A Study of the Function of Hormones Present in Taste Buds
A Study of the Function of Hormones Present in Taste Buds
批准号:
7592087
负责人:
Josephine Egan
金额:
$52.11万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至
关键词:
Blood specimenCarbohydratesCellsCephalicCranial NervesDeglutitionDiabetes MellitusEndocrineEnhancersEsthesiaFabaceaeFatty acid glycerol estersFirst Degree RelativeFishesFlavoringFoodGlucoseGlutamatesHormonalHormonesHumanImpairmentIndividualIngestionInsulinInterventionL CellsMasticationMeatMusNon-Insulin-Dependent Diabetes MellitusObesityParticipantPatientsPeptide YYPhaseProteinsPurposeRattusRecruitment ActivitySensorySmell PerceptionSodium GlutamateStimulusTaste BudsTaste PerceptionThinkingVisionVisitfeedingglucagon-like peptide 1glucose toleranceimpaired glucose toleranceimprovedinsulin secretioninterestoral sensoryresponsesham feedingsweet receptorsweet taste perception
中文摘要
胰岛素分泌的头部阶段由自主神经和内分泌对食物相关的感官刺激(如视觉、嗅觉和味觉)的反应调节。人类的味觉至少包括五种不同的特征:苦、咸、酸、甜和鲜味,即谷氨酸引起的感觉,通常存在于蛋白质(肉、鱼和豆类)和味精(味精)等风味增强剂中。甜味和鲜味刺激都被证明会在大鼠的头部阶段非法释放胰岛素。改良的假喂养(MSF,食物可以闻到、咀嚼,但不能吞咽)的口腔感觉刺激已经被证明在健康受试者的头部阶段增加胰岛素释放,降低餐后血糖水平,并改善葡萄糖耐量。胰岛素吸收前期反应的丧失已被证明损害了葡萄糖耐量。此外,2型糖尿病患者及其一级亲属已被证明甜味受损。
我们已经确定葡萄糖通过激活L细胞中的甜味受体来刺激胰升糖素样肽-1(GLP-1)。L细胞是肠道中含有GLP-1的特殊细胞,甜味受体被认为只存在于味蕾中的味觉细胞上。
最近,我们发现GLP-1和YY(PYY)多肽存在于小鼠味蕾中的味觉细胞中。这些新发现提出了几个有趣的问题,即严格品尝不摄入的食物是否会刺激味觉细胞分泌GLP-1和PYY,它们的分泌是否涉及脑神经的传入输入,以及这种分泌在肥胖症和糖尿病前期或2型糖尿病患者中是否受损。我们还想调查不同的口味,如甜味和鲜味,以及不同的食物含量,如脂肪百分比和碳水化合物组成,是否会引起不同的荷尔蒙反应。
这项研究的目的是确定GLP-1和PYY是否确实参与了头位相反应。如果是这样的话,健康的瘦人、健康的肥胖者和有糖尿病前期或2型糖尿病的人的反应是否有差异。参与者在七次研究访问中的每一次都接受不同的品尝者作为干预,并在每次干预前后进行频繁的血液采样。我们正在积极招募健康瘦身受试者、健康肥胖受试者、糖尿病前期受试者和2型糖尿病受试者进行这项研究。
英文摘要
Cephalic phase of insulin secretion is regulated by autonomic and endocrine responses to food-related sensory stimulation such as sight, smell, and taste. Human taste perception comprises of at least five distinct qualities: bitterness, saltiness, sourness, sweetness, and umami, the sensation elicited by glutamate, commonly found in protein (meat, fish, and legumes) and flavor enhancer such as monosodium glutamate (MSG). Both the sweet and umami taste stimuli had been shown to illicit cephalic-phase insulin release in rats. Oral sensory stimulation in human with modified sham feeding (MSF where food is smelled, chewed, but not swallowed) had been shown to enhance insulin release during the cephalic phase, lower postprandial glucose level, and improve glucose tolerance in healthy subjects. The loss of pre-absorptive insulin response has been shown to impair glucose tolerance. Furthermore, patients with type 2 diabetes and their first degree relatives had been shown to have impairment of sweet taste.
We have determined that glucose stimulates glucagon-like peptide-1 (GLP-1) through activation of sweet receptors in L cells. The L cells are the specialized cells of the gut that contain GLP-1, and sweet receptors were thought to be present only on tast cells within taste buds.
Recently, we found that GLP-1 and peptide YY (PYY) are prsent in the taste cells located in the taste buds of mice. These new findings raise several interesting questions of whether strict tasting of food without ingestion may stimulate secretion of GLP-1 and PYY from the taste cells, whether their secretion is involved in the afferent input of the cranial nerves, and whether this secretion is impaired in obesity and in patients with pre-diabetes or type 2 diabetes. We also want to investigate whether different tastants, such as sweet versus umami, and different food contents such as percent fat versus carbohydrate compositions, would elicit different hormonal responses.
The purpose of this study is to determine if GLP-1 and PYY are indeed involved in the cephalic-phase response. If so, are there differences in response among healthy lean individuals, healthy obese individuals, and individuals with pre-diabetes or type 2 diabetes. Participants receive different tastants as interventions at each of their seven study visits and frequent blood samplings are performed before and after each intervention. We are actively recruiting healthy lean subjects, healthy obese subjects, subjects with pre-diabetes and subjects with type 2 diabetes for this study.
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