GLP1 is an incretin and therefore increased

during the post-prandial period solely due to the increase glucose

Ghrelin secretion is preferentially increased

by glucose in response to ingestion of a meal.

PYY is secreted in response to a caloric load, with FA

having a greater effect than glucose

X/A-like

cells in the stomach increase ghrelin production to activate the Area Postrema

and enhance gastric emptying.

I-cells

in the upper gut release CCK in response to fatty acids to signal satiety via

vagal afferents, while L-cells release PYY to inhibit NPY/AgRP neurons in the

ARC.

Intramuscular

arrays (IMAs) detect a decrease in gastric wall tension, which triggers the

release of GLP-1 from the colon to stimulate insulin.

L-cells in

the duodenum release CCK to activate POMC neurons in the Arcuate Nucleus (ARC)

directly.

It reduces

food intake exclusively via the Y2 receptor, which is located only on NPY/AgRP

neurons in the hypothalamus.

Its primary

role is to increase the rate of gastric emptying post-prandially to facilitate

faster nutrient absorption in the duodenum.

It

is an incretin secreted from L-cells in the intestine that inhibits gastric

emptying and reduces food intake by directly stimulating POMC neurons in the arcuate

nucleus.

It is a

hunger-inducing hormone released from X/A-like cells in the stomach that

activates NPY/AgRP neurons via the GHSR receptor.

I-cells of

the duodenum; levels increase within 60 minutes of a low-fat meal.

K-cells of

the small intestine; levels decrease in proportion to caloric intake.

X/A-like

cells of the stomach; levels peak immediately before eating.

Vagal

afferents integrate mechanical information from stretch-sensitive endings

(IGLEs and IMAs) with chemical signals from nutrients and hormones, relaying

these satiety signals primarily to the Nucleus of the Solitary Tract (NTS) in

the brainstem.

The vagal

system is the primary pathway for meal initiation, where Intramuscular Arrays

(IMAs) sense gastric emptiness to trigger the systemic release of acylated

ghrelin from the liver.

Vagal

afferent nerves act solely as mechanoreceptors in the large intestine and are

incapable of responding to chemical stimuli such as Cholecystokinin (CCK) or

fatty acids.

Signaling

via the vagus nerve is an endocrine process that bypasses the brainstem to

deliver nutrient information directly to the fenestrations of the Area Postrema.

IGLEs are located in the myenteric plexus and

only detect longitudinal stretch

IMAs are located in the circular muscle and detect

longitudinal stretch

IMAs are located in the myenteric plexus and

detect longitudinal stretch

IGLEs are located in the circular muscle and

detect longitudinal stretch

The removal

of the C-18 fatty diacid chain to increase the rate of renal clearance.

Modification

of the peptide to allow it to bypass the brainstem and act exclusively on the

reward pathways of the prefrontal cortex.

Conjugation

with ghrelin-O-acyltransferase (GOAT) to allow for acylation and improved

receptor binding.

Specific

amino acid substitutions and the addition of a spacer/fatty diacid chain to

protect the molecule from metabolic degradation and decrease renal clearance,

thereby increasing its half-life