Physio: Feeding Regulation

Question 1

Define:
Hunger
Appetite
Satiety
Hyperphagia
Aphagia

Answer 1

Hunger – carving for food, activated during energy deficits (maybe jones carves and eats pumpkins?)

Appetite – desire for food, often a particular type

Satiety – successful quest for food, would turn off hunger

Hyperphagia – vigorous eating

Aphagia – reversal to eat (maybe jones reverses her raincoats and then eats?)

Question 2

Hypothalamic nucleus involved in satiety.

Answer 2

Ventromedial

-lesions increase eating (same with paraventricular nucleus lesions)

Question 3

Hypothalamic nucleus involved in feeding.

Answer 3

Lateral

-lesions lead to satiety (same with dorsal medial nucleus lesions)

Question 4

Hypothalamic nucleus that controls GI hormones

Answer 4

Arcuate Nucleus

Question 5

Name 5 GI hormones that decrease feeding.

Answer 5

1. CCK
2. Glucagon-Like Protein 1 (GLP-1)
3. Insulin
4. Peptide Tyrosine-Tyrosine (PYY)
5. Leptin (from adipocytes)

Question 6

Name 2 GI hormones that increases feeding.

Answer 6

Ghrelin

Somatostatin

Question 7

Receptor that is activated in neurons to suppress eating.

Answer 7

MCR-4

Question 8

Neurons that antagonize the MCR-4 receptor to increase feeding. (orexigenic)

Answer 8

AGRP/NYP

Question 9

Neurons that activate the MCR-4 receptor to decrease feeding. (anorexigenic)

Answer 9

POMC/CART

Question 10

Protein used to measure the body’s insulin production.

Answer 10

C-peptide

Question 11

Name 3 incretins that stimulate insulin release.

Answer 11

1. CCK
2. GLP-1
3. GIP

Question 12

Main stimulator of insulin release.

Answer 12

Increased plasma glucose

Question 13

Describe the mechanism of insulin release in response to glucose.

Answer 13

1. Glucose enters beta cells thru GLUT-2
2. Glucose metabolized to ATP
3. ATP closes potassium channels and depolarizes the cell
4. Calcium channels open signaling the ER to produce insulin and send it in vesicles to be released into the blood.

Question 14

How do amino acids stimulate insulin release?

Answer 14

Glucogenic AA are converted to pyruvate, which is converted to ATP thru the citric acid cycle and electron transport chain. The ATP follows the same pattern as the glucose mechanism.

Ketogenic AA are converted to Acetyl CoA and then converted to ATP in the CAC and ETC.

Question 15

How do CCK and ACh (parasympathetics) stimulate inslulin release?

Answer 15

They increase IP3 which leads to calcium influx in the beta cells.

Question 16

Enzyme that breaks down chylomicrons and releases dietary fatty acids so they can be stored in adipose tissue.

Answer 16

Lipoprotein Lipase (LPL)

Question 17

Enzyme that liberates stored fatty acids from adipose tissue so they can be sent to the liver for fatty acid oxidation.

Answer 17

Hormone Sensitive Lipase (HSL)

• inhibited by insulin
• stimulated by low blood glucose

Question 18

Why is it important for the body to release glucagon after a protein-rich meal?

Answer 18

AA from the meal will stimulate insulin release. High protein meals do not contain much glucose so the insulin would cause severe hypoglycemia. The glucagon is stimulated by insulin to maintain blood sugar.