1.

Studying all night

 Sleep loss
o Increased sympathovagal balance
 Affects
 Insulin secretion
 Leptin secretion (appetite-suppressing hormone)

o Increase CORTISOL SECRETION

o Increases appetite
o Decreased LEPTIN SECRETION

 Arcuate nucleus of the hypothalamus

A. Acute Stress

 Corticotropin-releasing hormone (CRH) is released from the medial parvocellular (mp) paraventricular nucleus
of the hypothalamus (PVN) in response to the stressor
a. Release of ACTH
 Glucocorticoid release

b. INHIBIT NEUROPEPTIDE Y (NPY)/AGOUTI-RELATED PEPTIDE (AGRP) NEURONS (population of cells is

normally responsible for stimulating feeding behavior and suppressing energy expenditure)

B. Chronic

 With longer-term stressors, however, the energy used coping needs to be replaced
o Glucocorticoids is elevated
 Stimulates appetite
 Stimulate leptin release → leptin resistance
 Stimulate insulin (normally an appetite-suppressant) → insulin resistance
 Reduced ability of insulin to inhibit NPY/AGRP neurons in the ARC, which has the
converse effect of lessening appetite suppression

 Stimulate ghrelin release

 Modulate ACTH release from the pituitary and regulate glucocorticoid negative
feedback
 Increased ghrelin-mediated stimulation of NPY/AGRP and increased food intake
Stress response

1. activation of the sympathetic adrenal medullary system, with release of catecholamines (adrenaline and
noradrenaline) that is typical during periods of acute stress

2. hypothalamic-pituitary-adrenal (HPA) axis

o a neuroendocrine system with inhibitory feedback loops
o Stress stimulates the release of corticotropin-releasing factor (CRF) from the paraventricular nucleus
(PVN) of the hypothalamus which in turn stimulates the synthesis of adrenocorticotropic hormone
(ACTH) from the anterior pituitary

 Prolonged exposure to high levels of cortisol dysregulate HPA axis

II. GUT-BRAIN CONNECTION

 CHOLECYSTOKININ
o Satiety factor that decreases meal size


Regulation of Digestion
The activities of the digestive system are regulated by both hormones and neural reflexes. Four important
hormones and their effects on target cells follow:

 GASTRIN
o Stimulation of gastric juice (especially HCl) secretion by gastric glands.
o Stimulation of smooth muscle contraction in the stomach, small intestine, and large intestine,
which increases gastric and intestinal motility.
o Relaxation of the pyloric sphincter, which promotes gastric emptying into the small intestine.

 SECRETIN
o Stimulation of bicarbonate secretion by the pancreas, which stabilizes the pH of the chyme when
released into the duodenum.
o Stimulation of bile production by the liver.
o Inhibition of gastric juice secretions and gastric motility, which in turn slows digestion in the
stomach and retards gastric emptying.
  CHOLECYSTOKININ (CCK)
o Stimulation of bile release by the gallbladder.
o Stimulation of pancreatic juice secretion.
o Relaxation of the hepatopancreatic ampulla and opening of the hepatopancreatic sphincter, which
allows the flow of bile and pancreatic juices into the duodenum.

 GLUCOSE INSULINOTROPIC PEPTIDE (GIP) is produced and released by the enteroendocrine cells
of the duodenal mucosa in response to the presence of the glucose in the small intestine. This hormone
stimulates the pancreas to begin releasing insulin. Some researchers refer to this hormone as glucose‐
dependent insulinotropic peptide (still maintaining the abbreviation of GIP; some also use GDIP).

The second regulatory agent of the digestive system is the nervous system. Stimuli that influence digestive
activities may originate in the head, the stomach, or the small intestine. Based on these sites, there are three
phases of digestive regulation:

1.The CEPHALIC PHASE comprises those stimuli that originate from the head: sight, smell, taste, or
thoughts of food, as well as emotional states. In response, the following reflexes are initiated:

1. Neural response: Stimuli that arouse digestion are relayed to the hypothalamus, which in turn initiates
nerve impulses in the parasympathetic vagus nerve. These impulses innervate nerve networks of the GI
tract (enteric nervous system), which promote contraction of smooth muscle (which causes peristalsis)
and secretion of gastric juice. Stimuli that repress digestion (emotions of fear or anxiety, for example)
innervate sympathetic fibers that suppress muscle contraction and secretion.
2. General effects: The stomach prepares for the digestion of proteins.

2. The GASTRIC PHASE describes those stimuli that originate from the stomach. These stimuli include
distention of the stomach (which activates stretch receptors), low acidity (high pH), and the presence of
peptides. In response, the following reflexes are initiated:

1. Neural response: Gastric juice secretion and smooth muscle contraction are promoted.
2. Hormonal response: Gastrin production is promoted.
3. General effects: The stomach and small intestine prepare for the digestion of chyme, and gastric
emptying is promoted.

3. The INTESTINAL PHASE describes stimuli originating in the small intestine. These include distention of the
duodenum, high acidity (low pH), and the presence of chyme (especially fatty acids and carbohydrates). In
response, the following reflexes are initiated:

1. Neural response: Gastric secretion and gastric motility are inhibited (enterogastric reflex). Intestinal
secretions, smooth muscle contraction, and bile and pancreatic juice production are promoted.
2. Hormonal response: Production of secretin, CCK, and GIP is promoted.
3. General effects: Stomach emptying is retarded to allow adequate time for digestion (especially fats) in
the small intestine. Intestinal digestion and motility are promoted.
 GhrelinA hormone produced in the stomach that boosts appetite, slows metabolism and reduces fat
burning. It may be involved in the development of obesity. is produced in the stomach, and its
function is to tell the brain that the body has to be fed. It increases appetite.

 Gastrin is produced in the stomach when it is stretched. It stimulates the release of gastric juice rich
in pepsin and hydrochloric acid.

 Secretin is produced in the duodenum and has the effect of stimulating the pancreas to produce
alkaline secretions as well as slowing the emptying of the stomach.

 Cholecystokinin (CCK) is produced in the duodenum. It reduces appetite, slows down the emptying
of the stomach and stimulates the release of bile from the gall bladder.

 Peptide YY (PYY) is produced in the last part of the small intestine known as the ileum as well as
parts of the large intestine. It plays a role in slowing down the passage of food along the gut, which
increases the efficiency of digestion and nutrient absorption after meal.

 Glucagon-like peptide 1 (GLP-1) is produced in the small intestine and colon and has multiple
actions including inhibition of gastric emptying and appetite as well as the stimulation of insulin
release.