# Taste Changes in a Rat Model of Spinal Cord Injury: Impact of High-Fat Diet and Weight Loss Surgery

## TL;DR

Spinal cord injury in rats changes taste preferences, making them more prone to obesity, and weight loss surgery helps reduce sweet cravings more effectively in these rats.

## Contribution

This study shows that spinal cord injury alters taste functions and that weight loss surgery has a stronger effect on sweet taste responsivity in SCI rats.

## Key findings

- SCI rats showed reduced sucrose licking at high concentrations and increased salt preference before high-fat diet exposure.
- VSG reduced sucrose licking more significantly in SCI rats compared to non-SCI rats.
- cFos staining revealed increased neuronal activation in the dorsal vagal complex after sucrose ingestion in SCI rats.

## Abstract

Background: Approximately two-thirds of individuals with spinal cord injury (SCI) become overweight or obese. Weight loss surgery, including vertical sleeve gastrectomy (VSG), is one of the most effective long-term treatments for obesity and type 2 diabetes. Introduction: The main objective of this study was to test in our diet induced obesity rat model whether subjects respond to VSG in the same way as subjects with or without SCI. Methods: To address this question, male Wistar rats underwent either T3 contusion injuries or sham spinal surgeries (Sham). Following recovery, all rats were fed a high-energy, high-fat diet (HFD) for six weeks before undergoing VSG. Taste responsivity and preferences were assessed at multiple time points. Results: Prior to HFD exposure, SCI rats exhibited significantly reduced lick responses for sucrose at higher concentrations and increased licking for low concentrations of sodium, although 2BC sucrose preference was unchanged. HFD feeding in SCI rats enhanced salt and sucrose licking overall. Importantly, VSG reduced sucrose licking, with SCI rats showing greater sensitivity to this effect. cFos immunohistochemistry further revealed enhanced neuronal activation to sucrose ingestion in the dorsal vagal complex, including the rostral subnucleus of the nucleus of the solitary tract. Discussion and Conclusions: Together, these findings support the hypothesis that SCI alters taste functions, thereby increasing vulnerability to diet-induced obesity and that VSG may restore sweet taste responsivity even more effectively in SCI-associated obesity than in non-SCI obesity. Future studies are needed to clarify the neural and hormonal mechanisms mediating these effects and to determine their translational relevance to human SCI populations.