Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.

Effects of Intraduodenal Infusion of the Bitter Tastant, Quinine, on Antropyloroduodenal Motility, Plasma Cholecystokinin, and Energy Intake in Healthy Men

´ëÇѼÒÈ­°ü¿îµ¿ÇÐȸÁö 2019³â 25±Ç 3È£ p.413 ~ 422
Bitarafan Vida, Fitzgerald Penelope C. E., Little Tanya J., Meyerhof Wolfgang, Wu Tongzhi, Horowitz Michael, Feinle-Bisset Christine,
¼Ò¼Ó »ó¼¼Á¤º¸
 ( Bitarafan Vida ) 
University of Adelaide Adelaide Medical School

 ( Fitzgerald Penelope C. E. ) 
University of Adelaide Adelaide Medical School
 ( Little Tanya J. ) 
University of Adelaide Adelaide Medical School
 ( Meyerhof Wolfgang ) 
Saarland University Center for Integrative Physiology and Molecular Medicine
 ( Wu Tongzhi ) 
University of Adelaide Adelaide Medical School
 ( Horowitz Michael ) 
University of Adelaide Adelaide Medical School
 ( Feinle-Bisset Christine ) 
University of Adelaide Adelaide Medical School

Abstract


Background/Aims: Nutrient-induced gut hormone release (eg, cholecystokinin [CCK]) and the modulation of gut motility (particularly pyloric stimulation) contribute to the regulation of acute energy intake. Non-caloric bitter compounds, including quinine, have recently been shown in cell-line and animal studies to stimulate the release of gastrointestinal hormones by activating bitter taste receptors expressed throughout the gastrointestinal tract, and thus, may potentially suppress energy intake without providing additional calories. This study aims to evaluate the effects of intraduodenally administered quinine on antropyloroduodenal pressures, plasma CCK and energy intake.

Methods: Fourteen healthy, lean men (25 ¡¾ 5 years; BMI: 22.5 ¡¾ 2.0 kg/m2) received on 4 separate occasions, in randomized, double-blind fashion, 60-minute intraduodenal infusions of quinine hydrochloride at doses totaling 37.5 mg (¡°Q37.5¡±), 75 mg (¡°Q75¡±) or 225 mg (¡°Q225¡±), or control (all 300 mOsmol). Antropyloroduodenal pressures (high-resolution manometry), plasma CCK (radioimmunoassay), and appetite perceptions/gastrointestinal symptoms (visual analog questionnaires) were measured. Ad libitum energy intake (buffet-meal) was quantified immediately post-infusion. Oral quinine taste-thresholds were assessed on a separate occasion using 3-alternative forced-choice procedure.

Results: All participants detected quinine orally (detection-threshold: 0.19 ¡¾ 0.07 mmol/L). Intraduodenal quinine did not affect antral, pyloric or duodenal pressures, plasma CCK (pmol/L [peak]; control: 3.6 ¡¾ 0.4, Q37.5: 3.6 ¡¾ 0.4, Q75: 3.7 ¡¾ 0.3, Q225: 3.9 ¡¾ 0.4), appetite perceptions, gastrointestinal symptoms or energy intake (kcal; control: 1088 ¡¾ 90, Q37.5: 1057 ¡¾ 69, Q75: 1029 ¡¾7 0, Q225: 1077 ¡¾ 88).

Conclusions: Quinine, administered intraduodenally over 60 minutes, even at moderately high doses, but low infusion rates, does not modulate appetite-related gastrointestinal functions or energy intake.

Å°¿öµå

Cholecystokinin; Energy intake; Gastrointestinal hormones; Pylorus; Quinine

¿ø¹® ¹× ¸µÅ©¾Æ¿ô Á¤º¸

  

µîÀçÀú³Î Á¤º¸

KCI
KoreaMed
KAMS