Regulation of Food Intake Flashcards
1
Q
- Neuronal Centers that control satiety and feeding in the hypothalamus
A
- Lateral Nucleus (LH)
- Ventromedial Nucleus (VM)
- Paraventricular Nucleus (PV)
- Dorsomedial nucleus (DM)
- Arcuate nucleus (Arc)
2
Q
- _% of the vagus carries afferent fibers to the hypothalamus
A
- 80%
3
Q
- What hormone is important for long term control of satiety?
- What cells secrete it?
A
- Leptin
- Adipose cells
4
Q
- Where does the hypothalamus receive signals from to maintain energy balance?
A
- Neural signals from GI tract
- Chemical signals from nutrients in the blood
- Signals from GI hormones
- Signals from adipose tissue
- Signals from cerebral cortex (sight, smell, taste)
5
Q
- What hormones are part of the anorexigenic pathway?
A
- Leptin
- CCK
- Insulin
(Lept CCK in)
6
Q
-
Describe the anorexigenic pathway
- What does it stimulate
- What does it inhibit
A
- Insulin/CCK/Leptin bind to LepR on POMC/CART cell in the arcuate nucleus
- Alpha MSH is released and binds MCR 4 on neuron of PVN
- Inhibits food intake
- *Alpha MSH also inhibits MCR 3 R on AGRP/NPY cells of the orexigenic pathway
7
Q
- What are thre orexigenic hormones?
A
- Ghrelin
- (H in ghrelin-hunger)
8
Q
- How does the orexigenic pathway work?
A
- Ghrelin released from the stomach binds to AGRP/NPY cell and releases NPY and AGRP
- NPY binds Y1R in neurons of PVN
- AGRP released bings and antagonizes MCR-4 receptor on same neuron to inhibit anorexigenic pathway
- Overall increase in food intake
9
Q
- Most of the integration signaling regulating food intake and energy expenditure happens in the _
A
- Arcuate nucleus (which then sends its signals to the PVN)
10
Q
- Mutations in _ and _ genes have been related to some cases of obesity
- What pathway are these molecules involved in?
A
- POMC
- MCR-4
- Anorexigenic
11
Q
_ that stimulate satiety decrease feeding activate receptors on vagal afferents
Vagus sends signals to _ which then sends signals to the hypothalamus
What happens if vagal activity is blocked?
A
- Peptides
- NTS
- Amount of material in stomach no longer influences meal size
12
Q
- _ is able to regulate food intake in response to peripheral signals even in the absence of higher center input
A
- Hindbrain
13
Q
-
Ghrelin
- Where is it secreted?
- What does it bind to?
- What does it stimulate?
- Actions?
A
- Endocrine cells in the stomach
- Binds to GHSR (growth hormone secretagouge receptors)
- Stimulates neurons that release NPY
- Actions:
- Increase appetite
- Increase gastric motility
- Increase adipogenesis
- Increase acid secretion
- Increase and decrease insulin secretion
14
Q
-
Insulin
- Where does it bind? (does it excite or inhibit these pathways?)
- Actions
A
- Binds to NPY system-inhibits
- Binds to POMC pathway-stimulates
- Actions:
- Decrease appetite
- Increase metabolism
15
Q
- In patients with Type I DM, there is an increase in food intake associated with _ insulin
A
Decreased
16
Q
-
CCK
- What cells release it?
- Where does it act and what are its effects?
A
- Released by I cells in the duodenum
-
Elicits satiety by:
- Acting on vagal-NTS-hypothalamic circuit to inhibit ghrelin
- Inhibits gastric emptying
- Increases gastric distension
17
Q
-
PYY
- Where is it released?
- Where does it bind? (on what receptor)
- What are its effects?
A
- Released by L cells of ileum and Colon AFTER LARGE MEAL
- Binds to Y2R in hypothalamus
- Actions:
- Inhibits NPY neurons
- Releases inhibition of POMC neurons
- Anorexigenic
18
Q
-
Leptin
- Where is it secreted?
- What receptors does it bind (does it have stimulatory or inhibitory effects)?
- Actions
A
- Secreted by adipose tissue
- Binds to NPY (inhibits)
- Binds to POMC (stimulates)
-
Actions: Appetite-Suppressing hormone
- Decreases appetite
- Increases metabolism
- Decreases ghrelin release
19
Q
- Does administration of leptin aid in treatment for obese patients?
A
- In obese children with congenital leptin deficiency-yes
- Obesity in most of population-not responsive to exogenous leptin tx
20
Q
- Summary integration of signals regulating food intake and energy expenditure
A
21
Q
-
GLP -1 (Glucagon like peptide-1)
- What is it derived from?
- Co-secreted with what molecule in L cells of small intestine
- Acts as a _
- _ after a meal and _ during fasting
- Actions
A
- Derived from glucagon-like peptide
- PYY
- Incretin-works to decrease BGL
- Increases after meal
- Decreases during fasting
-
ACTIONS:
- Decreases food intake
- Suppresses Glucagon Secretion
- Delays Gastric emptying
22
Q
-
Oxyntomodulin
- Derived from what?
- Released from _ in intestine in response to ingested food
- Has _ effect
A
- Proglucagon
- L Cells
- Anorectic
23
Q
- Pancreatic Peptide
- Secreted from?
- Actions and MOA
- _ effect
- Can also act on vagus n.
A
- Islets of Langerhans (endocrine pancreas)
- Decreases food intake thru Y4R in hypothalamus
- Anorectic
24
Q
-
Glucagon
- Where is it secreted?
- Functions?
A
- Secreted by pancreatic islets
- Reduces food intake
- Increases BGL and insulin secretion
25
* ***Amylin***
* ******Stored and released with _ in response to food intake
* _ effects
* Insulin
* Anorectic ( inhibits NPY release)
26
***KEY FEATURES OF ANOREXIA NERVOSA:***
* _ in genes involved in eating attitudes, regulation of eating behavior, motivation and reward mechanisms (EX: AgRP)
* Basal and pulsatile secretion of _ is REDUCED in association w/ reductions in fat masses
* _ resistance helps with restrictive diet
* Elevated levels of _ (contribute to decreased nutrient intake and disordered eating psychopathology)
* Polymorphism
* LEPTIN (decreased)
* GHRELIN RESISTANCE
* PYY (elevated)
