation arising from obesity reduces taste bud abundance and inhibits renewal.

Despite evidence that the ability to taste is weakened by obesity and can be rescued with weight loss intervention, few studies have investigated the molecular effects of obesity on the taste system. Taste bud cells undergo continual turnover even in adulthood, exhibiting an average life span of only a few weeks, tightly controlled by a balance of proliferation and cell death. Recent data reveal that an acute inflammation event can alter this balance. We demonstrate that chronic low-grade inflammation brought on by obesity reduces the number of taste buds in gustatory tissues of mice-and is likely the cause of taste dysfunction seen in obese populations-by upsetting this balance of renewal and cell death.

The Impact of Pregnancy on Taste Function.

It is common for women to report a change in taste (for instance an increased bitter or decreased sweet response) during pregnancy, however specifics of any variation in taste with pregnancy remain elusive. Here we review studies of taste in pregnancy, and discuss how physiological changes occurring during pregnancy may influence taste signaling. We aim to consolidate studies of human pregnancy and "taste function" (studies of taste thresholds, discrimination, and intensity perception, rather than hedonic response or self-report), discussing differences in methodology and findings. Generally, the majority of studies report either no change, or an increase in threshold/decrease in perceived taste intensity, particularly in the early stages of pregnancy, suggesting a possible decrease in taste acuity when pregnant. We further discuss several non-human studies of taste and pregnancy that may extend our understanding. Findings demonstrate that taste buds express receptors for many of the same hormones and circulating factors that vary with pregnancy. Circulating gonadal hormones or other contributions from the endocrine system, as well as physiological changes in weight and immune response could all bear some responsibility for such a modulation of taste during pregnancy. Given our growing understanding of taste, we propose that a change in taste function during pregnancy may not be solely driven by hormonal fluctuations of progesterone and estrogen, as many have suggested.

Decrease in sweet taste response and T1R3 sweet taste receptor expression in pregnant mice highlights a potential mechanism for increased caloric consumption in pregnancy.

While much is known on how the maternal diet affects offspring fitness, less is known on the role of taste in guiding and promoting food intake during this crucial period. Women have intense food cravings and exhibit altered taste preferences during pregnancy, however the mechanistic details underlying these changes are presently unclear. We performed longitudinal brief-access taste testing in female mice before, during, and after pregnancy, along with quantitative PCR on taste buds and morphological analysis of taste tissues from pregnant and non-pregnant mice. Sucrose licking response decreased progressively during pregnancy compared to that prior to mating, with partial recovery in the post-partum period. No change in taste morphology was evident between pregnant and non-pregnant mice, however a notable decrease in T1R3 sweet taste receptor mRNA expression was recorded in pregnant dams. We conclude that altered taste preferences during pregnancy likely result from changes in the expression profile of taste buds in the mother, which may promote a less healthy diet while expecting.

Offspring of obese mice display enhanced intake and sensitivity for palatable stimuli, with altered expression of taste signaling elements.

Maternal body mass index and gestational weight gain predict future obesity status of the offspring. In studies of both rodents and non-human primates, maternal obesity also predicts a preference for palatable foods in the offspring. In this study, we used C57BL/6J mice to investigate whether an underlying cause for an increase in palatable food consumption in the offspring of obese mice was a change in taste function. Adult female mice were fed a normal chow (NC) or a high fat diet (HFD) for 5 weeks before mating, then also during the gestation (3 weeks) and lactation (3 weeks) periods, with offspring always maintained on a normal chow diet; thus the only experience offspring had with high fat food was via maternal exposure. Offspring exhibited similar weight, blood glucose levels and baseline water and chow intake in adulthood. Taste response was assessed after reaching maturity, using brief-access taste testing, with female offspring of obese dams showing an enhanced response to sucrose, and both sexes consuming more sucrose, sucralose and high fat diet if from obese mothers. Offspring also exhibited increased taste bud expression of mRNA for sweet receptor subunits T1R (Taste receptor type) 2 and 3, as well as other markers associated with taste signaling. Taste morphology in both groups appeared similar. Results indicate that obesity in the mother may lead to unhealthy feeding behavior in the offspring, correlating with altered expression of taste signaling elements, which likely drive increased avidity for palatable foods.

No detriment in taste response or expression in offspring of mice fed representative levels of sucrose or non-caloric sucralose while pregnant.

Recent studies in mice indicate that consumption of acesulfame K (a high intensity sweetener) while pregnant, can lead to deficits in taste or enhanced sweet consumption in the offspring, leading to concerns the same may be common in human populations. However, this work employed a relatively unpopular sweetener, fed in quantities amounting to over 20× the FDA's Acceptable Daily Intake (ADI). The aims of this study were to test the effects of sucralose, the USA's most popular high intensity sweetener, along with sucrose, on the taste system of the offspring of mice supplemented at a level commensurate with ADIs while pregnant. The hypothesis was that feeding a dam intensely sweet solutions would produce offspring with enhanced response to sweet taste, when compared to offspring of dams given only water. Females were mated following a 4-week period in which one group was given a measured ration of sucrose or sucralose in addition to chow and water, with the control group given chow and water only. Sucrose and sucralose solutions were removed two weeks after parturition to prevent direct consumption by the offspring. The offspring at 8weeks of age for both the sucrose and sucralose supplementation showed no change in their taste response to sucrose or sucralose. No effect of maternal sweet supplementation was detected at the taste bud level, with fungiform taste bud density and taste bud gene expression remaining unchanged. Overall, this study suggests that sucrose and sucralose consumption at human-relevant levels during pregnancy and lactation do not produce any long-term changes to the offspring's peripheral taste system.

Caffeine May Reduce Perceived Sweet Taste in Humans, Supporting Evidence That Adenosine Receptors Modulate Taste.

Multiple recent reports have detailed the presence of adenosine receptors in sweet sensitive taste cells of mice. These receptors are activated by endogenous adenosine in the plasma to enhance sweet signals within the taste bud, before reporting to the primary afferent. As we commonly consume caffeine, a powerful antagonist for such receptors, in our daily lives, an intriguing question we sought to answer was whether the caffeine we habitually consume in coffee can inhibit the perception of sweet taste in humans. 107 panelists were randomly assigned to 2 groups, sampling decaffeinated coffee supplemented with either 200 mg of caffeine, about the level found in a strong cup of coffee, or an equally bitter concentration of quinine. Participants subsequently performed sensory testing, with the session repeated in the alternative condition in a second session on a separate day. Panelists rated both the sweetened coffee itself and subsequent sucrose solutions as less sweet in the caffeine condition, despite the treatment having no effect on bitter, sour, salty, or umami perception. Panelists were also unable to discern whether they had consumed the caffeinated or noncaffeinated coffee, with ratings of alertness increased equally, but no significant improvement in reaction times, highlighting coffee's powerful placebo effect. This work validates earlier observations in rodents in a human population.