#hindgut

~ Weeks 4 through 6

Three embryologic divisions of the thoracic and abdominal gastrointestinal tube:

Foregut

Supplied by the celiac artery

Gives rise to the:

Esophagus

Stomach - Liver buds, which ultimately form the liver

Gallbladder

Ventral and dorsal pancreatic buds (aka, diverticula), which will later fuse to form the pancreas

Proximal duodenum

Midgut

Supplied by the superior mesenteric artery

Comprises primary intestinal loop, which connects to the yolk sac via the vitelline duct

Gives rise to the:

Distal duodenum

Jejunum

Ileum

Ascending colon

Proximal 2/3 of the transverse colon

Hindgut

Supplied by the inferior mesenteric artery

Gives rise to the allantois before ending blindly at the cloaca

Gives rise to the:

Distal 1/3 of the transverse colon - Descending and sigmoid colons

The proximal 2/3 of the anorectal canal

INNERVATION

The enteric nervous system, which is derived from neural crest cells, regulates motility to propel the contents of the GI tract.

MESENTERIES

Mesenteries divide the peritoneal cavity and suspend the gastrointestinal tract. Additionally, they provide a protective covering for neurovascular structures.

The ventral mesentery is derived from the septum transversum, and will give rise to ligaments associated with the liver.

The dorsal mesentery secures the gastrointestinal tract to the posterior body wall.

The meso-esophagus attaches the esophagus to the dorsal wall

The mesogastrium anchors the stomach

The mesoduodenum anchors the duodenum

The mesentery proper anchors the primary loop of the midgut

I was lucky enough to find a log full of termites behind my house. You know what that means? Gut protists!

Termites can’t actually digest wood for themselves, so they form symbiotic relationships with protists and bacteria to help break down the wood for them

I squished a termite under a slide and saw all these flagellates come out. These unicellular creatures make up a third of the body weight of termites, and I’m lucky enough to be studying them as a lab intern

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