Fructose- and glucose-conditioned preferences in FVB mice: strain differences in post-oral sugar appetition

Abstract

Recent studies indicate that, unlike glucose, fructose has little or no post-oral preference conditioning actions in C57BL/6J (B6) mice. The present study determined whether this is also the case for FVB mice, which overconsume fructose relative to B6 mice. In experiment 1, FVB mice strongly preferred a noncaloric 0.1% sucralose ϩ 0.1% saccharin (SϩS) solution to 8% fructose in a 2-day choice test but switched their preference to fructose after separate experience with the two sweeteners. Other FVB mice displayed a stronger preference for 8% glucose over SϩS. In a second experiment, ad libitum-fed FVB mice trained 24 h/day acquired a significant preference for a flavor (CSϩ) paired with intragastric (IG) selfinfusions of 16% fructose over a different flavor (CSϪ) paired with IG water infusions. IG fructose infusions also conditioned flavor preferences in food-restricted FVB mice trained 1 h/day. IG infusions of 16% glucose conditioned stronger preferences in FVB mice trained 24-or 1 h/day. Thus, fructose has post-oral flavor conditioning effects in FVB mice, but these effects are less pronounced than those produced by glucose. Further studies of the differential post-oral conditioning effects of fructose and glucose in B6 and FVB mice should enhance our understanding of the physiological processes involved in sugar reward.post-oral flavor conditioning; sucralose; saccharin; C57BL/6J mice IT IS WELL ESTABLISHED THAT inbred mouse strains differ in their taste responses to caloric and noncaloric sweeteners. This is due, in part, to allelic variations in the Tas1r3 gene that encodes the T1r3 sweet taste receptor protein (6,25). Mouse strains with the Sac B variant of the Tas1r3 gene are more sensitive to sugars (e.g., sucrose) and noncaloric sweeteners (e.g., saccharin) than are strains with the Sac D variant. In addition, sugar intake and preference are stimulated by the post-oral actions of sugars, a process referred to as appetition to distinguish it from the satiation process that inhibits sugar intake (27). Appetition is demonstrated by the intake and preference-stimulating effects of intragastric (IG) sugar infusions in mice and rats (3,21,27,30). Conceivably, strain differences in post-oral sugar appetition may contribute to variations in sugar intake in mice, but this has yet to be documented. One study reported mouse strain differences in sugar-conditioned flavor preferences, but because the sugars were orally consumed, the conditioning effects may have been mediated by the taste and/or post-oral actions of the sugars (24). In another study, we compared IG sucrose conditioning in The present study sought evidence for strain differences in the post-oral conditioning response to glucose and fructose, the constituent monosaccharide sugars of sucrose. B6 mice acquire strong preferences for flavors paired with IG glucose infusions but fail to prefer flavors paired with isocaloric fructose infusions (29, 43). Related findings were obtained with B6 mice given oral choice tests with 8% glucose or 8% fructose vs. a ...

The role of dopamine in the pursuit of nutritional value

“…Glucose is the most commonly used nutrient in experiments of this kind and other sugars that support conditioning include sucrose, maltose, and polycose [41,46]. Interestingly, in most situations fructose does not support conditioning [47][48][49] suggesting that it is not simply caloric value that drives this process, but rather nutrient-specific signalling mechanisms [50,51]. A number of flavours have been used in this paradigm and flavour-nutrient preferences even develop to innately aversive flavours, such as sour-or bitter-tasting compounds, after pairing with nutrients [43].…”

Does Nutrient Sensing Determine How We “See” Food?

“…Importantly, and similar to the negative feedback mechanisms described above, the reinforcement quality of intestinal nutrients, however, is not determined by the energy density alone. While initial evidence supported intestinal calories rather than nutrient condition preferences (i.e., lipids and glucose being equipotent) [84], subsequent work demonstrates that lipids are less potent than carbohydrates when infused isocalorically [86]. Furthermore, for each nutrient, the reinforcing quality is a function of concentration and follows an inverse U-shaped curve [97,98].…”

“…Both carbohydrates and lipids activate brain reward centers that contribute to increased food consumption. Similar to the gut and brain being important regulators of energy homeostasis (described above), these organs stimulate consumption and induce conditioning of food intake and preference [84].…”

“…For example, intestinal lipid or carbohydrate infusions stimulate intake of a paired non-calorically flavored solution as well as increase the preference of the paired solution [85]. This collective process is aptly named "appetition" [84]. Intestinal nutrient reinforcement is an incredibly strong phenomenon as well with reinforcement occurring after a single infusion [86] and persisting up to weeks following the initial infusion [87].…”

“…Furthermore, for each nutrient, the reinforcing quality is a function of concentration and follows an inverse U-shaped curve [97,98]. Part of this reason may be due to highly concentrated nutrients stimulating intestinal satiety signals and interfering with the stimulatory signals evoked by intestinal nutrients [84]. Thus, while appetition and satiation may share nutrient-sensing mechanisms, the signals are likely to be different as intestinal satiety signals do not generally condition preferences [99,100].…”