Taste Responses in the Nucleus of the Solitary Tract of Awake Obese Rats Are Blunted Compared With Those in Lean Rats

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.

Reduced Olfactory Bulb Volume in Obesity and Its Relation to Metabolic Health Status

“…More specifically, Thiebaud et al (2014) reported that hyperlipidemic diet in mice and associated obesity leads to a loss of olfactory sensory neurons and a decrease in olfactory function (Thiebaud et al, 2014). Moreover, it might be possible that the neural response to sensory input is blunted as it has been shown in taste processing (Weiss et al, 2019).…”

Persistent epigenetic reprogramming of sweet taste by diet

“…Evidence is emerging that the levels of salt, sugar, and fat in diets can alter taste sensation in humans (3)(4)(5), raising the question of whether these sensory changes may influence food intake, obesity, and metabolic disease (6,7). This idea is supported by a number of recent animal studies that found changes in taste, neural responses, and food preferences in rodents fed high-nutrient diets (8)(9)(10)(11)(12)(13). However, because of the complexity of the mammalian taste system and the lack of genetic tools, we know next to nothing about the molecular mechanisms through which diet composition affects taste sensation and obesity.…”

Dietary sugar inhibits satiation by decreasing the central processing of sweet taste

“…Consumption of diets high in sugar and fat decreases the perception of taste stimuli, influencing food preference and promoting food intake (Bartoshuk et al 2006;Sartor et al 2011;Kaufman et al 2018;Ahart et al 2019;May et al 2019;Weiss et al 2019) . Recent studies have examined the effects of these diets on the sensitivity of the peripheral taste system and the intensity of taste experience (Maliphol, Garth, and Medler 2013;Kaufman et al 2018;May et al 2019;Weiss et al 2019) , but how exactly taste deficits increase feeding behavior is not known.…”