Systemic administration of anorexic gut peptide hormones impairs hedonic-driven sucrose consumption in mice

Physiol Behav. 2017 Mar 15:171:158-164. doi: 10.1016/j.physbeh.2016.12.034. Epub 2016 Dec 28.

Abstract

A number of reports suggest that gut hormones such as cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1), and peptide YY(3-36) (PYY3-36), which are released postprandially, suppress homeostatic food intake and result in satiety and the termination of feeding. However, it remains unclear whether these peptide hormones also suppress non-homeostatic consumption of palatable foods or fluids. To examine whether gut hormones reduce hedonically motivated sugar consumption, we assessed the effects of intraperitoneal administration of these gut hormones on the consumption of a highly palatable sucrose solution, using a mouse model we previously established for binge-like sucrose overconsumption (Yasoshima and Shimura, 2015). To reduce homeostatic hunger, chow was available at nighttime prior to testing. After a limited-access training procedure for 10days, during which access to both sucrose and chow were controlled, on the test day, control mice injected with saline consumed significantly more sucrose than during the pre-training period. In contrast, sucrose consumption on the test day in the mice injected with CCK-8 (2 and 4μg/kg), GLP-1 (500 and 1000nmol/kg), or PYY3-36 (12.5 and 25nmol/kg) was significantly less than that in saline-injected mice. In a separate cohort of mice, the higher doses of CCK-8 and GLP-1 and a greater dose of PYY3-36 (50nmol/kg) did not produce conditioned taste aversion to saccharin, suggesting that the doses of exogenous hormones in the present study do not cause aversive visceral distress. The present findings suggest that the systemic administration of these three gut hormones suppresses hedonic-driven sugar consumption due to the anorexic, but not aversive-visceral, effects of these hormones.

Keywords: Cholecystokinin; Conditioned taste aversion; Glucagon-like peptide 1; Hedonic-driven consumption; Peptide YY(3–36); Sucrose.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Antimanic Agents / pharmacology
  • Avoidance Learning / drug effects
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Eating / drug effects*
  • Gastrointestinal Hormones / pharmacology*
  • Glucagon-Like Peptide 1 / pharmacology
  • Lithium Chloride / pharmacology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Peptide Fragments / pharmacology
  • Peptide YY / pharmacology
  • Philosophy
  • Sincalide / pharmacology
  • Sucrose / administration & dosage*
  • Sweetening Agents / administration & dosage*
  • Taste / drug effects
  • Time Factors

Substances

  • Antimanic Agents
  • Gastrointestinal Hormones
  • Peptide Fragments
  • Sweetening Agents
  • Peptide YY
  • peptide YY (3-36)
  • Sucrose
  • Glucagon-Like Peptide 1
  • Lithium Chloride
  • Sincalide