Abstract
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.
Highlights
The idea that obesity, an epidemic for United States adults (Ogden et al, 2015), is caused by a chronic surplus of energy from food belies the complexity of its etiology, and the obesity-related changes that occur in the body
Because we have shown that cells in the nucleus tractus solitarius (NTS) of awake rats respond to both taste and odor stimuli (Escanilla et al, 2015), we hypothesized that the optimal stimuli for NTS cells would be those that represented actual food, i.e., naturalistic tastants
Body Composition data from 14 lean rats and 7 dietinduced obesity (DIO) rats revealed that rats fed a 45% high fat diet (HED) had a significantly different body composition compared to animals on a standard lab diet, F(1,54) = 62.0, p < 0.0001 (Figure 1)
Summary
The idea that obesity, an epidemic for United States adults (Ogden et al, 2015), is caused by a chronic surplus of energy from food belies the complexity of its etiology, and the obesity-related changes that occur in the body. An increase in visceral fat is negatively correlated with both olfactory and taste function (Fernandez-Garcia et al, 2017). In both humans and rodents, taste sensitivity changes with body weight, for taste. It is unsurprising that there are multiple taste-related neural structures that are sensitive to an animal’s internal state. A high protein diet (Darcel et al, 2005), changes in blood glucose (Giza and Scott, 1983), changes in blood insulin (Giza and Scott, 1987), gastric distention (Baird et al, 2001), and obesity (Kovacs and Hajnal, 2008) can all alter taste processing in the brain
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