Gut vagal afferents are necessary for the eating-suppressive effect of intraperitoneally administered ginsenoside Rb1 in rats

Ling Shen, David Q.H. Wang, Chunmin C. Lo, Myrtha Arnold, Patrick Tso, Stephen C. Woods, Min Liu

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Ginsenoside Rb1 (Rb1) reduces food intake in both lean and high-fat diet induced-obese rats; however, the sites and/or mediation of the eating-suppressive effect of Rb1 have not previously been identified. We hypothesized that intraperitoneally (ip) administered Rb1 exerts its anorectic action by enhancing sensitivity to satiation signals, such as cholecystokinin (CCK), and/or that it acts through vagal afferent nerves that relay the satiating signaling to the hindbrain. To test these hypotheses, we gave ip bolus doses of Rb1 (2.5-10.0. mg/kg) and CCK-8 (0.125-4.0. μg/kg) alone or in combination and assessed food intake in rats. Low doses of Rb1 (2.5. mg/kg) or CCK-8 (0.125. μg/kg) alone had no effect on food intake whereas higher doses did. When these subthreshold doses of Rb1 and CCK-8 were co-administered, the combination significantly reduced food intake relative to saline controls, and this effect was attenuated by lorglumide, a selective CCK1-receptor antagonist. Interestingly, lorglumide blocked food intake induced by an effective dose of CCK-8 alone, but not by Rb1 alone, suggesting that Rb1's anorectic effect is independent of the CCK1 receptor. To determine whether peripherally administered Rb1 suppresses feeding via abdominal vagal nerves, we evaluated the effect of ip Rb1 injection in subdiaphragmatic vagal deafferentation (SDA) and control rats. Rb1's effect on food intake was significantly attenuated in SDA rats, compared with that in SHAM controls. These data indicate that the vagal afferent system is the major pathway conveying peripherally administered Rb1's satiation signal.

Original languageEnglish (US)
Pages (from-to)62-67
Number of pages6
JournalPhysiology and Behavior
Volume152
DOIs
StatePublished - Dec 1 2015
Externally publishedYes

Fingerprint

Eating
Satiation
Appetite Depressants
Rhombencephalon
Cholecystokinin
High Fat Diet
ginsenoside Rb1
Injections
cholecystokinin 8
lorglumide

Keywords

  • CCK
  • Food intake
  • Ginsenoside
  • Vagus nerve

ASJC Scopus subject areas

  • Experimental and Cognitive Psychology
  • Behavioral Neuroscience

Cite this

Gut vagal afferents are necessary for the eating-suppressive effect of intraperitoneally administered ginsenoside Rb1 in rats. / Shen, Ling; Wang, David Q.H.; Lo, Chunmin C.; Arnold, Myrtha; Tso, Patrick; Woods, Stephen C.; Liu, Min.

In: Physiology and Behavior, Vol. 152, 01.12.2015, p. 62-67.

Research output: Contribution to journalArticle

Shen, Ling ; Wang, David Q.H. ; Lo, Chunmin C. ; Arnold, Myrtha ; Tso, Patrick ; Woods, Stephen C. ; Liu, Min. / Gut vagal afferents are necessary for the eating-suppressive effect of intraperitoneally administered ginsenoside Rb1 in rats. In: Physiology and Behavior. 2015 ; Vol. 152. pp. 62-67.
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AU - Tso, Patrick

AU - Woods, Stephen C.

AU - Liu, Min

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AB - Ginsenoside Rb1 (Rb1) reduces food intake in both lean and high-fat diet induced-obese rats; however, the sites and/or mediation of the eating-suppressive effect of Rb1 have not previously been identified. We hypothesized that intraperitoneally (ip) administered Rb1 exerts its anorectic action by enhancing sensitivity to satiation signals, such as cholecystokinin (CCK), and/or that it acts through vagal afferent nerves that relay the satiating signaling to the hindbrain. To test these hypotheses, we gave ip bolus doses of Rb1 (2.5-10.0. mg/kg) and CCK-8 (0.125-4.0. μg/kg) alone or in combination and assessed food intake in rats. Low doses of Rb1 (2.5. mg/kg) or CCK-8 (0.125. μg/kg) alone had no effect on food intake whereas higher doses did. When these subthreshold doses of Rb1 and CCK-8 were co-administered, the combination significantly reduced food intake relative to saline controls, and this effect was attenuated by lorglumide, a selective CCK1-receptor antagonist. Interestingly, lorglumide blocked food intake induced by an effective dose of CCK-8 alone, but not by Rb1 alone, suggesting that Rb1's anorectic effect is independent of the CCK1 receptor. To determine whether peripherally administered Rb1 suppresses feeding via abdominal vagal nerves, we evaluated the effect of ip Rb1 injection in subdiaphragmatic vagal deafferentation (SDA) and control rats. Rb1's effect on food intake was significantly attenuated in SDA rats, compared with that in SHAM controls. These data indicate that the vagal afferent system is the major pathway conveying peripherally administered Rb1's satiation signal.

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