Capsaicin-sensitive intestinal mucosal afferent mechanism and body fat distribution

Leung, Felix W.

doi:10.1016/j.lfs.2008.04.018

Cited by 62 publications

(43 citation statements)

References 36 publications

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“…One potential role could be in adjustment of energy expenditure by controlling the intake of nutrients and fat. Recently it was shown that intra-abdominal desensitization of TRPV1 blocks the regulation of body temperature (54), and control of adipocyte fat storage by TRPV1 has been documented (31). Because vanilloids are used clinically, a clear characterization of their targets/receptors will be necessary to fully understand their mode of actions (TRPV1 dependent or not) on the different tissues to avoid potential side effects.…”

Section: Discussionmentioning

confidence: 99%

Capsaicin induces NKCC1 internalization and inhibits chloride secretion in colonic epithelial cells independently of TRPV1

Bouyer

Tang

Weber

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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Colonic chloride secretion is regulated via the neurohormonal and immune systems. Exogenous chemicals (e.g., butyrate, propionate) can affect chloride secretion. Capsaicin, the pungent ingredient of the chili peppers, exerts various effects on gastrointestinal function. Capsaicin is known to activate the transient receptor potential vanilloid type 1 (TRPV1), expressed in the mesenteric nervous system. Recent studies have also demonstrated its presence in epithelial cells but its role remains uncertain. Because capsaicin has been reported to inhibit colonic chloride secretion, we tested whether this effect of capsaicin could occur by direct action on epithelial cells. In mouse colon and model T84 human colonic epithelial cells, we found that capsaicin inhibited forskolin-dependent short-circuit current (FSK-I(sc)). Using PCR and Western blot, we demonstrated the presence of TRPV1 in colonic epithelial cells. In T84 cells, TRPV1 localized at the basolateral membrane and in vesicular compartments. In permeabilized monolayers, capsaicin activated apical chloride conductance, had no effect on basolateral potassium conductance, but induced NKCC1 internalization demonstrated by immunocytochemistry and basolateral surface biotinylation. AMG-9810, a potent inhibitor of TRPV1, did not prevent the inhibition of the FSK-I(sc) by capsaicin. Neither resiniferatoxin nor N-oleoyldopamine, two selective agonists of TRPV1, blocked the FSK-I(sc). Conversely capsaicin, resiniferatoxin, and N-oleoyldopamine raised intracellular calcium ([Ca(2+)](i)) in T84 cells and AMG-9810 blocked the rise in [Ca(2+)](i) induced by capsaicin and resiniferatoxin suggesting the presence of a functional TRPV1 channel. We conclude that capsaicin inhibits chloride secretion in part by causing NKCC1 internalization, but by a mechanism that appears to be independent of TRPV1.

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Section: Discussionmentioning

confidence: 99%

Capsaicin induces NKCC1 internalization and inhibits chloride secretion in colonic epithelial cells independently of TRPV1

Bouyer

Tang

Weber

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…In accord, desensitization of these nerves to RTX exerts a marked antiemetic effect in different species, including dogs and ferrets (Yamakuni et al, 2002). Furthermore, mice fed capsaicin-containing chow gain less weight compared with littermates on a regular diet (Zhang et al, 2007b;Leung, 2008). In addition, there is anecdotal evidence that human capsaicin consumption leads to early satiety and weight loss (see Whiting et al, 2012).…”

Section: Transient Receptor Potential Channels: Acquired Diseasesmentioning

confidence: 99%

Transient Receptor Potential Channels as Drug Targets: From the Science of Basic Research to the Art of Medicine

2014

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“…Capsaicin administration could regulate adipose tissue distribution by activating intestinal mucosal afferent nerves and modulate visceral adipose tissue blood flow. Activation of intestinal mucosal afferent could be a mechanism by which visceral obesity can be reduced [146]. Administration TRPV1 agonists is associated with the loss of abdominal fat and oxidation of fat [147].…”

Section: Trpv1 and Metabolic Disordersmentioning

confidence: 99%

Disease-Related Changes in TRPV1 Expression and Its Implications for Drug Development

Premkumar¹,

Bishnoi²

2011

CTMC

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The transient receptor potential vanilloid 1 (TRPV1) channel has been a topic of great interest, since its discovery in 1997. It is a homotetrameric non-selective cation channel predominantly expressed in a population of sensory neurons and its involvement in different modalities of pain has been extensively studied. However, TRPV1 has also been shown to be expressed in non-sensory neurons and non-neuronal cells. TRPV1 is considered as a potential target for drug development, based on its tissue distribution and its role in physiological functions. Here, we summarize the evidences for disease-related alterations in TRPV1 expression and function and review the current perspectives for the therapeutic potential of TRPV1 agonists and antagonists in the treatment of a wide range of diseases.

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Capsaicin-sensitive intestinal mucosal afferent mechanism and body fat distribution

Cited by 62 publications

References 36 publications

Capsaicin induces NKCC1 internalization and inhibits chloride secretion in colonic epithelial cells independently of TRPV1

Capsaicin induces NKCC1 internalization and inhibits chloride secretion in colonic epithelial cells independently of TRPV1

Transient Receptor Potential Channels as Drug Targets: From the Science of Basic Research to the Art of Medicine

Disease-Related Changes in TRPV1 Expression and Its Implications for Drug Development

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