04b: Appetite regulation

Question 1

Energy intake from (X) and E output via (Y).

Answer 1

X = food/EtOH
Y = BMR, thermogenesis, exercise

Question 2

T/F: Obesity refers to excess body weight.

Answer 2

False - excess body fat (adiposity)

Question 3

T/F: Biologically, weight gain is “defended”; our body holds on to to the weight, making it difficult to lose.

Answer 3

True

Question 4

Short-term satiety signal peptides are secreted mainly from (X). List some examples.

Answer 4

X = GI tract

1. GLP-1
2. CCK

Question 5

New methods to treat T2DM: drugs (gliptins) that (inhibit/enhance) GLP-1 activity. What would this do?

Answer 5

Enhance;

Increase satiety signals and insulin secretion

Question 6

GLP-1 levels (rise/fall) before meal and (rise/fall) afterwards.

Answer 6

Fall; rise (signaling satiety)

Question 7

(X) is the only gut peptide to increase appetite.

Answer 7

X = Ghrelin

Question 8

Long-term signals affecting hunger/satiety are (X) hormones. The levels parallel (Y).

Answer 8

X = Y = adiposity (report status of fuel stores)

Question 9

Vaccines against (X) lead to reduced
food intake in rodents. This could develop into (Y) therapy in humans.

Answer 9

X = ghrelin
Y = anti-obesity

Question 10

T/F: Insulin crosses the BBB and binds directly to receptors in the hypothalamus that suppress appetite.

Answer 10

True

Question 11

GI tract neural signals: (X) produces hunger feelings and (Y) produces satiety feelings.

Answer 11

X = gastric emptying
Y = gastric distension

Question 12

Appetite signals from adipose tissue involve (X) hormone, which binds (Y) and (stimulates/inhibits) appetite.

Answer 12

X = leptin
Y = hypothalamic neurons (ARC)
Inhibits

Question 13

Satiety peptides (increase/decrease) rate of gastric emptying.

Answer 13

Decrease

Question 14

Insulin directly (stimulates/inhibits) appetite at (X) part of brain.

Answer 14

Inhibits;

X = arcuate nucleus (hypothalamus)

Question 15

List the Leptin mutations discovered. Star the one which can be treated by (X).

Answer 15

1. Leptin deficiency* (mutation in leptin)
2. Leptin resistance (mutation in receptor)

X = exogenous leptin

Question 16

T/F: Most obesity is associated with high insulin and low leptin levels.

Answer 16

False - both high (and resistance to both)

Question 17

(X) condition, the loss of menstrual cycle under strenuous conditions (exercise excess, malnutrition) is a result of (rise/drop) in (Y) hormone.

Answer 17

X = hypothalamic amenorrhea

Drop
Y = leptin

Question 18

List the primary longer-term peripheral effectors on appetite.

Answer 18

1. Leptin
2. Insulin
3. Ghrelin

Question 19

T/F: Ghrelin is a satiety peptide.

Answer 19

False

Question 20

List the two main neuronal populations (in ARC) that act as circuits in processes related to energy homeostasis. Star the appetite-stimulating center.

Answer 20

1. Orexigenic center*

2. Anorexigenic center

Question 21

T/F: Satiety peptides act directly at the ARC.

Answer 21

False - act via vagal pathways

Question 22

T/F: Both orexigenic center and anorexigenic center are active at the same time.

Answer 22

True (but at varying levels)

Question 23

The (orexigenic/anorexigenic) center increases energy expenditure.

Answer 23

Anorexigenic

Question 24

In hungry (EAT) state, elevated (X) hormone levels activate receptors on (Y) neurons. This will (increase/decrease) food intake and (increase/decrease) E conservation.

Answer 24

X = ghrelin
Y = orexigenic center ARC

Increase both

Question 25

Activated ghrelin receptors stimulate the (X) cells to secrete:

Answer 25

X = orexigenic ARC neurons 1. NPY (neuropeptide Y) 2. AgRP (Agouti-related peptide)

Question 26

NPY (neuropeptide Y) is released from (X) and binds (Y) receptor on (Z) cells.

Answer 26

``` X = orexigenic ARC neurons Y = NPY Z = second-order neurons ```

Question 27

AgRP (Agouti-related peptide) is released from (X) and binds (Y) receptor on (Z) cells.

Answer 27

``` X = orexigenic ARC neurons Y = NPY Z = second-order neurons ```

Question 28

Activation of NPY receptor, via (X) neuropeptide, has which effect(s)?

Answer 28

X = NPY or AgRP (neuropeptides from orexigenic center) 1. Initiates feeding behavior/metabolic processes 2. Reduces E expenditure

Question 29

In general, (X) hormone acts | as the accelerator for eating and weight gain, while (Y) acts as the brakes.

Answer 29

``` X = ghrelin Y = leptin ```

Question 30

Leptin binds (orexigenic/anorexigenic) neurons and (stimulates/inhibits) (X).

Answer 30

Both; Stimulates anorexigenic center to secrete neuropeptides; Inhibits orexigenic release of neuropeptides

Question 31

In fed (DO NOT EAT) state, elevated (X) hormone levels activate receptors on (Y) neurons. This will (increase/decrease) feeding behavior and (increase/decrease) E conservation.

Answer 31

``` X = leptin Y = anorexigenic ARC ``` Decreases both (increase E expenditure)

Question 32

Activated leptin receptors, on anorexigenic ARC neurons, (stimulate/inhibit) secretion of:

Answer 32

Stimulate; 1. CART 2. POMC (both neuropeptides)

Question 33

(Anorexigenic/orexigenic) neurons release (X) neuropeptide, which is proteolytically cleaved into (Y).

Answer 33

Anorexigenic; X = POMC Y = alpha-MSH

Question 34

Alpha-MSH (promotes/inhibits) feeding behavior by binding (X) receptor. (Y) is a potent inhibitor of this pathway.

Answer 34

Inhibits; X = melanocortin (on second-order neurons) Y = AgRP (from orexigenic neurons)

Question 35

Melanocortin receptor | defects likely to cause (anorexia/obesity).

Answer 35

Obesity - problem with anorexigenic center signals

Question 36

Release of (X) neuropeptide from (orexigenic/anorexigenic) center is increased in prolonged stress.

Answer 36

X = NPY | orexigenic

Question 37

T/F: Education | mediates the effects of visual cues on appetite/food intake.

Answer 37

False - even dietitians served themselves more if given larger plates/spoons

Question 38

T/F: A low-energy-dense first course lowers energy intake at a meal.

Answer 38

True