Brainscape's Knowledge GenomeTM

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


See full index

GI > Control of Food Intake > Flashcards

Control of Food Intake Flashcards

1
Q

Where’s ghrelin secreted from?

A

stomach fundus

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

Role of gherlin?

A

increases hunger + stimulates gastric emptying

stimulates neuropeptide Y + AgRP neurons

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

Role of PYY?

A

signals satiety + inhibits gut motility

inhibits same AgRP neurons

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

What’s obestatin?

A

peptide derived from same prohormone as ghrelin + opposes effects of ghrelin

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

Role of amylin?

A

reduce food intake via medulla of brainstem by delaying gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are enterogastrones eg secretin, CCK (cholecystokinin), GIP (gastric inhibitory peptide)?

A

hormone secreted by ‘mucosa of the duodenum’ in lower GI tract in response to dietary lipids that inhibit the aboral motion of chyme

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

What’s relaxation of gastric reservoir (fundus) mediated by?

A

Reflexes :

  • Receptive (mechanical stimulation of pharynx-mechanoreceptors, sight)
  • Adaptive (vagal innervation NO/VIP, tension of stomach)
  • Feedback (nutrients, CCK)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the reflexes (receptive, adaptive, feedback-relaxation) mediated by?

A

non-adrenergic, non-cholinergic (NANC) mechanisms (inhibition involving NO, VIP,) + reflex chains involving release of NA from sympathetic nerve fibres helping stomach to relax via constriction of blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What’s pituitary adenylate cyclase (AC)-activating peptide (PACAP)?

A

secretin family of peptides that’s isolated from pituitary,

high levels in brain, but also found in myenteric + submucosal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Role of PACAP?

A
  • Stimulate adenylate cyclase activity in anterior pituitary
  • Mediates neuronal regulation of gastric acid secretion; intestinal motility
  • Stimulates relaxation of colonic smooth muscle
  • Stimulates pancreatic secretions
  • Stimulates insulin + glucagon secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Implications of vagotomy?

A
  • Impairs accommodation, gastric compliance, emptying
  • Ccause for early satiety in 5% patients
  • Nausea + bloating from gastric stasis in absence of a mechanical obstruction
  • Disturbances of fundic + antral contractility (but cause can be non-motor factors)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What’s gastroparesis?

A

delayed gastric emptying

5% of patients who undergo vagotomy

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

Define Gastric compliance

A

accommodation + perception of distension

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

Role of vagotomy?

A

surgical correction for peptic ulcer disease or malignancy

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

Define hunger

A

discomfort caused by lack of food + desire to eat – a strong physiological craving/drive for food/sensation of emptiness in the stomach

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

Define satiety

A

state of being full after eating food (joyous moments – no longer need to continue eating)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Define aphagia

A

inability or refusal to swallow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define hyperphagia/polyphagia

A

abnormal desire for food (extreme unsatisfied drive to eat)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define appetite

A

psychological desire/drive to satisfy the body’s needs of food; a hunger-stimulated response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Role of satiety?

A

signals function to prolong the interval until hunger or the onset of next meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What’s appetite influenced by?

A

social situations, food palatability, emotional, habitual, circadian factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What’s BMI?

A 
70% due to genes, how much we eat + its composition
BMI:
<18.5kg/m^2 = underweight
>30kg/m^2 = overweight
>35kg/m^2 = obese
>40kg/m^2 = morbidly obese
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How hypothalamus controls appetite + food intake?

A

base has several nuclei that regulate energy homeostasis → control appetite, size of helping, ingestive behaviour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What has executive control of food intake?

A

prefrontal cortex + limbic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Role of prefrontal cortex?

A

Food-seeking

  • Integration of sensory information from inside + outside body
  • Receive emotional + cognitive info from limbic system
  • Helps make choices by translating all homeostatic + environmental info into adaptive behavioural response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Role of limbic system?

A

Complex system of nerves + networks in brain : areas concerned with instinct + mood

  • Control emotions, pleasure (fear, anger)
  • Satiation of feeding behaviour associated with motor planning + execution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Role of cortico-limbic?

