Neuroscience

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Smoking may dull obese women’s ability to taste fat and sugar

Cigarette smoking among obese women appears to interfere with their ability to taste fats and sweets, a new study shows. Despite craving high-fat, sugary foods, these women were less likely than others to perceive these tastes, which may drive them to consume more calories.

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M. Yanina Pepino, PhD, assistant professor of medicine at Washington University School of Medicine in St. Louis, and Julie Mennella, PhD, a biopsychologist at the Monell Center in Philadelphia, where the research was conducted, studied four groups of women ages 21 to 41: obese smokers, obese nonsmokers, smokers of normal weight and nonsmokers of normal weight. The women tasted several vanilla puddings containing varying amounts of fat and were asked to rate them for sweetness and creaminess, a measure of fat content.

“Compared with the other three groups, smokers who were obese perceived less creaminess and sweetness,” Pepino said. “They also derived less pleasure from tasting the puddings.”

The findings are published in the April issue of the journal Obesity.

Pepino cautioned that the study only identified associations between smoking and taste rather than definitive reasons why obese smokers were less likely to detect fat and sweetness. But the findings imply that the ability to perceive fat and sweetness — and to derive pleasure from food — is compromised in female smokers who are obese, which could contribute to the consumption of more calories.

“Obese people often crave high-fat foods,” she said. “Our findings suggest that having this intense craving but not perceiving fat and sweetness in food may lead these women to eat more. Since smoking and obesity are risk factors for cardiovascular and metabolic diseases, the additional burden of craving more fats and sugars, while not fully tasting them, could be detrimental to health.”

Interestingly, it was the combination of smoking and obesity that created something of a “double-whammy” because smokers who were not overweight could perceive fat and sweetness that was similar to women who did not smoke.

Previous studies have linked smoking to increased food cravings and greater consumption of fat, regardless of whether a smoker is obese. Studies also have found that smokers tend to have increased waist-to-hip ratios. That is, they tend to be shaped more like apples than pears, another risk factor for heart disease and metabolic problems.

The findings contribute to a growing body of knowledge that challenges the lingering perception that smoking helps a person maintain a healthy weight.

“Women are much more likely than men to take up smoking as an aid to weight control,” Pepino said. “But there is no good evidence showing that it helps maintain a healthy weight over the long term. And in the case of obese women who smoke, it appears the smoking may make things even worse than previously thought.”

(Source: news.wustl.edu)

Filed under smoking obesity taste perception flavor perception health

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How the Body’s Energy Molecule Transmits Three Types of Taste to the Brain
Saying that the sense of taste is complicated is an understatement, that it is little understood, even more so. Exactly how cells transmit taste information to the brain for three out of the five primary taste types was pretty much a mystery, until now.
A team of investigators from nine institutions discovered how ATP – the body’s main fuel source – is released as the neurotransmitter from sweet, bitter, and umami, or savory, taste bud cells. The CALHM1 channel protein, which spans a taste bud cell’s outer membrane to allow ions and molecules in and out, releases ATP to make a neural taste connection. The other two taste types, sour and salt, use different mechanisms to send taste information to the brain.
Kevin Foskett, PhD, professor of Physiology at the Perelman School of Medicine, University of Pennsylvania, and colleagues from the Monell Chemical Senses Center, the Feinstein Institute for Medical Research, and others, describe in Nature how ATP release is key to this sensory information path. They found that the calcium homeostasis modulator 1 (CALHM1) protein, recently identified by the Foskett lab as a novel ion channel, is indispensable for taste via release of ATP.  
“This is an example of a bona fide ATP ion channel with a clear physiological function,” says Foskett. “Now we can connect the molecular dots of sweet and other tastes to the brain.”
Taste buds have specialized cells that express G-protein coupled receptors (GPCRs) that bind to taste molecules and initiate a complex chain of molecular events, the final step of which Foskett and collaborators show is the opening of a pore in the cell membrane formed by CALHM1. ATP molecules leave the cell through this pore to alert nearby neurons to continue the signal to the taste centers of the brain. CALHM1 is expressed specifically in sweet, bitter, and umami taste bud cells.
Mice in which CALHM1 proteins are absent, developed by Feinstein’s Philippe Marambaud, PhD, have severely impaired perceptions of sweet, bitter and umami compounds; whereas, their recognition of sour and salty tastes remains mostly normal. The CALHM1 deficiency affects taste perception without interfering with taste cell development or overall function.
Using the CALHM1 knockout mice, team members from Monell and Feinstein tested how their taste was affected. “The mice are very unusual,” says Monell’s Michael Tordoff, PhD. “Control mice, like humans, lick avidly for sucrose and other sweeteners, and avoid bitter compounds. However, the mice without CALHM1 treat sweeteners and bitter compounds as if they were water. They can’t taste them at all.”
From all lines of evidence, the team concluded that CALHM1 is an ATP-release channel required for sweet, bitter, and umami taste perception. In addition, they found that CALHM1 was also required for  “nontraditional” Polycose, calcium, and aversive high-salt tastes, implying that the deficit displayed in the knockout animals might best be considered as a loss of all GPCR-mediated taste signals rather than simply sweet, bitter and umami taste.
Interestingly, CALHM1 was originally implicated in Alzheimer’s disease, although the link is now less clear. In 2008, co-author Marambaud identified CALHM1 as a risk gene for Alzheimer’s. They discovered that a CALHM1 genetic variant was more common among people with Alzheimer’s and they went on to show that it leads to a partial loss of function. They also found that this novel ion channel is strongly expressed in the hippocampus, a brain region necessary for learning and memory. So far, there is no connection between taste perception and Alzheimer’s risk, but Marambaud suspects that scientists will start testing this hypothesis.

