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Hormone dynamics

L-cell key to hormone dynamics post-RYGB

RYGB in rats was associated with gut hypertrophy and increased PYY and preproglucagon gene expression

The production of L-cell following Roux-en-Y gastric bypass (RYGB) in rats could be the key to explaining the enhanced gut hormone dynamics following a bypass procedure, according to a study published online in the journal Plos One.The study authors claim that this latest study showed that RYGB in rats was associated with gut hypertrophy, an increase in L-cell number, but not density, and increased peptide YY (PYY) and preproglucagon gene expression.

Although it is known that RYGB leads to a rapid remission of type 2 diabetes mellitus, the underlying mode of action is not fully understood. It is believed that L-cell derived gut hormones such as glucagon-like peptide-1 (GLP-1) and PYY play a key role in the anti-diabetic effects of the bypass procedure.

Therefore, the authors sought investigate the mechanisms by which both these hormones are produced and secreted primarily as a result of an increase in the number of enteroendocrine cells (endocrine L-cells).

Using 15 male normoglycemic Wistar rats (weight 432±7.1g), investigators recorded the quantitative morphological changes in the gut after RYGB, as well as alterations in the number and distribution of endocrine L-cells in the intestine. Five rats underwent RYGB and ten a sham-operation.

Results

They researchers report that after a short initial period of postoperative weight loss, SHAM rats returned to normal weight gain for the remainder of the study. At the day of termination, the body weight in the SHAM group was significantly higher than in the RYGB group (SHAM 617±10.8 and RYGB 395±19.2; p<0.001).

The RYGB surgery induced hypertrophy of the gut mucosa in the food exposed regions of the small intestine coupled with a doubling in the total number of L-cells. No changes in L-cell density were observed in any region regardless of surgery or food restriction.

The total gene expression capacity of the entire gut revealed a near 200% increase in both PYY and preproglucagon mRNA levels in RYGB rats associated with both increased L-cell number, as well as region-specific increased transcription per cell.

The marked mucosal hypertrophy in RYGB animals was observed in all food exposed gut regions (alimentary channel, common channel and colon) but not the bypassed biliopancreatic limb. The greatest increase in RYGB mucosa volume was observed in the alimentary channel (150%, p<0.001), followed by the common channel (140%, p<0.01) and colon, though the latter did not reach statistical significance (50%, p>0.05).

The greatest increase in L-cell number was confined to the alimentary channel (170%, p<0.001) followed by the common channel (130%, p<0.05) and the colon, though the latter did not reach statistical significance (40%, p>0.05).

The authors report that the total and regional L-cell density remained unchanged among groups, with L-cell density was lowest in the duodenal region with increasing density along the proximal-distal axis. L-cell density was highest in the distal jejuno-ileum (common channel) and was slightly lower in the colon.

“The present study provides the first stereological report of morphological changes in the rat gut after RYGB surgery,” the authors write. “We show that this particular type of bariatric surgery results in a more than doubling of total mucosa volume in the small intestine with concomitant increases in the absolute number of L-cells, without affecting L-cell density.”

“The data suggest that elevated GLP-1 and PYY hormone levels after RYGB surgery are a consequence of L-cell proliferation secondary to gut hypertrophy and hereby provide further insight into the possible mechanisms underlying the marked remission of T2DM following RYGB,” the authors conclude.

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