# Glucose-dependent insulinotropic polypeptide stimulates post-absorptive lipid secretion in the intestine

## TL;DR

This study shows that glucose in the intestine, not in the blood, triggers the release of stored fats via the hormone GIP.

## Contribution

The study identifies GIP as a key hormone in stimulating intestinal lipid release during the post-absorptive state.

## Key findings

- Intraduodenal glucose increases GIP levels and intestinal lipid output.
- Intravenous glucose does not stimulate intestinal lipid output.
- GIP administration alone stimulates lipid release from the intestine.

## Abstract

It is increasingly recognized that the intestine can retain a portion of dietary fats for secretion during the post-absorptive state, which has strong implications in metabolic diseases. The regulatory mechanisms of gut lipid storage and release are not well defined. Previous studies showed that the intestine releases locally stored fats in response to several stimulatory cues, such as glucose delivered into the intestinal lumen. It remains unknown how the intestine responds to nutrient signals in this phenomenon. Here we tested the effects of intravenous glucose delivery on intestinal lipid output during the post-absorptive state in mesenteric lymph duct cannulated rats. Compared with intraduodenal glucose delivery, intravenous glucose did not stimulate intestinal lipid output. Intraduodenal glucose was also associated with increases in blood levels of metabolic hormones, among which glucose-dependent insulinotropic peptide (GIP) levels were significantly higher at timepoints corresponding to increased lipid output than in intravenous glucose. Intraperitoneal GIP administration per se robustly stimulated intestinal lipid output. These results support a mechanism that involves glucose sensing at the apical side of the enterocytes and GIP as a potent stimulus for the release of lipid storage from the intestine.