How the Body’s Energy Molecule Transmits Three Types of Taste to the Brain

Saying that the sense of taste is complicated is an understatement, that it is little understood, even more so. Exactly how cells transmit taste information to the brain for three out of the five primary taste types was pretty much a mystery, until now.

A team of investigators from nine institutions discovered how ATP – the body’s main fuel source – is released as the neurotransmitter from sweet, bitter, and umami, or savory, taste bud cells. The CALHM1 channel protein, which spans a taste bud cell’s outer membrane to allow ions and molecules in and out, releases ATP to make a neural taste connection. The other two taste types, sour and salt, use different mechanisms to send taste information to the brain.

Kevin Foskett, PhD, professor of Physiology at the Perelman School of Medicine, University of Pennsylvania, and colleagues from the Monell Chemical Senses Center, the Feinstein Institute for Medical Research, and others, describe in Nature how ATP release is key to this sensory information path. They found that the calcium homeostasis modulator 1 (CALHM1) protein, recently identified by the Foskett lab as a novel ion channel, is indispensable for taste via release of ATP.  

“This is an example of a bona fide ATP ion channel with a clear physiological function,” says Foskett. “Now we can connect the molecular dots of sweet and other tastes to the brain.”

Taste buds have specialized cells that express G-protein coupled receptors (GPCRs) that bind to taste molecules and initiate a complex chain of molecular events, the final step of which Foskett and collaborators show is the opening of a pore in the cell membrane formed by CALHM1. ATP molecules leave the cell through this pore to alert nearby neurons to continue the signal to the taste centers of the brain. CALHM1 is expressed specifically in sweet, bitter, and umami taste bud cells.

Mice in which CALHM1 proteins are absent, developed by Feinstein’s Philippe Marambaud, PhD, have severely impaired perceptions of sweet, bitter and umami compounds; whereas, their recognition of sour and salty tastes remains mostly normal. The CALHM1 deficiency affects taste perception without interfering with taste cell development or overall function.

Using the CALHM1 knockout mice, team members from Monell and Feinstein tested how their taste was affected. “The mice are very unusual,” says Monell’s Michael Tordoff, PhD. “Control mice, like humans, lick avidly for sucrose and other sweeteners, and avoid bitter compounds. However, the mice without CALHM1 treat sweeteners and bitter compounds as if they were water. They can’t taste them at all.”

From all lines of evidence, the team concluded that CALHM1 is an ATP-release channel required for sweet, bitter, and umami taste perception. In addition, they found that CALHM1 was also required for  “nontraditional” Polycose, calcium, and aversive high-salt tastes, implying that the deficit displayed in the knockout animals might best be considered as a loss of all GPCR-mediated taste signals rather than simply sweet, bitter and umami taste.

Interestingly, CALHM1 was originally implicated in Alzheimer’s disease, although the link is now less clear. In 2008, co-author Marambaud identified CALHM1 as a risk gene for Alzheimer’s. They discovered that a CALHM1 genetic variant was more common among people with Alzheimer’s and they went on to show that it leads to a partial loss of function. They also found that this novel ion channel is strongly expressed in the hippocampus, a brain region necessary for learning and memory. So far, there is no connection between taste perception and Alzheimer’s risk, but Marambaud suspects that scientists will start testing this hypothesis.

Filed under taste taste bud cells brain cells ion channel neurons taste perception neuroscience science

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