Mice learn to identify and discriminate sugar solutions based on odor cues.

This study examined how olfaction impacts ingestive responses of mice to sugar solutions. Experiment 1 asked whether naïve C57BL/6 (B6) mice could identify 1 M glucose, fructose, or sucrose solutions based on odor cues, during a 30-min 2-bottle acceptability test. We tested mice both before and after they were rendered anosmic with ZnSO4 treatment. We used 2 indirect measures of odor-mediated response: number of trials initiated and latency to initiate licking. Before ZnSO4 treatment, the mice learned how to identify 1 M glucose and fructose (but not sucrose) solutions based on odor cues. ZnSO4 treatment eliminated their ability to identify the glucose and fructose solutions. Experiment 2 asked whether 2 d of exposure to a 1 M glucose, fructose, or sucrose solution improved the identification of the same sugar solution. Following exposure, the B6 mice identified all 3 sugar solutions based on odor cues. Experiment 3 asked whether T1R3 knockout mice (i.e. mice lacking the T1R3 subunit of the T1R2 + R3 sweet taste receptor) could learn to discriminate 0.44 M glucose and fructose solutions based on odor cues. All mice were subjected to a 1-h preference test, both before and after exposure to the 0.44 M glucose and fructose solutions. During exposure, the experimental mice received ZnSO4 treatment, whereas the control mice received saline treatment. Before exposure, neither type of mouse preferred the glucose solution. After exposure, the control mice preferred the glucose solution, whereas the experimental mice did not. Our results reveal that mice can learn to use odor cues to identify and discriminate between sugar solutions.

Individual differences in cephalic-phase insulin response are stable over time and predict glucose tolerance in mice.

Oral stimulation by glucose triggers a rapid insulin response, which enhances glucose tolerance. This so-called cephalic-phase insulin response (CPIR) has been documented in many mammal species, but its functional properties are poorly characterized. Here, we studied CPIR in lean C57BL/6 mice. Experiment 1 asked whether the large individual differences in CPIR magnitude were real or reflected experimental noise. We measured CPIR magnitude four times across a period of 30 days in the same mice. The individual differences in CPIR magnitude were remarkably stable across the repeated trials, indicating that they were real. Experiment 2 examined the functional consequences of individual differences in CPIR magnitude. We found that higher CPIR magnitudes contributed to larger postprandial insulin responses and greater glucose tolerance. Experiment 3 examined the observation that the CPIRs in Experiments 1 and 2 were associated with a rapid rise in blood glucose. To determine whether the rapid rise in blood glucose caused the CPIRs, we asked whether mice would generate a CPIR if we prevented cephalic-phase stimulation of beta cells by either delivering the glucose intragastrically or blocking parasympathetic input to the pancreatic beta cells with atropine. The mice subjected to these treatments experienced a rapid rise in blood glucose, but they did not exhibit a CPIR. This indicates that it was the oral glucose stimulation, and not the rise in blood glucose, that triggered the CPIRs in Experiments 1 and 2. We conclude that (i) individual differences in CPIR magnitude are stable over time; (ii) CPIR magnitudes predicted postprandial insulin responses and glucose tolerance; and (iii) a rapid rise in blood glucose is not sufficient to trigger a CPIR in mice.