It is well known that taste perception influences food intake. After ingestion, gustatory receptors relay sensory signals to the brain, which segregates, evaluates, and distinguishes the stimuli, leading to the experience known as "flavor." It is well accepted that five taste qualities -sweet, salty, bitter, sour, and umami -can be perceived by animals. In this review, the anatomy and physiology of human taste buds, the hormonal modulation of taste function, the importance of genetic chemosensory variation, and the influence of gustatory functioning on macronutrient selection and eating behavior are discussed. Individual genotypic variation results in specific phenotypes of food preference and nutrient intake. Understanding the role of taste in food selection and ingestive behavior is important for expanding our understanding of the factors involved in body weight maintenance and the risk of chronic diseases including obesity, atherosclerosis, cancer, diabetes, liver disease, and hypertension.
Peptide YY3-36 is a satiation hormone released postprandially into the bloodstream from L-endocrine cells in the gut epithelia. In the current report, we demonstrate PYY3-36 is also present in murine as well as in human saliva. In mice, salivary PYY3-36 derives from plasma and is also synthesized in the taste cells in taste buds of the tongue. Moreover, the cognate receptor Y2R is abundantly expressed in the basal layer of the progenitor cells of the tongue epithelia and von Ebner's gland. The acute augmentation of salivary PYY3-36 induced stronger satiation as demonstrated in feeding behavioral studies. The effect is mediated through the activation of the specific Y2 receptor expressed in the lingual epithelial cells. In a long-term study involving diet-induced obese (DIO) mice, a sustained increase in PYY3-36 was achieved using viral vector-mediated gene delivery targeting salivary glands. The chronic increase in salivary PYY3-36 resulted in a significant long-term reduction in food intake (FI) and body weight (BW). Thus this study provides evidence for new functions of the previously characterized gut peptide PYY3-36 suggesting a potential simple and efficient alternative therapeutic approach for the treatment of obesity.
Hormone peptide tyrosine-tyrosine (PYY) is secreted into circulation from the gut L-endocrine cells in response to food intake, thus inducing satiation during interaction with its preferred receptor, Y 2 R. Clinical applications of systemically administered PYY for the purpose of reducing body weight were compromised as a result of the common side effect of visceral sickness. We describe here a novel approach of elevating PYY in saliva in mice, which, although reliably inducing strong anorexic responses, does not cause aversive reactions. The augmentation of salivary PYY activated forebrain areas known to mediate feeding, hunger, and satiation while minimally affecting brainstem chemoreceptor zones triggering nausea. By comparing neuronal pathways activated by systemic versus salivary PYY, we identified a metabolic circuit associated with Y 2 R-positive cells in the oral cavity and extending through brainstem nuclei into hypothalamic satiety centers. The discovery of this alternative circuit that regulates ingestive behavior without inducing taste aversion may open the possibility of a therapeutic application of PYY for the treatment of obesity via direct oral application.
The objective of this review is to shed light on the literature regarding the psychological impact of invasive cosmetic surgery and to discuss future implications for research and clinical practice. Articles published through October 2021 were reviewed to answer the question, "Does cosmetic surgery improve a patient's overall psychological health?" Psychological well-being was examined through the lens of body image, self-esteem, anxiety, and depression scores. The studies revealed that although cosmetic surgery seems to boost patients' body image, other crucial aspects of psychological well-being may or may not similarly benefit. Notably, factors such as a patient's preoperative mental status, level of education, type of cosmetic procedure, postoperative healing time, sex, and age play a role in determining the direction and magnitude of psychological change after surgery. Limitations include the lack of diversity in study populations and the potential role of body dysmorphic disorder. Overall, researchers have concluded that cosmetic surgery improves body image but remain in disagreement on its effects on self-esteem, anxiety, and depression.
In this report, we show that murine and human saliva contains gut peptide YY (PYY3‐36), a hormone characterized by its physiological function of increasing satiation but not altering appetite. The purpose of the study was to investigate whether changes in salivary PYY3‐36 concentration induced either pharmacologically (acute augmentation) or genetically (gene therapy) would modulate food intake (FI) and body weight (BW) in C57Bl6 mice. Short‐term augmentation resulted in transient decrease in FI followed by compensatory feeding. On the contrary, sustained PYY transgene expression in the salivary gland resulted in a significant reduction of FI and 24% decrease of BW in diet‐induced obese mice over the eight weeks study. A conditioned taste aversion (CTA) test was used to determine the mechanism of FI reduction. Intra‐peritoneal administration of PYY3‐36, or LiCl produced CTA to the paired flavored chow, whereas no such response was documented in response to the augmentation of the salivary PYY3‐36. Furthermore, hypothalamic c‐fos activation had been investigated in response to the acute salivary PYY3‐36 augmentation. Interestingly, the treatment induced hypothalamic nuclei similar to the ones activated during re‐feeding. In conclusion, we describe the existence of an alternative satiation pathway mediated by salivary PYY3‐36 suggesting novel pharmacological and/or genetic approaches to treat obesity.
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