(P16-013-23) Enhancing the Taste Metabolic Signal of Glucose Increases Licking in Rats and Liking in Humans

Objectives: In taste bud cells glucose stimulates sweet taste receptors, T1R2-T1R3, and an oral metabolic signaling (OMS) pathway, which is comprised of glucose transporters (GLUTs & SGLTs), glucokinase, and the ATP-gated potassium channel (K_ATP). We seek to determine first whether OMS influences lick responses to glucose in rats, and second whether activation of both sweet taste and OMS can be manipulated to hyperstimulate licking. Rats show a very strong preference for glucose (G) and saccharin (S) mixture (G+S) and can drink their body-weight of this mixture daily. Less is known of the short-term, oral controls of G+S preference and how the OMS contributes to this robust response. We hypothesize that OMS influences licking for glucose and contributes to appetitive synergy for licking G+S mixtures in rats.

Methods: Eight adult Sprague Dawley rats (4 males, 4 females) were given brief access tests with a concentration range of glucose and its non-metabolizable analog, methyl-D-glucopyranose (MDG), from 167 to 668 mM in a series of 30 sec presentations via a Davis-rig rodent gustometer. The rats were treated with 5 mM tolbutamide, the K_ATP closer (cellular activator), or with vehicle alone immediately prior to testing. Rats were separately tested with G+S and MDG+S. Additionally, five humans (18-58 years old) were asked to rate liking for 167 mM to 1.28 M glucose and MDG on a hedonic scale after rinsing with either 5 mM tolbutamide or vehicle.

Results: At baseline, rats had similar lick responses for glucose and MDG. Pre-treatment with tolbutamide increased licking for glucose, but not MDG. In addition, rats licked twice as much for G+S than for MDG+S. Humans tended to give higher liking ratings for strong concentrations of glucose after the tolbutamide pretreatment.

Conclusions: When oral K_ATP signaling is enhanced, rats and humans increase licking and liking for glucose but not MDG, which cannot be metabolized. Rats avidly lick for a mixture of G+S in brief access tests, but this effect is negated when glucose is replaced with the non-metabolizable glucose analog MDG. These results collectively implicate oral metabolic signaling in the reward and liking of oral carbohydrates. Future investigations will examine the interactions of T1R2-T1R3 signaling and OMS on taste-guided behaviors and neural activity.

Funding Sources: NIH R21, R01 and Busch Biomedical Grants to PASB and NIH R01 to NTB