Taste Responsiveness to Sweeteners Is Resistant to Elevations in Plasma Leptin

Glendinning, John I.; Elson, Amanda E.T.; Kalik, Salina; Sosa, Yvett; Patterson, Christa M.; Myers, Martin G.; Munger, Steven D.

doi:10.1093/chemse/bju075

Cited by 14 publications

(12 citation statements)

References 44 publications

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“…This issue warrants further research. It is also important to note that leptin may affect taste-receptor function (Glendinning et al, 2015; Kawai et al, 2000; Meredith et al, 2015; Yoshida et al, 2015), and a contribution of this to our data cannot be excluded.…”

Section: Discussionmentioning

confidence: 89%

RYGB progressively increases avidity for a low-energy, artificially sweetened diet in female rats

et al. 2016

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Weight re-gain within 2 y after Roux-en-Y gastric bypass (RYGB) is significantly associated with increased intake of and cravings for sweet foods. Here we describe a novel model of this late increase in sweet appetite. Ovariectomized RYGB and Sham-operated rats, with or without estradiol treatment, were maintained on Ensure liquid diet and offered an artificially sweetened low-energy diet (ASD) 2 h/d. First, we tested rats more than six months after RYGB. ASD meals were larger in RYGB than Sham rats, whereas Ensure meals were smaller. General physical activity increased during ASD meals in RYGB rats, but not during Ensure meals. Second, new rats were adapted to ASD before surgery, and were then offered ASD again during 4–10 wk following surgery. Estradiol-treated RYGB rats lost the most weight and progressively increased ASD intake to >20 g/2 h in wk 9–10 vs. ~3 g/2 h in Sham rats. Finally, the same rats were then treated with leptin or saline for 8 d. Leptin did not affect body weight, Ensure intake, or activity during meals, but slightly reduced ASD intake in estradiol-treated RYGB rats. Food-anticipatory activity was increased in estradiol-treated RYGB rats during the saline-injection tests. Because increased meal-related physical activity together with larger meals is evidence of hunger in rats, these data suggest that (1) RYGB can increase hunger for a low-energy sweet food in rats and (2) low leptin levels contribute to this hunger, but are not its only cause. This provides a unique rat model for the increased avidity for sweets that is significantly associated with weight recidivism late after RYGB.

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Section: Discussionmentioning

confidence: 89%

RYGB progressively increases avidity for a low-energy, artificially sweetened diet in female rats

et al. 2016

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“…Mechanisms are thought to involve release of endogenous opioids. Interestingly and perhaps indicative of the important role sweet taste plays in food selection and utilization are findings that leptin and endocabbinoids modulate sweet taste function at the receptor level [15–16, but see 17]. This modulatory effect of endocabbinoids may thereby play a significant role in regulating energy balance through their ability to alter taste perception.…”

Section: Sweet Taste and Powermentioning

confidence: 99%

Why do we like sweet taste: A bitter tale?

Beauchamp

2016

Physiology & Behavior

103

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Sweet is widely considered to be one of a small number of basic or primary taste qualities. Liking for sweet tasting substances is innate, although postnatal experiences can shape responses. The power of sweet taste to induce consumption and to motivate behavior is profound, suggesting the importance of this sense for many species. Most investigators presume that the ability to identify sweet molecules through the sense of taste evolved to allow organisms to detect sources of readily available glucose from plants. Perhaps the best evidence supporting this presumption are recent discoveries in comparative biology demonstrating that species in the order Carnivora that do not consume plants also do not perceive sweet taste due to the pseudogenization of a component of the primary sweet taste receptor. However, arguing against this idea is the observation that the sweetness of a plant, or the amount of easily metabolizable sugars contained in the plant, provides little quantitative indication of the plant’s energy or broadly conceived food value. Here it is suggested that the perceptual ratio of sweet taste to bitter taste (a signal for toxicity) may be a better gauge of a plant’s broadly conceived food value than sweetness alone and that it is this ratio that helps guide selection or rejection of a potential plant food.

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“…At oral cavity level, a physiological role of salivary leptin as a growth factor for keratinocyte proliferation was reported [ 21 ]. Recently, Glendinning and colleagues [ 16 ] suggested that salivary leptin might act at leptin receptor level present in taste cells, in a way similar to what was reported for the satiation peptide PYY [ 22 ]. Moreover, Fábián and colleagues [ 23 ], by reviewing the mechanisms of taste perception, hypothesized that leptin, besides having an endocrine action, may act in an exocrine manner, at the level of taste receptor cells.…”

Section: Introductionmentioning

confidence: 79%

“…The influence of leptin at the level of sweet taste perception has been considered in the last years, despite some conflicting results [ 7 , 15 ]. In a recent study [ 16 ] increases in plasma leptin levels did not induce changes in sweet taste responses. Although these authors confirmed the expression of leptin receptors in taste cells, they hypothesized that these receptors in taste cells might be not sufficiently accessible to circulating leptin and that the leptin effect in sweet taste might be through a paracrine route, possibly involving leptin present in saliva.…”

Section: Discussionmentioning

confidence: 99%

“…A relation between plasma leptin levels and sweet taste has been proposed by different authors based on studies performed both in humans [ 12 ] and in rodents [ 13 ]. However, studies are not totally in agreement: whereas some observed decreased responses to the sweet stimulus sucrose [ 7 , 14 ], others reported an increased responsiveness [ 15 ] or no observable effects on sweet taste response [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

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Association between Salivary Leptin Levels and Taste Perception in Children

Rodrigues

Espanca²,

Costa

et al. 2017

Journal of Nutrition and Metabolism

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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.

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Taste Responsiveness to Sweeteners Is Resistant to Elevations in Plasma Leptin

Cited by 14 publications

References 44 publications

RYGB progressively increases avidity for a low-energy, artificially sweetened diet in female rats

RYGB progressively increases avidity for a low-energy, artificially sweetened diet in female rats

Why do we like sweet taste: A bitter tale?

Association between Salivary Leptin Levels and Taste Perception in Children

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