A
  • mechanisms of reward under executive control of prefrontal cortex
  • prefrontal cortex receives sensory, emotional, cognitive info from limbic system
  • connected to cortical areas involved in motor planning + execution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Role of lateral hypothalamus (LH)?

A

hunger/thirst centre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Role of ventromedial nucleus (VMN)?

A

satiety centre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Role of dorsomedial nucleus (DMN)?

A

modulates energy intake (hunger centre)

release NPY into DMN to ↑ feeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Role of paraventricular nucleus (PVN)?

A

modulates feeding behaviour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Parts of brain that control feeding behaviour?

A 
Lateral hypothalamus (LH)
Ventromedial nucleus (VMN)
Dorsomedial nucleus (DMN)
Paraventricular nucleus (PVN)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Role of arcuate nucleus?

A

Neurons produce orexigenic signals (NPY, opioids, dynorphin, β-endorphin, POMC, galanin, AA, GABA + glutamate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Role of ventromedial nucleus + lateral hypothalamus?

A

restrain feeding if required; lesion of VMN to ↑appetite, with weight gain that tends to persist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Role of paraventricular nucleus + perifornical hypothalamus?

A

control feeding behaviour
NPY, opioids, GABA to ↑ feeding
leptin to↓ food intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Role of GABA?

A

reduces feeding behaviour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Role of suprachiasmatic nucleus or nuclei (SCN)?

A

each side of hypothalamus tiny above optic chiasm

controls circadian rhythms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Role of medial amygdaloid nucleus (MeA)?

A

sub-region of amygdaloid complex

mediates food intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Where’s human body clock located?

A

in suprachiasmatic nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Role of ligands 5-HT (via 5-HT2C + 5-HT1A receptors)-regulates appetite and food intake

A

regulation of food intake + appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Role of orexigenic + anorexigenic NT?

A

in hypothalamus

  • Orexigenic neurotransmitters: ↑appetite
  • Anorexigenic neurotransmitters: ↓ appetite
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe how serotonin agonist suppresses appetite

A
  • appetite suppressing neurons make precursor pro-opiomelanocortin (POMC)
  • POMC -> α-MSH
  • serotonin 5HT2C agonist eg meta-chlorphenylpiperazine (mCPP)
  • binds to 5HT2C receptors on POMC neurons
  • activates POMC neurons
  • release of α-melanocyte stimulating hormone (α-MSH)
  • binds to melanocortin 4 receptors (MC4R)
  • suppress appetite
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe how orexogenic factors (NPY + AGRP) suppress appetite

A
  • NYP + AGRP released in arcuate nucleus
  • bind to receptor
  • NPY bind to Y receptors
  • carry signal transduction mechanisms via GPCR
  • ↑appetite
  • AGRP a competitive antagonist to MCR4
  • natural agonist α-MSH bind to MCR4
  • ↓appetite
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What does appetite suppressing pathway release?

A

alpha-melanocyte stimulating hormone (alpha-MSH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does appetite suppressing pathway release?

A

α-melanocyte stimulating hormone (α-MSH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are GABA + dopamine?

A

anorexigenic factors so decrease appetite
5HT does
this by reacting with 2C and the 1A receptors. How do we know this? If we carry out
an experiment, we could use an agent called Zimelidine

47
Q

Why do zimelidine test?

A

inhibits reuptake of 5-HT from synaptic cleft, so 5HT persists + mediates its effects in suppressing appetite
-Side effects : dry mouth, hyperhidrosis, vertigo, nausea, dryness of nasal membranes

48
Q

Diff effects of GABA on feeding behaviour?

A

Injections of 100 ng of GABA into LH were variable:

  • Injection of GABA into VMH reliably ↑ food intake
  • Injection of GABA into origin of nigrostriatal dopamine (DA) neurons in substantia nigra (SN) suppressed food intake
  • Similar injections of GABA into the origin of mesolimbic DA cells in ventral tegmental area (VTA) irrelevant
49
Q

Highlights of data on zimelidine graphs?

A

Zimelidine (0.2, 2, 20nmol/100nL) in MeA evoked dose-dependent hypophagic effects in fasted rats;

  • MeA 5-HT2C receptors involved in hypophagic effect caused by zimelidine in MeA;
  • MeA 5-HT2C receptors target of zimelidine evoking hypophagic effect
50
Q

Features of satiety centre?

A

=Hypothalamus : ventromedial wall of paraventricular nuclei

  • Stimulation of ventromedial wall of paraventricular nuclei → aphagia
  • Lesions of ventromedial wall of paraventricular nuclei → hyperphagia (increased appetite or excessive hunger)
  • Brain has glucostat
51
Q

Features of feeding/hunger/thirst centre?

A

=Lateral hypothalamus

  • Stimulation of lateral hypothalamus → ↑feeding
  • Lesion → aphagia
52
Q

Effect of opioids + GRRH on appetite?

A

↑ appetite

53
Q

Effect of opioid agonist on appetite + eg?

A

Naltrexone (opioid antagonist) reduces positive ‘hedonic valence😊’ of food

54
Q

Effect of removing lateral hypothalamus?

A

hypophagia (decreased feeding) –> severe weight loss –> death

55
Q

Effect of removing ventromedial hypothalamus?

A

hyperphagia (increased feeding)

56
Q

Effect of recreational drugs on appetite?

A
  • Marijuana increases total daily caloric intake by 40%.

- Inject opioids increases food palatability + intake

57
Q

What controls nutrient intake?

A
  • Signals from periphery + CNS
  • Higher functions modulate responses to CNS + peripheral cues (eg gut; environment) → inhibition or stimulation of food intake
58
Q

Factors that affect if food is ingested?

A

Food preferences
Emotions
Environment
Life style

59
Q

How does stomach control food intake?

A

Stomach nerves act as clock to coordinate food intake due to circadian rhythm which may limit food intake to certain times throughout the day

60
Q

Effect of [glucose]blood on food intake?

A

-stimulates gluco-receptors in hypothalamus
↓[glucose]blood →up-regulation of hunger
↑[glucose]blood → up-regulation of satiety

61
Q

Why do diabetic patients feel hungry despite ↑[glucose]blood?

A

Cold environments stimulate feeding while hot environments inhibit appetite

62
Q

Afferent input

A

-Distension of full stomach inhibits appetite
-Contraction of empty stimulates appetite
Deposition of fat may control appetite (leptin)

63
Q

Why does enervation of intestines and stomach have no effect on food intake?

A

peripheral signals from adrenals, as pancreas, adipose tissue, GIT, CNS operates to control food intake + energy expenditure

64
Q

Effect of insulin on feeding behaviour?

A

decreases feeding behaviour
: It may have

65
Q

Effect of glucagon on feeding behaviour?

A

maintains euglycemia

66
Q

Why are type 1 DM not obese?

A

hyperphagic
not obese as insulin vital for adipocytes to store fat, so excess calories consumed wasted via inefficient utilisation + excretion in urine

67
Q

Role of calcitonin?

A

reduces appetite

has CNS effects involving regulation of feeding + appetite, inhibits food intake

68
Q

Role of CCK?

A
  • fat ingestion causes CCK release
  • slowing of gastric emptying (sense of fullness)
  • CCK (from I cells in intestine or nerve endings) + somatostatin inhibit further food intake - satiety factors
  • Injection of CCK in brain → reduction of appetite
69
Q

Role of somatostatin?

A

decreases appetite

It does the same thing as CCK and appears to work

70
Q

Describe how CCK + somatostatin works to decrease appetite

A
  • via vagus nerve too
  • appetite suppression because somatostatin is growth hormone-inhibiting hormone
  • inhibit appetite
  • infuse somatostatin or its analogue octreotide into humans –> hunger + food intake suppressed
71
Q

Describe how insulin (like leptin) is vital adiposity signal

A
  • insulin secreted into blood from pancreas proportion to fat stored in white adipose tissue
  • circulates via brain capillaries
  • insulin transported into brain
  • acts on insulin receptors on neurons with either net catabolic or anabolic activity
  • eg arcuate nucleus of hypothalamus
  • influence energy homeostasis (food intake + energy expenditure) + fat stored in body by exerting a net catabolic action
  • insulin in brain reduces food intake
  • food intake increases until body weight + insulin signal restored
  • insulin signal increases
  • reducing food intake until weight is lost
72
Q

Effect of insulin on other places?

A

-insulin stimulatory in POMC/CART (pro-opiomelanocortin/cocaine-amphetamine-regulated-transcript)
neurons
-promote satiety while in NPY/AgRP neurons
-mainly inhibitory to reduce appetite + increase energy expenditure

73
Q

What inhibits + induces lipolysis?

A
  • Insulin inhibits lipolysis in adipocytes

- Ghrelin, NA, A, GH, testosterone, cortisol induce lipolysis

74
Q

Effect of insulin, glucagon, amylin secreted from endocrine pancreas?

A

regulation of energy homeostasis

  • insulin acts at liver + forebrain to reduce energy intake + suppress hepatic glucose production
  • glucagon acts at liver to increase glucose production while generating a signal to reduce energy intake –> relayed to hindbrain
  • amylin acts at hindbrain to reduce energy intake
  • NTS (nucleus of the solitary tract)
  • AP (area postrema) is a medullary structure that controls vomiting + control autonomic functions by CNS
  • islet amyloid polypeptide or amylin is co-secreted with insulin from pancreatic β-cells
  • amylin acts as satiety signal
  • antagonists of amylin (amylin 8-37, AC 253, AC 187) if administered prior to meals systemically or directly into area postrema reduce anorectic action of exogenous amylin
  • amylin + CCK interact synergistically to reduce meal size
  • amylin reduces food intake via medulla + by delaying gastric emptying
  • glucagon like peptide-1 (glp-1): pre-pro-glucagon gene expressed in enteroendocrine L cells of intestine, pancreas, brainstem
  • cleaved by pro-hormone convertases 1+2
  • produces glucagon in pancreas, GLP-1, GLP-2, oxyntomodulin in CNS + intestine
  • after meal GLP-1 released into circulation
  • acts via vagus nerve
  • inhibit food intake
75
Q

Effect of insulin, glucagon, amylin secreted from endocrine pancreas?

A

regulation of energy homeostasis

act as anorexigenic agents

76
Q

How does glucagon regulate energy homeostasis?

A

acts at liver to increase glucose production while generating a signal to reduce energy intake –> relayed to hindbrain

77
Q

How does amylin regulate energy homeostasis?

A

acts at hindbrain to reduce energy intake

78
Q

Role of AP (area postrema)?

A

medullary structure controls vomiting + control autonomic functions by CNS

79
Q

Role of glucagon like peptide-1 (GLP-1)?

A

=pre-pro-glucagon gene expressed in enteroendocrine L cells of intestine, pancreas, brainstem

  • cleaved by pro-hormone convertases 1+2
  • produces glucagon in pancreas, GLP-1, GLP-2, oxyntomodulin in CNS + intestine
  • after meal GLP-1 released into circulation
  • acts via vagus nerve
  • inhibit food intake
80
Q

Role of glucagon like peptide-1 (GLP-1) on food intake?

A

=pre-pro-glucagon gene expressed in enteroendocrine L cells of intestine, pancreas, brainstem

  • cleaved by pro-hormone convertases 1+2
  • produces glucagon in pancreas, GLP-1, GLP-2, oxyntomodulin in CNS + intestine
  • after meal GLP-1 released into circulation
  • acts via vagus nerve
  • inhibit food intake
81
Q

Effect of amylin antagonists?

A

eg (amylin 8-37, AC 253, AC 187) if administered prior to meals systemically or directly into area postrema reduce anorectic action of exogenous amylin

82
Q

Role of amylin?

A
  • islet amyloid polypeptide or amylin is co-secreted with insulin from pancreatic β-cells
  • acts as satiety signal
  • amylin + CCK interact synergistically to reduce meal size
  • reduces food intake via medulla + by delaying gastric emptying
83
Q

Features of leptin?

A
  • Gene codes for a 16kDa protein-leptin
  • Gene expressed mainly in adipocytes (fat cells)
  • Administration can decrease food intake, induce weight loss + increase energy expenditure
84
Q

What are adiposity signals?

A

insulin + leptin determine food intake via fat-related lipostatic signal to brain

85
Q

Effect of leptin + ghrelin?

A
  • Leptin + ghrelin act reciprocally on food intake

- due to stimulation of their receptors in hypothalamus → changes in food intake

86
Q

Describe how leptin works?

A
  • white adipose tissue -> leptin (lipostat:signals fat stores in adipose tissue)
  • controls fat stores by operating a feedback mechanism between adipose tissue + brain
  • ↑adipose tissue size → ↑leptin secretion
87
Q

Effect of leptin or insulin abundance?

A

anorexigenic pathways prevail: increase of energy expenditure + thermogenesis, diminished food intake

88
Q

Effect of decreased leptin + insulin serum conc?

A

orexigenic pathways: low metabolic rate + enhanced appetite

89
Q

Effect of satiation?

A

suppresses food intake + weight w/o causing conditioned taste aversion

90
Q

Effect of insulin + leptin?

A

act agonistically reducing food intake via action on receptors within brain

91
Q

Role of leptin?

A

-Increases expression of anorexigenic factors
(pro-opiomelanocortin (POMC)
cocaine and amphetamineregulated transcript (CART)
corticotrophin-releasing hormone (CRH)
neurotensin
-Stimulates metabolic rate
-Inhibits neuropeptide Y, which stimulates feeding

92
Q

Effect of leptin resistance?

A
  • Binge eating, despite adequate or growing adipose tissue (obese)
  • Hyperphagia
93
Q

What secretes leptin?

A

white adipose tissue and gastric mucosa - contains epithelial endocrine, exocrine cells secreting leptin in blood stream + in gastric lumen

94
Q

What does microscopy show about leptin?

A

Light + electron microscopy show adipocytes + gastric epithelial cells contain leptin along their RER-Golgi-granules secretory pathway
synthesize soluble form of leptin receptor that’s secreted bound to leptin in blood –> gastric juice
-soluble receptor protect leptin + enhances half-life

95
Q

Features of gastric leptin?

A
  • Gastric cells leptin follow rapid regulated secretion pathway
  • Short term regulation of digestion, including delay of gastric emptying, absorption of nutrients by intestinal wall, secretion of gastric, intestinal, pancreatic hormones
96
Q

Features of adipocyte leptin?

A
  • Adipocytes secrete leptin in constitutive slow

- Acts on hypothalamus for long-term regulation of food intake

97
Q

Role of ghrelin?

A
  • Appetite-inducing hormone (an orexin)
  • Stimulates hunger
  • Fast-acting and stimulates food intake
  • Released by stomach, pancreas, adrenals in response to nutritional status
98
Q

Describe how gherlin stimulates food intake

A
  • high circulating gherlin before meal
  • low circulating gherlin after meal
  • increases central orexins eg NPY, AgRP
  • generate hunger signals
  • suppresses ability of leptin to stimulate anorexigenic factors
  • secretion of ghrelin can be inhibited by leptin
99
Q

Describe effect of gherlin

A
  • P/D1 cells in upper stomach produce gherlin
  • ↑glucose levels inhibit P/D1 expression
  • below blood glucose threshold activates ghrelin
  • reaches arcuate nucleus of the hypothalamus (ARC) via bloodstream + activates expression of agouti-related protein (AgRP), NPY (+ cannabinoids)
  • AgRP + NPY generate hunger signals by stimulating orexigenic neuron

(In brain NPY implicated in anxiety, depression, feeding, obesity, memory retention, neuronal excitability, endocrine function, metabolism)

100
Q

Features of obestatin?

A
  • Produced by stomach epithelial cells
  • Encoded by ghrelin gene, but opposes effects
  • Suppresses food intake (suppresses appetite; ↓ body weight gain)
  • Antagonises ghrelin-induced food intake (+ growth hormone secretion)
  • Mediates its effects via diff receptors to ghrelin
101
Q

Effect of decreased ghrelin/obestatin ratio?

A

obesity

102
Q

Describe tonic vs episodic signals

A
  • tonic signal for drive to eat that reflects body’s demand for energy arises from free fat mass (FFM) + resting metabolic rate (RMR)
  • drive under tonic inhibition from leptin
  • action reflects amount of stored energy reserves in body
  • as adipose tissue increases leptin insensitivity occurs
  • tonic inhibition reduced
  • drive to eat periodically interrupted + suppressed by episodic signals (peptides released from GI tract in response to food consumption)
103
Q

Why does prolonged exercise stimulate hunger?

A

by increasing post-prandial satiety signalling via an effect on GI peptides

104
Q

Role of stomach nerves?

A

responsible for telling the brain how much food a person has eaten + when to stop eating

105
Q

Summary of DMN (dorsomedial nucleus)?

A
  • Modulates energy intake
  • Destruction → hyperphagia + obesity
  • Injection of GABA, NPY, galanin (orexigenic agents) stimulates appetite/food intake
  • DMN receive projections from agRP/NPY neurons from ARC (arcuate nucleus)
  • Has NPY-expressing cells
106
Q

Summary of PFA (perifornical area)?

A
  • Sensitive hypothalamic site for NPY-induced eating
  • NPY in high conc within neurons of hypothalamus
  • If injected into hypothalamus stimulates stimulus to eat
107
Q

Summary of FX (fornix)?

A
  • C-shaped bundle of nerve fibres in brain
  • Carry signals from hippocampus to mammillary bodies (pair of small round bodies on under surface of brain that as part of diencephalon)
  • Anterior nuclei of thalamus
  • Part of limbic system
  • Involved in re-collective memory
108
Q

Summary of LHA (lateral hypothalamic area)?

A

hunger/thirst or feeding centre

109
Q

Summary of VMN (ventromedial nucleus)?

A

satiety centre

110
Q

Summary of ME (median eminence)?

A
  • Part of hypothalamus
  • Releases regulatory hormones
  • Integral to hypophyseal portal system (midline structure below 3rd cerebral ventricle connecting hypothalamus with pituitary gland)
111
Q

Summary of ARC (arcuate nucleus)?

A

=infundibular nucleus

  • Aggregation of neurons in mediobasal hypothalamus
  • Diff groups of arcuate nucleus neuroendocrine neurons secrete various types or combinations of neurotransmitters, neuropeptides (NPY, GnRH, AgRP, CART, kisseptin, dopamine, SP, GHRH, neurokinin B, β-endorphin, MSH, GABA, somatostatin, POMC = precursor polypeptide that’s cleaved to α-MSH + β-endorphin + expressed
  • Role in feeding involves neuropeptide Y (NPY), another peptide, agouti-related protein (AGRP), inhibitory neurotransmitter GABA
112
Q

Describe study on why ARC is primary site of satiety effect of leptin

A

-obese (ob) gene encodes a fat cell-derived circulating satiety factor (leptin) that’s involved in regulation of energy homeostasis
-effects of i.c.v. injection of recombinant human leptin on food intake + weight gain in rats
-effects of direct microinjections of leptin into ARC, VMH, LH
-1 injection reduced sig, dose-dependently food intake, body weight gain in rats
-microinjections into bilateral arc, VMH, LH caused dose-related decreases in food intake + weight gain
rank order of potency; Arc > VMH = LH

113
Q

HOW IS FOOD INTAKE CONTROLLED?

A

-Depends on the detection and integration of a variety of signals
-Energy stores and energy fluxes
-Inputs received (gut-brain axis): palatability, emotional, circadian, social/situational, habitual, GI handling of the food
-Some players at the cross-roads of energy metabolism:
Short-term: insulin, amylin, glucagon, CCK, NPY
Long-term: leptin, ghrelin, obestatin; insulin (and amylin)?
-Hormones have GI, metabolic and behavioural effects by modulating meal size and food intake
-Mediators (leptin, NPY, etc.) elicit their effects via noradrenaline has been suggested

114
Q

Role of NA?

A

α1 stimulation ↓ eating

α2 stimulation ↑ eating

GI (15 decks)

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