Summary: High-fat diets produce blunted, more prevalent responses to taste in the brain and weaken the association of taste responses with ingestive behaviors.
Source: Binghamton University
Obesity is connected with a reduced response to taste, according to a new study featuring faculty at Binghamton University, State of University of New York.
Taste perception is known to change with obesity, but the underlying neural changes remain poorly understood.
“It’s surprising that we know so little about how taste is affected by obesity, given that the taste of food is a big factor in determining what we choose to eat,” said Binghamton University Professor of Psychology Patricia Di Lorenzo.
To address this issue, a team of researchers including Di Lorenzo and former graduate student Michael Weiss aimed to detail the effects of obesity on responses to taste stimuli in the nucleus tractus solitarius, a part of the brain involved with taste processing. The researchers recorded the responses to taste stimuli from single cells in the brainstem of rats that were made obese by eating a high-fat diet. They found that taste responses in these obese rats were smaller in magnitude, shorter in duration and took longer to develop, compared with those in lean rats.
These results suggest that a high-fat diet produces blunted, but more prevalent, responses to taste in the brain, and a weakened association of taste responses with ingestive behavior.
While Di Lorenzo stressed that these findings currently only apply to rats, she said that this same process could possibly translate to humans.
“Others have found that the number of taste buds on the tongue are diminished in obese mice and humans, so the likelihood that taste response in the human brain is also blunted is good,” said Di Lorenzo.
She and her team are looking into the effects of gastric bypass surgery on brainstem responses to see if this procedure can recover some or all of the deficits in the taste system.
Source:
Binghamton University
Media Contacts:
John Brhel – Binghamton University
Image Source:
The image is adapted from the Binghamton University news release.
Original Research: Open access
“Taste Responses in the Nucleus of the Solitary Tract of Awake Obese Rats Are Blunted Compared With Those in Lean Rats”. Michael S. Weiss, Andras Hajnal, Krzysztof Czaja and Patricia M. Di Lorenzo.
Frontiers in Integrative Neuroscience. doi:10.3389/fnint.2019.00035
Abstract
Taste Responses in the Nucleus of the Solitary Tract of Awake Obese Rats Are Blunted Compared With Those in Lean Rats
Taste perception changes with obesity but the underlying neural changes remain poorly understood. To address this issue, we recorded taste responses from single cells in the nucleus tractus solitarius (NTS, the first synapse in the central gustatory circuit) in awake, diet-induced obese [(DIO; ≥ 8 weeks on a high-energy diet (45%fat, 17% sugar; HED)], and lean rats. Rats were implanted with a bundle of microelectrodes in the NTS and allowed to recover. Water-deprived rats were allowed to freely lick various tastants in an experimental chamber. Taste stimuli included an array of sapid stimuli dissolved in artificial saliva (AS). Each taste trial consisted of five consecutive licks followed by five AS licks presented on a VR5 schedule. Results showed that taste responses (n = 49 for DIO; n = 74 for lean rats) in NTS cells in DIO rats were smaller in magnitude, shorter in duration, and longer in latency that those in lean rats. However, there were proportionately more taste-responsive cells in DIO than in lean rats. Lick coherence in DIO rats was significantly lower than in lean rats, both in taste-responsive, and lick-related cells (n = 172 in lean; n = 65 in DIO). Analyses of temporal coding showed that taste cells in DIO rats conveyed less information about taste quality than cells in lean rats. Collectively, results suggest that a HED produces blunted, but more prevalent, responses to taste in the NTS, and a weakened association of taste responses with ingestive behavior. These neural adaptations may represent both negative effects and compensatory mechanisms of a HED that may underlie deficits in taste-related behavior associated with obesity.
