Dr. Robin Dando, assistant professor of Food Science at Cornell University, is a specialist in taste biology. It is tewnty years now that he faces the understanding of the relationships between human taste and its variation according to feeding and human disease. He is very interested on a curious effect of being obese: why the sense of taste of people seems opaque while they gain weight? Doctors have known the phenomenon in recent years, after reports published in the last decade have shown that obese people have performed poor results in taste tests compared to individuals with normal weight. But the fundamental question remained: why? Eat heavy foods has blurred the sensitivity of the tongue to the flavors? Or does this have anything to do with the mere presence of excess body fat? To find out, professor Dando studied the tongues of his fat and normal mice. Under the fatty diet, he found that the taste buds were regressing. The obese had about 25% less taste buds: the taste buds are structures on the tongue made up of about 100 cells and when the mice get fat, the older cells become extinct more quickly and are slowly replaced with new, young cells.
Dr. Dando worked with two groups of mice in the experiment: one was a set of mutants (genetically modified), which were practically unable to gain weight, no matter how fat their foods were. These mice have the same fatty food as normal obese mice but have not gained much weight. After eight weeks, Dando and his students sliced mice tongues and examined their taste buds, and they seemed totally normal: they had the same number of taste buds as skinny mice. This suggested that the diet itself was not responsible for the damage to the taste buds of mice – it had something to do with being obese. So Dando looked at another group of mice – a group of mutants that can not produce a molecule called TNF-alpha, a cytokine that creates inflammation in the body. TNF-alpha and other inflammatory cytokines are naturally higher in obese individuals – both humans and mice – and cause them a higher level of inflammation. Even when these mice became very fat, they did not even lose their taste buds. It means that the loss of taste buds is really related to that inflammatory state.
Scientists have known for some time that obesity is an inflammatory disease, but they did not know that there is a connection between inflammation and the proliferation of taste buds, and that actually leads to a decrease in sensitivity to taste. It is important to note that this study was conducted on simple mice, but the situation is probably the same for humans too. In this particular circumstance, it is reasonable to make that extrapolation to humans. Studies that have similar results have been done on humans. This smoothing of taste can make it harder for obese people to adhere to certain diets. With a diminished sense of taste, people need stronger and more flavored food to enjoy it as much as someone with 25% more taste buds. Often this means more sugar and fat and more calories, of course. It is not a permanent loss, though. Studies on patients undergoing bariatric surgery show that they begin to notice that food tastes are better and more intense after a couple of months of surgery. Earlier Dr. Dando presented evidence also for the presence of interferon (IFN)-mediated signaling pathways in taste bud cells.
IFN receptors, particularly the IFN-gamma receptor IFNGR1, are coexpressed with the taste cell-type markers neuronal cell adhesion molecule and alpha-gustducin, suggesting that both the taste receptor cells and synapse-forming cells in the taste bud can be stimulated by IFN. Incubation of taste bud-containing lingual epithelia with recombinant IFN-alpha and IFN-gamma triggered the classical gene expression patterns that are activated by interferons. Furthermore, the systemic administration of either IFN-alpha or IFN-gamma significantly increased the number of taste bud cells undergoing elimination. These findings suggest that interferons induced by bacterial and viral infections can act directly on taste bud cells, affecting their cellular function in taste transduction, A lot of persons have experienced that when sick with cold, flu, pneumonia and other similar conditions, their appetite changes as it is true with their taste, for intensity or the onset of “strange” tastes that do not make sense with what they are eating. According ot professor Dando, it is also possible that IFN-induced elimination in taste buds may cause abnormal cell turnover and skew the representation of different taste bud cell types, leading to the development of taste disorders.
- edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.
Kaufman A et al., Dando R. PLoS Biol. 2018 Mar; 16(3):e2001959.
Lv W, Finlayson G, Dando R. Appetite. 2018 Feb 12; 125:210-216.
Feng P, Huang L, Wang H. Chem Senses. 2014; 39(1):3-16.
Barlow LA. Development. 2015 Nov 1; 142(21):3620-9.
Dott. Gianfrancesco Cormaci
Ultimi post di Dott. Gianfrancesco Cormaci (vedi tutti)
- Ovary cancer eludes immunity? Chemical databases will show a natural way to hinge with - Giugno 23, 2022
- ALS4: un forma di SLA che coinvolge il sistema immunitario in modo diretto - Giugno 23, 2022
- Inquinamento e salute cerebrale: le prove che siamo a rischio a cominciare dai bambini - Giugno 23, 2022
- Dannata nausea: dà fastidio ma serve, ecco perchè gli scienziati vanno a caccia dei suoi circuiti - Giugno 22, 2022
- Stubborn prostate cancer: looking for new strategies against the receptAR to erase the Rsk of resistance - Giugno 22, 2022