Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GIGU test! > Regulation of food intake > Flashcards

Regulation of food intake Flashcards

1
Q

What are the Neuronal centers that control feeding and satiety in the hypothalamus?

A
  • Lateral nucleus (LH)
  • Ventromedial nucleus (VM)
  • Paraventricular nucleus (PV)
  • Dorsomedial nucleus (DM)
  • Arcuate nucleus (arc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

where does the hypothalamus receive signals to help with regulation of control?

A
  • Neural signals from the GI tract
  • Chemical signals from GI hormones
  • Signals from adipose tissue
  • Signals from cerebral cortex (sight, smell and taste)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where does most of the integration signaling regulating food intake and energy expenditure happen?

A

Arcuate nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the Anorexigenic pathway?

A

THe POMC/CART (pro-opiomelanocortin) in the arcuate nucleus will release a-melanocortin (a-MSH) on to the PVN
-these act on the MCR-4 receptor

this process will decrease food intake

this is activated by inulin, leptin and CCK

the POMC/CART also acts on the orexigenic pathway by inhibiting it via the release of a-MSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the Orexigenic pathway

A

Hunger signals from Ghrelin will stimulate the AGRP/NPY of the arcuate nucleus

  • release neuropeptide on to the PVN to stimulate food
  • neuropeptide will bind to the Y1R receptor
  • agouti-related peptide (AGRP) is also released to inhibit the MCR-4 (anorexigenic pathway)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how does the anorexigenic and orexigenic pathways influence each other?

A

Both pathways antagonize each other:
-peptides that stimulate the a-MSH pathway will inhibit the NPY system

-AGRP is an antagonist to MCR-4 and will inhibit the anorexigenic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clinical correlation of the POMC and MCR-4 genes

A

some cases of obesity have been related to mutations in the POMC and MCR-4 genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

genetic causes of obesity: Leptin

A

Leptin or leptin receptor gene deficiency

  • Early onset server obesity
  • infertility
  • hypogonadotropic and hypogonadism
  • hyperphagia
  • infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

genetic causes of obesity: MC4R

A

Melanocortin 4 receptor gene mutation

  • Early onset severe obesity,
  • increased linear growth
  • Hyperphagia
  • hyperinsulinemia
  • most common know genetic cause of obesity
  • homozygous worse than heterozygous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

genetic causes of obesity: Prader-Willi syndrome

A

Partial deletion of chromosome 15 or loss of paternally expressed genes

-Neonatal hypotonia
-slow infant growth
-small hands and feet
-mental retardation
-hypogonadism
-hyperphagia
elevated ghrelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

genetic causes of obesity: POMC gene

A

Loss of function of the Proopiomelanocortin (POMC)

  • obesity
  • red hair
  • adrenal insufficiency due to ACTH deficiency
  • hyperproinsulinemia
  • hyperphagia
  • pale skin
  • cholestatic jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

by inhibiting the Vagal nerve how could it affect the feeding behavior and metabolism?

A

if the vagal activity is blocked, the amount of materia in the stomach no longer influences meal size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the Vagal, BTS, hypothaamus circuit?

A

Nucleus tractus solitarus is crucial in the interpretation and relaying of peripheral signals

Vagal signaling to the NTS is integrated with info recieved by the hypothalamus to produce the appropriate feeding behavior and metabolic responses

THe hindbrain is able to regulate food intale in response to peripheral signals even in the absence of higher centers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the function of the Lateral hypothalamic area?

A

Hunger center
-neurons project throughout the brain and release the oxigenic peptides melanin concentrating hormone (MHC) or orexins A and B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the function of the Ventromedial hypothalamic nucleus?

A

satiety center

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the function of the Paraventricular nucleus:

A

THis nucleus contains neurons that in turn project to both the cerebral cortex and the areas of the brainstem

17
Q

what is Ghrelin and what are its actions and what does it bind to?

A

Secreted in the stomach by endocrine cells

Binds to growth hormone secretagogue receptors (GHSR)

Stimulates neurons that release NPY

Actions:

  • increase appetite
  • increase gastric motility
  • increase gastric acid secretion
  • increase adipogenesis
  • decrease insulin secretion (evidence for increase too)

Appears to initiate the feeding response

18
Q

What does insulin do towards regulating feeding behavior and what are its actions?

