Oxytocin knockout mice demonstrate enhanced intake of sweet and nonsweet carbohydrate solutions

Abstract

Sclafani A, Rinaman L, Vollmer RR, Amico JA. Oxytocin knockout mice demonstrate enhanced intake of sweet and nonsweet carbohydrate solutions. Am J Physiol Regul Integr Comp Physiol 292: R1828-R1833, 2007. First published February 1, 2007; doi:10.1152/ajpregu.00826.2006.-Oxytocin knockout (OT KO) mice display enhanced intake of nutritive and nonnutritive sweet solutions (i.e., sucrose and saccharin) compared with wild-type (WT) mice of the same C57BL/6 background strain. The present study further investigated the differential behavioral response of OT KO and WT mice to sucrose solutions and also examined intake preferences of OT KO and WT mice for palatable but nonsweet isocaloric solutions of carbohydrate and fat. A progressive ratio operant licking procedure demonstrated that OT KO and WT mice display a similar motivational drive to consume 10% sucrose. A series of two-bottle intake tests revealed that OT KO mice consume significantly larger amounts of both sweet and nonsweet carbohydrate solutions (i.e., sucrose, Polycose, and cornstarch) compared with WT cohorts. Intake pattern analyses revealed that OT KO mice overconsume carbohydrate solutions by initiating more drinking bouts compared with WT mice; bout sizes did not differ between the genotypes. In contrast, OT KO and WT mice did not differ in their intake of Intralipid, a palatable soybean oil emulsion. These findings indicate that the absence of OT in mice does not affect their appetitive drive to consume palatable sucrose solutions. Instead, the absence of OT may increase daily intake of palatable sweet and nonsweet solutions of carbohydrate (but not fat) by selectively blunting or masking processes that contribute to postingestive satiety. ingestive behavior; sucrose; Polycose; cornstarch; lipid; operant licking WE PREVIOUSLY REPORTED THAT oxytocin (OT) signaling pathways modulate intake of sweet solutions in mice. Compared with wild-type (WT) mice of the same C57BL/6 background strain, male and female OT gene knockout (OT KO) mice consume larger volumes of sucrose or saccharin solutions during initial and sustained exposure (3, 6). WT mice reach a plateau in daily sucrose or saccharin intake that is less than 50% of the daily intakes by OT KO mice (3, 6). Thus, the genetic absence of OT in male and female mice enhances their daily consumption of caloric and noncaloric sweet solutions. Despite their differential intake of sweet solutions, age-and sex-matched OT KO and WT mice have similar body weights and display similar hourly and cumulative daily food (i.e., mouse chow) and water intake during basal conditions (14). OT KO and WT mice also display similar water intake after overnight water deprivation (2), and similar food intake after an overnight fast with water available ad libitum (14). Given the apparent lack of effect of OT gene deletion on chow or water intake under basal conditions or after overnight food deprivation, the sustained excessive intake of sweetened water by male and female OT KO mice is striking.The first part of the present st...

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“…The hyperphagic obese KO mice had larger BPs and larger meal sizes than the WT mice suggesting a deficit in within-meal satiety in the KO mice. Sclafani et al (2007) also described a type of satiety deficit in oxytocin KO mice, who had more meals than WT mice. Of note was the finding that the BP for sucrose did not differ between WT and KO mice, indicating that sucrose per se was not more reinforcing, or more palatable, in KO mice.…”

Taste perception, associated hormonal modulation, and nutrient intake

“…Hormones that bind to receptors on taste cells alter the palatability of food and, therefore, intake. Current knowledge of the hormonal modulation of taste function is summarized in Table 1 [60][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75][76][77] and described in greater detail below.…”

“…72 Still, some studies suggest a role in the consumption of sweet and salty foods. 73,74 While these studies postulate an impact on food consumption, oxytocin has not been directly linked to modulation of a specific taste quality.…”

Reward systems and food intake: role of opioids

“…20 Oxytocin-deficient mice show increased intake of carbohydrate solutions (sweet and non-sweet); this effect was interpreted as support for a role of oxytocin in carbohydratespecific satiety. 21 Naloxone potentiated the effects of cholecystokinin and lithium chloride (LiCl) on oxytocin secretion and feeding, 22 and butorphanol, a mixed m/kopioid agonist, reduced the number of c-Fos-positive oxytocin cells in the PVN at a time associated with the termination of feeding. 19 Naltrexone increased c-Fos immunoreactivity in rat arcuate nucleus a-MSH neurons, 23 and chronic morphine administration reduced proopiomelanocortin gene expression and a-MSH levels in the medial basal hypothalamus.…”