TRPV1 Desensitization Abolishes Metabolic Effects of Time-Restricted Feeding in Rats

Jun 28, 2025Journal of biological rhythms

Blocking TRPV1 Stops Metabolic Benefits of Time-Restricted Feeding in Rats

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Abstract

Rats treated with the TRPV1 agonist resiniferatoxin (RTX) demonstrated changes in locomotor activity and body temperature during time-restricted feeding (TRF) but did not show certain metabolic improvements.

TRF is associated with increased spontaneous locomotor activity before mealtime and a phase shift in clock gene expression, especially in the liver.
RTX treatment resulted in increased locomotor activity and body temperature at the beginning of the light phase.
While RTX-treated rats experienced decreased body weight gain and food intake compared to fed controls, they did not show reduced oxygen consumption or improved glucose tolerance typically induced by TRF.
RTX treatment eliminated the temporal changes in the expression of specific clock genes and leptin levels in the liver.
The findings suggest that TRPV1 may play a role in mediating the metabolic changes associated with TRF through its influence on liver gene expression and leptin secretion.

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Time-restricted feeding (TRF) can improve metabolic outcomes. Rodents experiencing TRF exhibit an increase in spontaneous locomotor activity before mealtime and show a phase shift in the rhythm of clock gene expression in peripheral organs, particularly in the liver. Because activation of the transient receptor potential vanilloid-1 (TRPV1) channel produces similar beneficial effects on metabolism as TRF, we hypothesized that this channel mediates the metabolic changes induced by TRF. To assess the role of TRPV1 in metabolism and circadian responses, we utilized the agonist resiniferatoxin (RTX), which at a dosage of 20 µg/kg desensitizes TRPV1. After treatment with RTX or its vehicle, adult male rats were exposed to 21 days of TRF during the light phase. RTX-treated rats show some effects of TRF similar to vehicle-treated controls, with increased locomotor activity and body temperature at the beginning of the light phase, decreased body weight gain and food intake relative to-fed controls. However, RTX-treated rats did not show a decrease in VOconsumption or an improvement in glucose tolerance induced by TRF. In addition, RTX treatment eliminated the temporal changes in the expression of clock genesandin the liver as well as leptin blood levels. In addition, RTX abolished the temporal alterations of thegene in the liver, which encodes a protein that negatively modulates insulin signaling without affecting the expression of insulin,, or other clock genes in the liver. In conclusion, TRPV1 may participate in the TRF-induced alterations in metabolism, most likely through its regulation of the temporal changes in,, andexpressions in the liver, along with leptin secretion. ad-libitum Per1Rev-Erba Trb3Ppar, Pck1, G6pc α Per1Rev-Erba Trb3 2

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TRPV1 Desensitization Abolishes Metabolic Effects of Time-Restricted Feeding in Rats

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