More Bypass => More Satiety => Less Food Intake

In a model of direct glucose delivery to the hindgut, the length of foregut bypassed directly correlated with degree of GLP-1 increase and ghrelin decrease.[52]

Amplify’d from bariatrictimes.com
In a model of direct glucose delivery to the hindgut, the length of foregut bypassed directly correlated with degree of GLP-1 increase and ghrelin decrease.[52]

Many diet modifications and metabolic surgical techniques have relied on the up-regulation of GLP-1 and peptide YY to exert a strong satiating effect. Exenatide is the first of the antidiabetic drugs related to GLP-1 to receive FDA approval, and its use has shown improvement in diabetes as well as modest weight loss.[51] Intestinal resection or bypass in patients is accompanied by a GLP-1 and PYY surge to meal stimulus that contributes to decreased food intake and improved glucose homeostasis.[35,39] In a model of direct glucose delivery to the hindgut, the length of foregut bypassed directly correlated with degree of GLP-1 increase and ghrelin decrease.[52] Clinically, this correlates to operations with a “malabsorptive” component achieving greater overall weight loss and diabetes resolution.[50] Sleeve gastrectomy seems unique in that increased gastric emptying contributes to less mechanical breakdown of food and resultant greater hindgut stimulation than seen with other purely restrictive procedures.[16]

Hindgut Hormones: Glugagon-Like Peptide (GLP-1) and Peptide-YY (PYY)
The “ileal brake” was recognized clinically as the strong feeling of satiation that developed once nutrients reached the hindgut. This phenomenon makes evolutionary sense because further ingestion of food in the presence of nutrients within the distal small bowel would only result in calorie loss in the stool. To prevent this, the hindgut L-cells within the terminal ileum and colon produce GLP-1 and peptideYY to stop ingestion and improve nutrient utilization. GLP-1 is a potent stimulator of insulin secretion and is trophic to beta cell function.[2] It is the hormone believed to play a key role in diabetes resolution after gastric bypass and duodenal switch, but is also likely to be the culprit behind the rare hypoglycemic hyperinsulimia reported after these operations.[48] Both peptideYY and GLP-1 have receptors in the central satiety and metabolism centers, where they exert strong effects to terminate hunger and increase the basal metabolic expenditure rate. Obese and diabetic patients seem to release less circulating GLP-1 and peptide YY in repsonse to a meal than their lean counterparts.[35,49] This is likely because many obese people are “early-intestine dominant” with an excessively long small bowel that is too efficient at processing and absorbing calories. This leaves little residual intraluminal nutrients downstream to stimulate the release of hindgut hormones.[50]

Read more at bariatrictimes.com

 

Advertisements

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s