Hypothalamic Control of Eating

Question 1

What is the role of the short term signals in eating?

Answer 1

Short term signals come form satiety factors in the GI tract.

This is how the stomach tells the brain it has HAD ENOUGH.

Question 2

What are the two types of short term signal factors–give examples of each.

Answer 2

Pre-absorptive satiety factors (before nutrients absorbed)

1. Oropharyngeal- respond to taste, texture and smell (can increase or decrease appetite depending on whether you’re in a fed/fasted state)

2. Gastric Distension/Intestinal nutrients– will decrease food intake

Post-absorbitve satiety factors (affected after food is absorbed)

1. Liver! --> decreases food intake

Question 3

What three short term satiety factors effect the CNS?

Answer 3

1. Gastric Distension
2. CCK
3. Grehlin

Question 4

How does gastric distension affect the CNS?

Answer 4

A stomach stretch activates mechanoreceptors that increase the firing of vagal afferents and stimulate the nucleus of hte solitary tract (medulla) which leads to a DECREASE in food intake.

This is our stomach telling us HEY, I’M FULL…NO MORE.

Question 5

How does CCK affect the CNS?

Answer 5

Releasing CCK, like gastric distension, increases firing on the vagal afferents, ultimately leading to a decrease in food intake.

When fat enters the stomach, CCK is secreted by the duodenum and causes gallbladder and pyloric contraction as well as increased gastric contraction.

gallbladder contraction- secretes bile to digest fats

pyloric contraction- slows gastric emptying so you ahve more time to digest

gastric contractions- increased digestion

CCK is making sure you digest the HELL outa that food.

Question 6

What does Ghrelin do?

Answer 6

The OPPOSITE of CCK and gastric distension.

Grhelin is made in the stomach.

Increased by fasting.

INCREASES food intake/apetite.

Question 7

What is Prader-Willi Syndrome?

Answer 7

Deletion of chromosome 15 leads to uncontrolled appetite d/t excessive ghrelin secretion.

Sx:

fetal hypotonia

mental retardation

hypogonadotropic hypogonadism > decreased gonadal fxn

obesity

hyperphagia = excessive eating

Question 8

What is the primary hormone related to long term satiety signals?

Answer 8

Leptin!

Adipocytes release leptin which acts on the brain and hypothalums to decrease food intake.

Question 9

What are the hypothalamic nuclei that control food intake?

Answer 9

1. LHA
2. PVN
3. ARC

Question 10

What happens when the lateral hypothalamic area is stimulated?

Answer 10

Stimulatoin of LHA leads to the release of orexin (a anabolic NT in the brainstem) which INCREASES food intake.

Question 11

A lesion of the LHA leads to what deficit?

Answer 11

Aphagia= stop eating

D/t

1. Damage to the medial forebrain bundle > reduced motivation/motor function
2. Loss of neurons synthesizing orexigenic peptide

Question 12

What happens when the PVN is stimulated?

Answer 12

The PVN releases a catabollic NT (CRH- Corticotropin Releasing hormone) that affects the brainstem and leads to a DECREASE in food intake.

Question 13

What is ARC?

Answer 13

Arc is at the base of the hypothalamus and contains two typse of neurons.

NPY neurons project to the LHA and PVN and lead to INCREASED food intake. Leptin INHIBITS these neurons leading to decreased food intake.

Melanocortiocon neurons also project to the LHA and PVN and act to DECREASE food intake. Leptin ACTIVATES mel neurons in order to decrease food intake.