Oxytocin decreases sweet taste sensitivity in mice

Abstract

Oxytocin (OXT) suppresses food intake and lack of OXT leads to overconsumption of sucrose. Taste bud cells were recently discovered to express OXT-receptor. In the present study we tested whether administering OXT to wild-type mice affects their licking behavior for tastants in a paradigm designed to be sensitive to taste perception. We injected C57BL/6J mice intraperitoneally (i.p.) with 10 mg/kg OXT and assayed their brief-access lick responses, motivated by water deprivation, to NaCl (300 mM), citric acid (20 mM), quinine (0.3 mM), saccharin (10 mM), and a mix of MSG and IMP (100 mM and 0.5 mM respectively). OXT had no effect on licking for NaCl, citric acid, or quinine. A possible effect of OXT on saccharin and MSG+IMP was difficult to interpret due to unexpectedly low lick rates to water (the vehicle for all taste solutions), likely caused by the use of a high OXT dose that suppressed licking and other behaviors. A subsequent experiment focused on another preferred tastant, sucrose, and employed a much lower OXT dose (0.1 mg/kg). This modification, based on our measurements of plasma OXT following i.p. injection, permitted us to elevate plasma [OXT] sufficiently to preferentially activate taste bud cells. OXT at this low dose significantly reduced licking responses to 0.3 M sucrose, and overall shifted the sucrose concentration – behavioral response curves rightward (mean EC50saline = 0.362 M vs. EC50OXT = 0.466 M). Males did not differ from females under any condition in this study. We propose that circulating oxytocin is another factor that modulates taste-based behavior.

Cocaine decreases saccharin preference without altering sweet taste sensitivity

“…Training Day 3 serves to familiarize mice with repeated presentations of varying concentrations of saccharin, representing a novel taste (Sinclair et al , 2014). On Training Day 3 and on all test days, seven bottles were filled with either water or a solution of sodium saccharin (0.9mM, 2mM, 7mM, 9mM, 18mM, or 45mM corresponding to 0.018%, 0.041%, 0.18%, 0.37%, 0.92% g/ml, respectively) and were presented in computer-generated random order.…”

“…This assay has been used to quantify differences of taste sensitivity in mice with mutations in taste-related genes (Tordoff and Ellis, 2013, Treesukosol et al , 2009) and to compare orosensory ability and drug preference for both nicotine (Glatt et al , 2009) and alcohol (Brasser et al , 2012). Brief-access lickometry has been optimized to elicit concentration-dependent licking for different taste stimuli and to effectively separate mice with altered taste function (Glendinning et al , 2002, Sinclair et al , 2014). A brief-access lickometer assay generates a concentration-response curve of the acceptance of a taste stimulus.…”

Oxytocin – The Sweet Hormone?

“…These studies typically show reductions in food intake, and Ott et al [82] reported a marked reduction in intake of sweet snacks after intranasal administration of 24 IU (~50µg). This does not necessarily imply a central action, as in humans and in mice, taste buds express oxytocin receptors [8], and in mice oxytocin decreases sweet taste sensitivity [83]. Intranasal oxytocin has also been reported to improve glucose tolerance by effects on pancreatic beta cells [84].…”

Can We Selectively Reduce Appetite for Energy-Dense Foods? An Overview of Pharmacological Strategies for Modification of Food Preference Behavior

“…Indeed, peripherally administered oxytocin reduced food intake in humans [ 357 ] and animals [ 358 - 361 ]. Rodent studies indicated that endogenous oxytocin was an inhibitor of carbohydrate (especially sucrose) but not fat intake [ 362 - 364 ] that decreased sweet taste sensitivity [ 365 ]. Importantly, these findings were confirmed by human studies reporting the suppressory effect of intranasal oxytocin on snack, i.e.…”