04b: Appetite regulation Flashcards
Energy intake from (X) and E output via (Y).
X = food/EtOH Y = BMR, thermogenesis, exercise
T/F: Obesity refers to excess body weight.
False - excess body fat (adiposity)
T/F: Biologically, weight gain is “defended”; our body holds on to to the weight, making it difficult to lose.
True
Short-term satiety signal peptides are secreted mainly from (X). List some examples.
X = GI tract
- GLP-1
- CCK
New methods to treat T2DM: drugs (gliptins) that (inhibit/enhance) GLP-1 activity. What would this do?
Enhance;
Increase satiety signals and insulin secretion
GLP-1 levels (rise/fall) before meal and (rise/fall) afterwards.
Fall; rise (signaling satiety)
(X) is the only gut peptide to increase appetite.
X = Ghrelin
Long-term signals affecting hunger/satiety are (X) hormones. The levels parallel (Y).
X = Y = adiposity (report status of fuel stores)
Vaccines against (X) lead to reduced food intake in rodents. This could develop into (Y) therapy in humans.
X = ghrelin Y = anti-obesity
T/F: Insulin crosses the BBB and binds directly to receptors in the hypothalamus that suppress appetite.
True
GI tract neural signals: (X) produces hunger feelings and (Y) produces satiety feelings.
X = gastric emptying Y = gastric distension
Appetite signals from adipose tissue involve (X) hormone, which binds (Y) and (stimulates/inhibits) appetite.
X = leptin
Y = hypothalamic neurons (ARC)
Inhibits
Satiety peptides (increase/decrease) rate of gastric emptying.
Decrease
Insulin directly (stimulates/inhibits) appetite at (X) part of brain.
Inhibits;
X = arcuate nucleus (hypothalamus)
List the Leptin mutations discovered. Star the one which can be treated by (X).
- Leptin deficiency* (mutation in leptin)
- Leptin resistance (mutation in receptor)
X = exogenous leptin
T/F: Most obesity is associated with high insulin and low leptin levels.
False - both high (and resistance to both)
(X) condition, the loss of menstrual cycle under strenuous conditions (exercise excess, malnutrition) is a result of (rise/drop) in (Y) hormone.
X = hypothalamic amenorrhea
Drop
Y = leptin
List the primary longer-term peripheral effectors on appetite.
- Leptin
- Insulin
- Ghrelin
T/F: Ghrelin is a satiety peptide.
False
List the two main neuronal populations (in ARC) that act as circuits in processes related to energy homeostasis. Star the appetite-stimulating center.
- Orexigenic center*
2. Anorexigenic center
T/F: Satiety peptides act directly at the ARC.
False - act via vagal pathways
T/F: Both orexigenic center and anorexigenic center are active at the same time.
True (but at varying levels)
The (orexigenic/anorexigenic) center increases energy expenditure.
Anorexigenic
In hungry (EAT) state, elevated (X) hormone levels activate receptors on (Y) neurons. This will (increase/decrease) food intake and (increase/decrease) E conservation.
X = ghrelin Y = orexigenic center ARC
Increase both
Activated ghrelin receptors stimulate the (X) cells to secrete:
X = orexigenic ARC neurons
- NPY (neuropeptide Y)
- AgRP (Agouti-related peptide)
NPY (neuropeptide Y) is released from (X) and binds (Y) receptor on (Z) cells.
X = orexigenic ARC neurons Y = NPY Z = second-order neurons
AgRP (Agouti-related peptide) is released from (X) and binds (Y) receptor on (Z) cells.
X = orexigenic ARC neurons Y = NPY Z = second-order neurons
Activation of NPY receptor, via (X) neuropeptide, has which effect(s)?
X = NPY or AgRP (neuropeptides from orexigenic center)
- Initiates feeding behavior/metabolic processes
- Reduces E expenditure
In general, (X) hormone acts
as the accelerator for eating and weight gain, while (Y) acts as the brakes.
X = ghrelin Y = leptin
Leptin binds (orexigenic/anorexigenic) neurons and (stimulates/inhibits) (X).
Both;
Stimulates anorexigenic center to secrete neuropeptides;
Inhibits orexigenic release of neuropeptides
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.
X = leptin Y = anorexigenic ARC
Decreases both (increase E expenditure)
Activated leptin receptors, on anorexigenic ARC neurons, (stimulate/inhibit) secretion of:
Stimulate;
- CART
- POMC
(both neuropeptides)
(Anorexigenic/orexigenic) neurons release (X) neuropeptide, which is proteolytically cleaved into (Y).
Anorexigenic;
X = POMC
Y = alpha-MSH
Alpha-MSH (promotes/inhibits) feeding behavior by binding (X) receptor. (Y) is a potent inhibitor of this pathway.
Inhibits;
X = melanocortin (on second-order neurons)
Y = AgRP (from orexigenic neurons)
Melanocortin receptor
defects likely to cause (anorexia/obesity).
Obesity - problem with anorexigenic center signals
Release of (X) neuropeptide from (orexigenic/anorexigenic) center is increased in prolonged stress.
X = NPY
orexigenic
T/F: Education
mediates the effects of visual cues on appetite/food intake.
False - even dietitians served themselves more if given larger plates/spoons
T/F: A low-energy-dense first course lowers energy intake at a meal.
True
