CSIRO Agriculture and Food, Sydney, Australia.
CSIRO Health and Biosecurity, Sydney, Australia.
Int J Obes (Lond). 2019 Jul;43(7):1475-1484. doi: 10.1038/s41366-018-0303-y. Epub 2019 Jan 29.
The role of taste perception in the development and persistence of obesity is currently unclear due to conflicting results from psychophysical and other studies. No study to date has assessed whether there is an underlying fundamental difference in the physiology of taste tissue between lean and obese individuals.
METHOD/SUBJECTS: We analysed the transcriptomic profile (RNA-seq) of human fungiform taste papillae biopsied from lean (n = 23) and obese (n = 13) Caucasian females (age range 18-55) to identify differences in gene expression.
Obesity status was the major contributor to variance in global gene expression between individuals. A total of 62 genes had significantly different gene expression levels between lean and obese (P < 0.0002), with the specific taste associated genes phospholipase C beta 2 (PLCβ2) and sonic hedge-hog (SHH) having significantly reduced expression in obese group. Genes associated with inflammation and immune response were the top enriched biological pathways differing between the lean and the obese groups. Analysis of a broader gene set having a twofold change in expression (2619 genes) identified three enriched theme groups (sensory perception, cell and synaptic signalling, and immune response). Further, analysis of taste associated genes identified a consistent reduction in the expression of taste-related genes (in particular reduced type II taste cell genes) in the obese compared to the lean group.
The findings show obesity is associated with altered gene expression in tastebuds. Furthermore, the results suggest the tastebud microenvironment is distinctly different between lean and obese persons and, that changes in sensory gene expression contribute to this altered microenvironment. This research provides new evidence of a link between obesity and altered taste and in the future may help design strategies to combat obesity.
由于来自心理物理学和其他研究的结果相互矛盾，味觉感知在肥胖的发展和持续中的作用目前尚不清楚。迄今为止，尚无研究评估瘦人和肥胖个体之间的味觉组织的生理学是否存在潜在的根本差异。
方法/受试者：我们分析了从瘦（n=23）和肥胖（n=13）白种女性（年龄范围为 18-55 岁）中活检的人味蕈状乳头的转录组谱（RNA-seq），以鉴定基因表达的差异。
肥胖状况是个体之间整体基因表达差异的主要原因。共有 62 个基因在瘦人和肥胖者之间的基因表达水平存在显著差异（P<0.0002），特定的味觉相关基因磷脂酶 Cβ2（PLCβ2）和 Sonic Hedgehog（SHH）在肥胖组中的表达显著降低。与炎症和免疫反应相关的基因是肥胖和瘦组之间差异最大的生物途径。对表达水平变化两倍的更广泛的基因集（2619 个基因）进行分析，确定了三个富集的主题组（感觉感知，细胞和突触信号，以及免疫反应）。此外，对味觉相关基因的分析表明，与瘦组相比，肥胖组中味觉相关基因的表达明显降低（特别是味觉 II 型细胞基因的表达降低）。
这些发现表明肥胖与味蕾中的基因表达改变有关。此外，结果表明，味蕾的微环境在瘦人和肥胖者之间明显不同，并且感觉基因表达的变化促成了这种改变的微环境。这项研究为肥胖与味觉改变之间的联系提供了新的证据，并且将来可能有助于设计对抗肥胖的策略。
