Leptin Suppresses Mouse Taste Cell Responses to Sweet Compounds

Yoshida, Ryusuke; Noguchi, Kenshi; Shigemura, Noriatsu; Jyotaki, Masafumi; Takahashi, Ichiro; Margolskee, Robert F.; Ninomiya, Yuzo

doi:10.2337/db14-1462

Cited by 59 publications

(59 citation statements)

References 54 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: 88%

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: 88%

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

et al. 2016

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“…We used immunofluorescent confocal microscopy to investigate the expression of NK 1 receptors on taste bud cells. Several laboratories have shown previously that GLAST is expressed only in Type I taste cells and thus a marker for Type I cells (Lawton et al, ; Vandenbeuch et al, ; Yoshida et al, ). To verify the expression of NK 1 receptors on Type I taste cells, we double‐immunostained isolated and fixed vallate taste buds with antibodies directed against NK 1 receptors and GLAST.…”

Section: Resultsmentioning

confidence: 99%

“…Isolated taste buds were fixed in 4% paraformaldehyde in PBS for 10–20 min at 4°C and immunostained following the procedures as described in Huang and Wu (, ). is exclusively expressed in Type I cells in vallate taste buds (Lawton et al, ; Vandenbeuch et al, ; Yoshida et al, ). To localize two different antigens, NK 1 receptor/GLAST and/or GABA /GLAST, in isolated taste buds, a mixture of two primary antibodies generated in two different species against different antigens was used.…”

Section: Methodsmentioning

confidence: 99%

Substance P as a putative efferent transmitter mediates GABAergic inhibition in mouse taste buds

Huang

2018

British J Pharmacology

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Combined with the recent findings that GABA depresses taste-evoked ATP secretion, the current results indicate that SP elicited secretion of GABA, which provided negative feedback onto Type II (receptor) cells to reduce taste-evoked ATP secretion. These findings are consistent with a role for SP as an inhibitory transmitter that shapes the peripheral taste signals, via GABAergic signalling, during the processing of gustatory information in taste buds. Notably, the results suggest that SP is intimately associated with GABA in mammalian taste signal processing and demonstrate an unanticipated route for sensory information flow within the taste bud.

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“…While most studies have made progress in the identification of leptin action in the brain, Yoshida et al (15) present a study revealing a role for leptin outside of the brain-in taste buds. They discovered that leptin regulates sweet taste responses in taste buds, thus putting forward the first peripheral mechanism linking sweetness to leptin.…”

mentioning

confidence: 99%

“…Sensory and central systems are likely to have coevolved complementary strategies to modulate behavior. The regulation of sugar intake by leptin seems to be very complex, and Yoshida et al (15) propose a model that adds another layer of regulation.…”

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confidence: 99%

Sweet and Low on Leptin: Hormonal Regulation of Sweet Taste Buds

2015

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Since 1980, the incidence of obesity in the world has more than doubled (1), but most prescribed treatments still rely on voluntary modifications of eating behavior (dieting). Longterm compliance to dieting is difficult (2) as it requires eating less and forcefully deciding about what foods to eat. Sugar restriction, for instance, is a common theme in many weightcontrol diets and a must for patients with diabetes. The appetite for sugar is mediated by nutrient-sensing circuits in the brain, which play a role that seems to be conserved across species (3-5). These brain nutrient-sensing circuits are regulated to allow adaptive food intake behavior in response to the metabolic state and hormones such as leptin (6-9).Leptin is an adipose tissue hormone that functions as an afferent signal in a negative feedback loop that maintains homeostatic control of adipose tissue mass (10,11). Leptin is synthesized by adipose tissue and released into the bloodstream in amounts that are proportional to the amount of fat, thus informing the brain about the status of energy reserves. Leptin is a primordial hormone in the regulation of energy homeostasis that acts in hypothalamic neurons to increase energy expenditure and reduce appetite (12). Moreover, leptin controls sugar reward via the central nervous system by acting on glucose-sensing neural circuitry (8,13,14).While most studies have made progress in the identification of leptin action in the brain, Yoshida et al. (15) present a study revealing a role for leptin outside of the brain-in taste buds. They discovered that leptin regulates sweet taste responses in taste buds, thus putting forward the first peripheral mechanism linking sweetness to leptin.In this study, the authors used in situ hybridization to investigate which types of taste cells (TCs) express the long form of the leptin receptor (Ob-Rb). Ob-Rb colocalizes with approximately 40% of taste receptor family 1 member 3 (T1R3)-expressing TCs, which are the sweet-sensing TCs. The study also included electrophysiological analyses of the effect of leptin on TC responses to different taste stimuli: sweet, sour, or bitter. Yoshida et al. discovered that leptin exhibits selective action on T1R3-expressing TCs, suppressing their response to natural sweet sweeteners, such as sucrose, and artificial sweeteners, such as sucralose and saccharin. This suppressive effect of leptin was reversible, dose-dependent, and did not extend to other sensory modalities, such as bitter or sour perception. The authors used mutant mice lacking Ob-Rb (db/db) to discover that the suppressive effect of leptin on TC responses to saccharin was mediated by Ob-Rb. In addition, the study demonstrated by in situ hybridization that the gene SUR1, which encodes for a K ATP channel, was expressed in Ob-Rb/T1R3-expressing TCs. Pharmacological inhibition of this K ATP channel blunts the suppressive effect of leptin on T1R3-expressing TC responses to saccharin. Reciprocally, pharmacological activation of K ATP channels phenocopied the effect of leptin on sac...

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Leptin Suppresses Mouse Taste Cell Responses to Sweet Compounds

Cited by 59 publications

References 54 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

Substance P as a putative efferent transmitter mediates GABAergic inhibition in mouse taste buds

Sweet and Low on Leptin: Hormonal Regulation of Sweet Taste Buds

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