Peptide YY and glucagon-like peptide-1 contribute to decreased food intake after Roux-en-Y gastric bypass surgery

Abstract

Blockade of actions from only one of the two L-cell hormones, GLP-1 and PYY, resulted in concomitant increased secretion of the other, probably explaining the absent effect on food intake on these experimental days. Combined blockade of GLP-1 and PYY actions increased food intake after RYGB, supporting that these hormones have a role in decreased food intake postoperatively.

Anti-Obesity Therapy: from Rainbow Pills to Polyagonists

“…These data suggest that enhanced GLP-1 action alone cannot explain the metabolic benefits of this surgery. Consistent with this notion, singular inhibition of either GLP-1 or PYY alone does not affect food intake in humans following RYGB (Svane et al, 2016). However, as shown in the same study, when GLP-1 and PYY signaling are both collectively blocked, food consumption is increased by ;20%.…”

“…However, as shown in the same study, when GLP-1 and PYY signaling are both collectively blocked, food consumption is increased by ;20%. Consequently, it has been proposed repeatedly that GLP-1, when acting in concert with other gastrointestinal peptides, might play a role in the sustained weight loss associated with bariatric surgery (Svane et al, 2016). Notably, also signaling via the farnesoid-X-activated receptor seems to play an important role in the metabolic benefits achieved by bariatric surgery because the efficacy of VSG to decrease body weight is strikingly reduced in mice lacking farnesoid-X-activated receptor (Ryan et al, 2014).…”

“…Endocrine changes in gastrointestinal hormone secretion following RYGB or VSG include enhanced postprandial secretion of GLP-1 (le Roux et al, 2006;Korner et al, 2007;Isbell et al, 2010;Jacobsen et al, 2012;BojsenMoller et al, 2014;Svane et al, 2016) and peptide YY (PYY) (le Roux et al, 2006;Svane et al, 2016), whereas circulating levels of glucose-dependent insulinotropic polypeptide (GIP) and ghrelin are typically diminished (Cummings et al, 2002;Korner et al, 2007). The observation that RYGB and VSG lead increased postprandial GLP-1 secretion has widely resulted in the hypothesis that enhanced GLP-1 action contributes to reduced food intake, weight loss, and improved glucose metabolism typically observed after these surgical procedures.…”

Enteroendocrine K and L cells in healthy and type 2 diabetic individuals

“…Biopsies were sampled from nine anatomically well-defined areas: the duodenum (1), the area around the ligament of Treitz (2), the ileocaecal region (10), caecum (11), ascending colon (12), transverse colon (13), descending colon (14), sigmoid colon (15) and rectum (16). Furthermore, biopsies were taken every 30 cm in the small intestine and divided equally into seven groups (3)(4)(5)(6)(7)(8)(9) Immunohistochemistry The other biopsy sampled from each site was immediately fixated and then embedded in paraffin, cut in thin slide sections and dewaxed. Subsequently, antigen retrieval was performed, with incubations with (1) specific primary antibodies, (2) a second layer of antibodies and (3) a third layer of an avidin-biotin complex.…”

“…Enteroendocrine cells and their secretory products have turned out to constitute important players in the regulation of glucose homeostasis and appetite [1][2][3][4]. Some of the most exhaustively studied gut hormones are the so-called incretin hormones: glucose-dependent insulinotropic polypeptide (GIP) from enteroendocrine K cells, and glucagon-like peptide-1 (GLP-1) from enteroendocrine L cells [5,6].…”