A

BInds to receptors in POMC and NPY systems

  • inhibits NPY pathway
  • Stimulates POMC pathway

Actions:

  • decrese appetite
  • increase metabolism

in patients with type 1 DM there is an increase in food intake associated with a decrease in insulin

19
Q

what does CCK do in the regulation of the feeding behavior

A
  • Released by I cells in the duodenum
  • Elicts satiety

acts on vagal, NTS, hypothalamus circuit

  • decreases ghrelin
  • increases gastric emptying when there is an increase in gastric distention
20
Q

what does PYY do in regulation of feeding behavior?

A

Released by L cells of the ileum and colon following a meal

Binds to Y2R in the hypothalamus

  • inhibits NPY neurons
  • releases inhibition of POMC neurons
  • promotes satiety
21
Q

what does leptin do in the regulation of feeding behavior?

A

Secreted by cells in adipose tissue

Binds to receptors in POMC and NPY systems

  • inhibits NPY pathway
  • stimulates POMC pathway

Appetite supressing hormone

  • decrease in appetite
  • increase in metabolism
  • decrease in ghrelin release
22
Q

leptin in obese children

A

In obese children with congenital leptin deficiency, subcutaneous administration of recombinant leptin reduces fat mass, hyperinsulinaemia and hyperlipidaemia

However obesity in humans is often associated with high leptin levels and failure to respond to exogenous leptin ( leptin resistant)

23
Q

Source, site of action, and effect: Insulin

A

source: pancreatic Beta cells

site of action: hypothalamus

effect: decrease in appetite
increase in metabolism

24
Q

Source, site of action, and effect: Leptin

A

source: Fat cells and endocrine cells of the stomach

site of action:
-Hypothalamus, decrease in NPY, AgRP
increase in POMC
Vagal afferents

Effect:

  • decrease appetite
  • increase metabolism
  • decrease ghrelin release
25
Q

Source, site of action, and effect: CCK

A

source: I cells of the duodenum

Site of action: Vagal afferents

Effect:

  • decrease appetite
  • decrease gastric emptying
26
Q

Source, site of action, and effect: PYY

A

Source: L cells of the ileum and colon

Site of action: hypothalamus
-decrease in NPY, and AgRP
-increase in POMC
stomach

Effect:

  • decrease in appetite
  • decrease in gastric emptying
  • increase in metabolism
27
Q

Source, site of action, and effect: Ghrelin

A

Source: Endocrine cells of the stomach
hypothalamus
large and small intestines

Site of action: Hypothalamus
-increase NPY and AgRP
vagal afferents

Effect:

  • increase appetite
  • decrease metabolism
  • decrease leptin release
28
Q

Summary integration of signals regulating food intake and energy expenditure

A

Adiposity signals are involved in the long term regulation of energy balance

while gut peptides modullate food intake on a meal by meal basis

29
Q

How does Glucagon like peptide-1 affect the body

A

GLP-1

  • Proglucagon derived peptide
  • Co-secreted with PYY from L cells in the intestine
  • Incretin
  • levels rise after a meal and fall during fasting
  • reduces food intake, suppresses glucagon secretion and delays gastric emptying
30
Q

How does Oxyntomodulin affect the body

A
  • Proglucagon derived peptide
  • relleased from L cells of the intestine in response to ingested food and in proportion to caloric intake
  • anorectic effect
31
Q

how does Pancreatic Peptide affect the body?

A
  • secreted from cells in the pancreatic islet of langerhans

- Putatively decreases food intake through Y4R in the brainstem and hypothalamus

32
Q

How does Glucagon affect the body?

A
  • secreted by a cells of the pancreatic islets
  • increases blood glucose levels and insulin secretion
  • reduces food intake
33
Q

How does Amylin affect the body?

A
  • Stored and relleased with insulin in response to food intake
  • anorectic effects (inhibition of NPY release)
34
Q

what is Anorexia nervosa? and what physiological changes are occuring?

A

Characterized by self starvation and excessive weight loss

Patients become severely manourished and significantly emaciated leading to endorinological and cardiological dysfunctions and abnormalities within the digestive, skeletal, and reproductive systems

Polymorphisms in genes in eating attitudes, the regulation of eating behavior, motivation and reward mechanism (AgRP)

Basal and pulsatile secretion of leptin is reduced in association with reductions in fat mass

Ghrelin resistance appears to be a conductive factor to a restrictive diet

Elevated levels of PYY
-might contribute to decreased nutrient intake and disordered eating psychopathology

GIGU test! (40 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions