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YEAR 2 - Applied Physiology & Pharmacology > 56. Metabolism, Growth and Appetite (HT) > Flashcards

56. Metabolism, Growth and Appetite (HT) Flashcards

1
Q

Give some experimental evidence relating to The Biggest Loser.

[EXTRA]

A

(Fothergill, 2016):

  • Investigated 14 participants of the TV program “The Biggest Loser”
  • 13 of these participants had regained weight in the 6 years after the competition
  • The participants had a greater decrease in the resting metabolic rate (RMR) than would be predicted based on just the changes in body composition.
  • This is evidence for the existence of “metabolic adaptation”, which is an evolutionary adaptation to prevent weight loss.

However, this is a controversial topic. There are uncertainty as to how persistent metabolic adaptation is, what factors increase metabolic adaptation and who is affected most.

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2
Q

Give some experimental evidence for the best rate for weight loss.

[EXTRA]

A

(Purcell, 2014):

  • It is often stated that you are more likely to maintain lost weight if you lose the weight slowly.
  • However, this study showed that te rate of weight loss does not affect the proportion of weight regained within 144 weeks.
  • This goes against many current dietary guidelines.
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3
Q

What percentage of BMI is determined by genetics?

A

40% to 70%

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4
Q

Where is leptin secreted?

A

Adipose tissue

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5
Q

What is the role of leptin and when is it secreted?

A
  • Leptin leads to decreased appetite
  • Leptin production increases exponentially with body fat mass, so it acts as direct feedback, maintaining weight within a narrow range
  • However, leptin levels can also be dissociated from this relationship by various events, such as starvation
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6
Q

Give some experimental evidence surrounding the discovery of leptin.

[EXTRA]

A

(Coleman, 1973):

  • Studied two types of overweight mice, known as ob/ob (for obese) and db/db (for diabetic)
  • Used a technique known as parabiosis, which involves surgically joining two mice’s circulatory systems
  • Parabiosis of an ob/ob mouse and normal mouse caused the ob/ob mouse to lose weight
  • Parabiosis of a db/db mouse and normal mouse caused the normal mouse to stop eating and become cachexic
  • Parabiosis of an ob/ob mouse and db/db mouse caused the ob/ob mouse to lose weight
  • These results suggest the existence of a signal that controls adipocity that was overproduced by the db/db mouse but not produced at all by the ob/ob mouse -> This was confirmed to be leptin

(Zhang, 1994):

  • Positionally cloned the mouse obesity gene and its homologue (leptin) in humans
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7
Q

Give some clinical relevance for leptin.

[EXTRA]

A

(Montague, 1997):

  • Congenital leptin deficiency is associated with severe early-onset obesity in humans.

(Farooqi, 1999):

  • Recombinant leptin therapy in children with congenital leptin deficiency leads to significant weight loss.

(Brown, 2018):

  • Leptin can be used to reverse the metabolic syndrome that is seen in generalised lipodystrophy (lack of adipocytes). This is because these patients do not produce leptin since they do not have much adipose tissue. Improvements in insulin sensitivity are independent of food intake.
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8
Q

How did the discovery of leptin change understanding of adipose tissue?

[IMPORTANT]

A

It lead to the idea that adipose was an endocrine organ involved in energy homeostasis via the secretion of leptin.

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9
Q

How does leptin affect apetite?

A
  • It reduces appetite because it regulates the activity of first order neurons in the arcuate nucleus.
  • It reduces firing of AgRP neurons and increases firing of POMC neurons.
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10
Q

What is some evidence for leptin not only having an effect on weight loss by suppressing food intake?

A

(Levin, 1996):

  • Leptin-deficient mice that were treated with leptin were compared to pair-fed mice (i.e. where mice that are leptin-deficient but not treated are given as much food as those treated with leptin eat)
  • This showed that leptin did not only cause weight loss via reducing appetite
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11
Q

How does leptin affect the body apart from reducing appetite?

A

Leptin is in a neuroendocrine loop with sympathetic nerves:

  • Leptin from adipose tissue feeds back to the brain
  • This drives sympathetic nerve activity, which leads to release of noradrenaline onto the adipose tissues
  • In turn, this leads to increased lipolysis and thermogenesis
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12
Q

Why do high levels of leptin in obesity not lead to weight loss? And why can we not treat obesity by administering more leptin to suppress appetite? Give some experimental evidence.

A
  • Hyperleptinemia causes leptin resistance, perhaps because the levels get so high that a desensitisation threshold is reached (LeDuc, 2019).
  • It might instead be advantageous to instead reduce the leptin levels, so that the sensitivity is increased.
  • (Zhao, 2019) found that using antibodies against leptin in obese individuals helps to increase sensitivity to leptin and thus return to a lower body weight.
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13
Q

Apart from improving leptin sensitivity, how can obesity be treated with relevance to leptin?

A

The action of efferent sympathetic nerves (usually activated by leptin) that stimulate lipolysis and thermogenesis may be amplified using sympathofacilitators. These do not affect the brain, so they have cardioprotective effects.

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14
Q

What are some consequences of obesity?

A

Increased risk of diabetes, hypertension, heart disease, some cancers, obstructive sleep apnoea, hepatic steatosis, biliary disease, neurodegeneration, osteoarthritis.

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15
Q

What are the differences between visceral and subcutaneous fat?

[IMPORTANT]

A

Visceral fat is more unhealthy than subcutaneous fat, which gives rise to the idea of metabolically “healthy” obesity, where the majority of the fat is not centrally located.

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16
Q

How does metabolically healthy obesity compare with being normal weight?

A
  • Being metabolically healthy obese does not increase your risk of hypertension, type 2 diabetes or dyslipidemia
  • However, there is still an increased risk of cardiovascular disease
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17
Q

Give some experimental evidence for the importance of brown adipose tissue.

[EXTRA?]

A

(Bercher, 2021):

  • Brown adipose is associated with cardiometabolic health
  • Of the over 52,000 participants, individuals with detectable brown fat were less likely than their peers to suffer cardiac and metabolic conditions (such as type 2 diabetes and coronary artery disease)
  • Brown adipose tissue can be detected in PET scans using 2-deoxyglucose as a marker

(Hanssen, 2015):

  • Found that short-term cold acclimation improves insulin sensitivity in patients with type 2 diabetes mellitus
  • This is thought to be due to changes in brown adipose tissue activity
  • There are questions about whether this is a sustainable strategy in the longer term, since the patient must remain in a room at around 15*C and there is uncertainty about whether the effect is sustained
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18
Q

What are the differences between subcutaneous and visceral fat?

[IMPORTANT]

A

Subcutaneous fat:

  • Contains beige adipocytes (Similar to brown adipocytes. Made by browning of white adipocytes.)
  • Thermogenic function
  • Protects from metabolic diseases

Visceral fat:

  • Loss of beige adipocyte function
  • Inflammatory action
  • Increases risk of metabolic diseases
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19
Q

How can visceral and subcutaneous fat be exchanged between?

A
  • Various factors can control the transition between the two types of fat
  • PRDM16 activates beige adipocytes, prompting them to burn calories rather than store them.
  • In PRDM16 KO mice develop obesity, insulin resistance, and fatty liver as beige adipocytes no longer functioned properly.
  • Subcutaneous fat “visceralizes”, both at molecular and morphological levels
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20
Q

Describe the concept of browning.

A
  • Adipose tissue is a dynamic tissue that can respond to environmental stimuli.
  • Browning is the increase in the number of brown adipocyte-like cells, named beige adipocytes, upon sustained cold exposure or direct β-adrenergic activation.
  • These beige adipocytes are functionally similar to classic brown adipocytes, since they have many mitochondria, multilocular lipid droplets and express UCP1.
  • This is relevant because it is a target for treatment of obesity.
  • Subcutaneous fat appears to show more browning than visceral fat, so it is considered the healthier type of fat.
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21
Q

How does 2,4-dinitrophenol work? Why is it not used to treat obesity anymore?

[EXTRA]

A
  • It is a protonophore, so it allows protons to bypass the ATP synthatase, dissipating the proton gradient and making ATP synthesis less efficient.
  • It is no longer used because it is difficult to control the thermogenic effect.
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22
Q

Give some experimental evidence surrounding new drugs to be created for treating obesity.

[EXTRA?]

A

Saxenda:

  • One of the most recently approved drugs that effectively treats obesity
  • It is a derivative of Glucagon-like peptide-1 (GLP-1), which is one of the gut hormones regulating food intake & glucose homeostasis
  • It has only been approved for the treatment of diabetes, but many of these patients suffer from obesity as a co-morbidity so it is useful in treating the obesity too

(Müller, 2018):

  • Various peptides derived from gut peptides can be combined into a chimeric structure
  • This produces a structure that can act as an agonist at multiple sites receptors
  • A GLP-1/GIP/Glucagon triagonist would be most effective at reducing body weight and glycaemic control
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23
Q

Give some experimental evidence for the potential of GLP-1 derivatives in treating diabetes.

[EXTRA]

A

Gastric bypass surgery in obese individuals with T2 diabetes tends to lead to some recovery from diabetes before weight loss is observed. This is seen alongside an increase in GLP-1, which suggests that this may be involved in the return to normal insulin sensitivity.

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24
Q

How does metformin lead to weight loss?

[EXTRA?]

A
  • Metformin is usually used to treat diabetes, but it also often leads to weight loss
  • The mechanism of action is not known, but the metformin leads to increases in GDF15.
  • The effects of metformin on weight are lost in a GDF15 KO mouse.
  • GDF15 agonises GFRAL in brainstem to mediate anorexia.
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25
Q

What are some genetic obesity syndromes?

[EXTRA]

A

At least 10% of children with severe obesity have chromosomal abnormalities, nonsense mutations, or missense mutations that strongly determine obesity.

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26
Q

Clinically, what does POMC deficiency cause?

[EXTRA]

A

Severe early-onset obesity, adrenal insufficiency and red hair.

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27
Q

What does melanocortin receptor 4 deficiency cause?

[EXTRA]

A

Hyperphagia, accelerated linear growth, increased bone density, increased adipose and lean tissue mass

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28
Q

What does Prohormone Convertase-1 (PC1) Deficiency cause?

[EXTRA]

A

Defective prohormone processing:

  • Abnormal glucose homeostasis
  • Very low insulin levels
  • Elevated plasma proinsulin and pro-POMC concentrations
  • Hypogonadotrophic
  • Hypogonadism
  • Hypocortisolism

Downregulation of PC1 is also seen in Prader-Willi syndrome.

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29
Q

What does Bardet–Biedl syndrome (BBS) cause?

[EXTRA]

A
  • Obesity, retinitis pigmentosa, polydactyly, hypogonadism, and kidney failure
  • It is a ciliopathic disorder, but it is still unclear how the cilia are involved in obesity
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30
Q

Describe the importance of inflammation in obesity.

[IMPORTANT]

A
  • Obesity is typically characterised by chronic inflammation in the adipose tissue
  • This involves recruitments of macrophages that secrete TNFα
  • This TNFα blocks insulin signalling, which leads to insulin resistance
  • Experimentally, removal of TNFα function leads to return of insulin sensitivity but not resolution of obesity
  • Clinically, Infliximab is an anti-TNFα neutralizing antibody, but it does not ameliorate human obesity.
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31
Q

How are sympathetic-associated macrophages involved in obesity?

A
  • Sympathetic-associated macrophages exist near sympathetic nerves and remove noradrenaline.
  • Since noradrenaline drives browning and activates thermogenesis, its removal leads to weight gain.
  • Therefore, a therapeutic target for treating obesity is the removal of these macrophages.
32
Q

How does the body detect dehydration?

A
  • Subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT) detect the changes in blood osmolarity
  • They can then activate the median preoptic nucleus (in the anterior pituitary), which initiates water seeking and ingestive behavior.
33
Q

What is the osmotic threshold for the stimulation of thirst/drinking?

A

A change of only 2-3 mOsm/L

(i.e similar to that for vasopressin secretion – sensitive to 1% change)

34
Q

How are thirst and blood volume control related?

A
  • Stimuli which cause thirst also switch on ADH to conserve body water
  • Angiotensin II is a very potent stimulus to drinking
  • Low pressure (volume) receptors induce thirst/drinking via the vagus nerve (X) and nucleus of tractus solitarius, which project to the hypothalamus
35
Q

How does taste change when you are thirsty?

A
  • Hypothalamic and orbitofrontal neurons respond to the taste of water if thirsty -> Water tastes better when thirsty
  • Even when not thirsty, the orbitofrontal neurons are involved in reward -> So you continue drinking a drink even if you are not thirsty
36
Q

How is drinking stopped (i.e. how is sufficient water intkae detected)?

A
  • Thirst satiation occurs before there is time for the water to be absorbed, so there must be some pre-absorptive mechanisms
  • Water in duodenum stops drinking so there could be some duodenal or portal vein osmoreceptors
37
Q

Summarise the various brain centres involved in thirst and blood volume control.

[EXTRA?]

A
38
Q

What part of the brain is the key controller of food intake?

[IMPORTANT]

A

Arcuate nucleus (in the hypothalamus)

39
Q

Describe the principle of how the arcuate nucleus controls appetite?

A
  • Arcuate nucleus receives input from various other parts of the brain and from hormones
  • In response, it controls the paraventricular nucleus (PVN) via stimulatory and inhibitory neurons
  • It also sends projections to the dorsomedial nucleus (DMN), lateral hypothalamus (LHA) and ventromedial nucleus (VMN)
40
Q

To what important target does the arcuate nucleus project in order to control appetite?

A

Paraventricular nucleus (PVN) of the hypothalamus

41
Q

What are the two populations of neurons in the arcuate nucleus and how do they control appetite?

A
  • POMC/CART neurons -> Project onto the PVN and inhibit appetite
    • POMC is converted into α-MSH, which is an agonist at MC4 receptors [EXTRA] in the PVN
  • NPY/AgRP neurons -> Project onto the PVN and stimulate appetite
    • NPY binds to NPY receptors (GPCR)
    • AgRP [EXTRA] is an antagonist at MC4 receptors [EXTRA] in the PVN

Thus, the two neuron populations have opposite effects on appetite via the paraventricular nucleus. They also project to the DMN, LHA and VMN.

42
Q

How does the arcuate nucleus control metabolism?

[EXTRA?]

A
  • α-MSH (released by POMC/CART neurons) is an agonist at MC4 receptors in the PVN -> Leads to increased metabolism via TRH release
  • AgRP (released by NPY/AgRP neurons) is an antagonist at MC4 receptors in the PVN -> Leads to decreased metabolism via decreased TRH release [EXTRA}
43
Q

What neurotransmitter do the neurons in the paraventricular nucleus (PVN) use that influences body weight?

A
  • Oxytocin
  • Experimentally, oxytocin administration induces weight loss.
44
Q

Give some clinical relevance of a disorder characterised by abnormal body weight.

[EXTRA]

A

Prader-Willi syndrome:

  • Features loss of oxytocin-producing neurons in the paraventricular nucleus
  • This leads to excessive eating and life-threatening obesity.
45
Q

Give some experimental evidence for the populations of neurons in the arcuate nucleus that affect appetite.

[EXTRA]

A

(Aponte, 2011):

  • Showed that POMC/CART and NPY/AgRP neurons acutely regulate feeding behaviour.
  • Also showed that NPY/AgRP neurons act not only by inhibiting α-MSH signalling via AgRP, but also that their activation alone is sufficient to promote food intake, presumably via NPY.
  • Used optogenetics to study this:
    • POMC stimulation reduces food intake and body weight in a melanocortin signalling dependent manner.
    • Light-stimulus induced feeding by activation of NPY/AgRP neurons.
46
Q

How does the arcuate nucleus know whether to drive or inhibit appetite?

A

It receives input from various other parts of the brain and also detects different hormones and levels of nutrients.

47
Q

What are the different hormones, nutrients and other neurons that the arcuate nucleus detects/receives input from?

A

Hormones:

  • From adipose tissue -> Leptin
  • From pancreas -> Insulin, Pancreatic polypeptide
  • From GI tract -> Ghrelin, Peptide Tyrosin Tyrosin (PYY), Cholecystokinin (CCK)

Nutrients:

  • Glucose
  • Free fatty acids
  • Amino acids

Other neurons:

  • Central: brain stem (NTS)
  • Peripheral
48
Q

For leptin, state:

  • Where it is produced
  • When it is produced
  • How it affects the arcuate nucleus
A
  • Produced in adipose tissue
  • Release is proportional to amount of adipose tissue
  • Binds to receptor tyrosine kinase in the arcuate nucleus:
    • POMC/CART neurons -> Leads to stimulation
    • NPY/AgRP neurons -> Leads to inhibition
  • Thus, it leads to decreased food intake and increased metabolism
49
Q

Where else in the brain (apart from the arcuate nucleus) does leptin act?

[IMPORTANT]

A
  • Ventromedial nucleus (VMN)
  • This is considered the “satiety centre” [IMPORTANT]
  • SF-1 neurons also express leptin receptors, so that stimulation decreases food intake
50
Q

Give some experimental evidence for both the arcuate nucleus and ventromedial nucleus being involved in satiety.

[EXTRA]

A

Selective deletion of leptin receptors in either the VMN or arcuate nucleus leads to less obese animals than knock-down of the receptor in both areas.

51
Q

For insulin, state:

  • Where it is produced
  • When it is produced
  • How it affects the arcuate nucleus
A
  • Produced in the pancreas (by β cell)
  • Circulating levels are proportional to body adipose mass and also released in response to rising blood glucose
  • Binds to receptor tyrosine kinase in the arcuate nucleus (just like leptin):
    • POMC/CART neurons -> Leads to stimulation
    • NPY/AgRP neurons -> Leads to inhibition
  • Thus, it leads to decreased food intake and increased metabolism
52
Q

For pancreatic polypeptide, state:

  • Where it is produced
  • When it is produced
  • How it affects the arcuate nucleus
A
  • Released from pancreatic PP cells in islets of Langerhans
  • Released in response to meal (in proportion to caloric intake)
  • Binds to Y4 receptors (GPCR) in the brainstem (NTS) and hypothalamus (arcuate nucleus and PVN)
  • Reduces food intake and increases metabolism
53
Q

For ghrelin, state:

  • Where it is produced
  • When it is produced
  • How it affects the arcuate nucleus
A
  • Produced by the stomach
  • Concentration increases before a meal and drops upon eating
  • Stimulates NPY/AgRP neurons -> This leads to inhibition of POMC/CART neurons since NPY/AgRP neurons make GABAergic contacts with POMC/CART neurons
  • Thus, ghrelin is the only gastric hormone to increase appetite and decrease metabolism
54
Q

Give some clinical relevance relating to ghrelin.

[EXTRA]

A
  • Circulating concentration of ghrelin is chronically elevated in people with Prader Willi Syndrome
  • This means that obesity is a feature of Prader Willi
55
Q

For peptide tyrosin tyrosin, state:

  • Where it is produced
  • When it is produced
  • How it affects the arcuate nucleus
A
  • Produced in ilium and colon
  • Produced in response to food intake (mainly fat)
  • Binds to Y receptors (GPCRs) in arcuate nucleus and brainstem
  • Leads to decreased appetite
56
Q

For cholecystokinin (CCK), state:

  • Where it is produced
  • When it is produced
  • How it affects the arcuate nucleus
A
  • Produced in the duodenum
  • Produced after a meal
  • High plasma CCK decreases meal size but increases meal frequency
57
Q

What are the two ways in which glucose sensing can be achieved?

A
  • Glucose is metabolised to give ATP, which leads to the closing of KATP channels, depolarising the cell
  • Allosteric modulation of enzymes by glucose
58
Q

Describe how the arcuate nucleus detects blood glucose.

A

Glucose-excited cells (GE):

  • Fire action potentials when glucose rises
  • This occurs because glucose is metabolised to ATP, leading to the closing of KATP channels and therefore depolarisation -> Unclear if this is the only mechanism
  • It would make sense if these were the POMC/CART neurons, but it is unclear

Glucose-inhibited cells (GI):

  • Stop firing action potentials when glucose rises
  • Unclear how glucose inhibits firing (likely mix of pathways)
  • It would make sense if these were the NPY/AgRP neurons, but it is unclear
59
Q

Describe how the arcuate nucleus detects blood fatty acids.

A
  • Neurons don’t use fatty acids as fuel but the fatty acids can diffuse across the blood brain barrier and can diffuse into cells
  • Here they are esterified to fatty acyl-coenzyme A (acyl-CoA)
  • Some theories about how cells detect fatty acids include:
    • The fatty acids are incorporated into the cell membrane and thus modulate the conductance of a variety of ion channels
    • Some neurons have the ability to oxidise the fatty acids and use them as fuels
60
Q

Describe how the arcuate nucleus detects blood amino acids.

A
  • The arcuate nucleus relies on the fact that there are certain amino acids we cannot produce (i.e. essential amino acids), meaning that their presence indicates that a mean has occurred
  • The arcuate nucleus detects leucine since leucine activates mTOR, which controls gene transcription
61
Q

What is mTOR?

[EXTRA?]

A
  • It is a serine/threonine kinase that is involved in gene transcription
  • Stimulation reduces food intake and increases metabolism
  • Leptin and insulin are thought to ultimately activate mTOR
  • It is inhibited by AMP kinase, whose activity is increased by ghrelin and decreased by leptin and insulin
62
Q

Which part of the brainstem is most involved in control of appetite?

A

Nucleus tractus solitarius (NTS) -> It has reciprocal connections with the arcuate nucleus.

63
Q

How does the nucleus tractus solitarius (NTS) detect hormones and nutrients? How does this affect appetite?

A
  • Leptin receptors -> Decreases food intake
  • Ghrelin receptors -> Promotes food intake
  • PYY3-36 receptors -> Decreases food intake
  • Glucose sensing neurons -> Decreases food intake
  • Gastric distention (conveyed via vagus nerve) -> Decreases food intake

There are reciprocal connections with the arcuate nucleus of the hypothalamus.

64
Q

What are some reasons why we eat, aside from meeting energy needs?

A
  • Emotions
  • Hedonic factors
  • Social factors
  • Convenience
  • Cost
65
Q

What are some parts of the brain involved in reward and perception of taste that affect appetite?

A
  • Orbitofrontal cortex (OFC)
    • Combines information on taste, smell and visual inputs
    • Critical for learning which foods to avoid and which to seek out
  • Ventral tegmental area (VTA)
    • Involved in reward via dopaminergic projections to the nucleus accumbens
  • Nucleus accumbens (NA)
    • Involved in reward
    • Cues previously paired with calories elicit neuronal activation, reflecting reinforcing value of food (i.e. Flavours paired with calories are liked more than flavours not paired with calories)
66
Q

Why does food taste better when hungry?

A
  • The ventral tegmental area has both leptin receptors and ghrelin receptors
  • Leptin decreases dopamine release
  • Ghrelin increases dopamine release
  • This explains why food tastes better when hungry, since the ghrelin levels are higher
67
Q

What is the role of the lateral hypothalamus in appetite?

[IMPORTANT]

A
  • It is the “feeding centre” [IMPORTANT]
  • It contains two populations of neurons that both drive appetite:
    • Orexin neurons -> Directly excite NPY/AgRP neurons in the arcuate nucleus
    • MCH neurons (melanin concentrating hormone) -> Promote NPY/AgRP release from the arcuate nucleus
  • Receives input from the arcuate nucleus, VTA, OFC and striatum -> This means that it essentially integrates homeostatic, satiety and reward related inputs to modulate feeding behaviour
68
Q

What are the satiety centre and feeding centre of the brain?

[IMPORTANT]

A
  • Ventromedial nucleus = ‘Satiety centre’
  • Lateral hypothalamus = ‘Feeding centre’
69
Q

What are some common pathologies of fetal growth and what causes them?

A

Growth abnormalities (either growth restriction or large for gestational age) are commonly caused by alteration of uterine environment caused by placental insufficiency, maternal metabolic syndrome, and under- or overnutrition of the fetus.

70
Q

What are the hormones involved in control of energy metabolism that are mentioned in the spec?

A
  • IGF1 (insulin-like growth factor 1)
  • IGF2 (insulin-like growth factor 2)
  • Insulin
  • Growth hormone
  • Human placental lactogen (hPL)
71
Q

What are the functions of ILGF-1 and ILGF-2?

A

Both are similar to insulin and are anabolic:

  • ILGF-1 plays more of a role in adults
  • ILGF-2 plays more of a role in the foetus

They essentially signal that there are sufficient nutrients for cell growth.

72
Q

What is the function of hPL?

A
  • It modifies the metabolic state of the mother during pregnancy to facilitate the energy supply of the fetus.
  • hPL has anti-insulin properties.
  • hPL is a hormone secreted by the syncytiotrophoblast during pregnancy.
73
Q

What are some metabolic responses to chronic malnutrition?

A
  • The main response in chronically malnourished populations is slow growth rate, delayed maturity, and small adult stature.
  • Small stature can be seen as a successful adaptation to low-energy intake because overall basal metabolic rate will be low.
  • There are also other adaptions, such as hormonal changes and retention of water (in the long-term).
74
Q

What does GLP-1 stand for?

A

Glucagon-like peptide

75
Q

What is the effect of GLP-1 on appetite?

A
  • GLP-1 inhibits appetite
  • The satiety effect of GLP-1 may involve both meal entero-enteric reflexes and across meal central signaling mechanisms to mediate changes in appetite and promote satiety.
  • GLP-1 delays gastric emptying and increases gastric volumes. GLP-1 enhances insulin secretion and inhibits glucagon-release.

YEAR 2 - Applied Physiology & Pharmacology (11 decks)

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