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Yr 2 LCRS - Endo > 14 - Obesity and The Endocrine Control of Food Intake > Flashcards

14 - Obesity and The Endocrine Control of Food Intake Flashcards

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1
Q

What is the balance between in body weight homeostasis?

A

Food Intake

Energy Expenditure

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2
Q

With regards to control of food intake, what overall things feed into the hypothalamus?

A

Ghrelin

PYY

Leptin

Other hormones

Neural input from the periphery and other brain regions

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3
Q

With regards to body weight homeostasis, what two factors can the hypothalamus influence?

A

Food Intake

Energy Expenditure

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4
Q

What is a hypothalamic nucleus?

A

A group of neuronal cell bodies

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5
Q

Where is the arcuate nucleus situated in the brain?

A

Situated either side of the 3rd ventricle

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6
Q

What is the arcuate nucleus and what is it’s function?

A

Hypothalamic nucleus

Key brain area involved in the regulation of food intake

Integrates peripheral and central feeding signals

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7
Q

What factor of the arcuate nucleus allows peripheral hormones to access it?

A

It has an incomplete blood brain barrier

This allows the integration of peripheral (hormones in the circulation) and central feeding signals

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8
Q

What two neuronal populations are present in the arcuate nucleus?

A

Stimulatory

  • NPY/Agrp neuron
  • Stimulate appetite

Inhibitory

  • POMC neuron
  • Suppresses appetite
  • Depending on where POMC is expressed alters what hormones are made from it
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9
Q

Where do the two neuronal populations in the arcuate nucleus extend to?

A

Both sets of neurons extend to other hypothalamic and extra-hypothalamic regions

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10
Q

What are the two key hypothalamic nuclei responsible for appetite regulation?

A

Paraventricular Nucleus

Arcuate Nucleus

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11
Q

What is the function of MC4Rs?

A

Paraventricular nucleus expresses Melanocortin 4 Receptors (MC4R)

When the are activated by α-MSH (made by the cleavage of POMC) from the arcuate nucleus, it decreases food intake

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12
Q

Outline the melanocortin system

A

SUPPRESSION OF APPETITE (activation of melanocortin system)

  • POMC cleaved into α-MSH in the arcuate nucleus
  • α-MSH activates MC4Rs in the paraventricular nucleus
  • Activation of MC4Rs decreases food intake

STIMULATION OF APPETITE (inhibition of melanocortin system)

  • Agrp released from arcuate nucleus
  • Agrp inhibits MC4Rs
  • Inhibition of MC4Rs increases food intake
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13
Q

What does α-MSH stand for?

A

α-Melanocyte Stimulating Hormone

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14
Q

What human CNS mutations have been found to affect appetite?

A

POMC Deficiency

  • causes morbid obesity

MC4-R Mutation

  • causes morbid obesity

No NPY or Agrp mutations associated with appetite discovered in humans as of yet

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15
Q

Are human CNS mutations the cause of rising obesity?

A

No, mutations are not responsible for the prevalence of obesity but they are important to remember

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16
Q

What part of the brain is responsible for appetite?

A

Mainly the hypothalamus

However, it communicates with many other brain regions and parts of the body such as the gut and fat

e.g. prefrontal cortex is important for decision making around food

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17
Q

What nerve links the gut to the brainstem?

A

Vagus Nerve

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18
Q

What is the Ob gene?

A

Ob gene codes for leptin

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19
Q

What is leptin?

A

Hormone released from white adipose tissue

It is a signal for how much fat a person has

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20
Q

Where are the receptors for leptin found?

A

In the hypothalamus (Ob-R)

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21
Q

What hormone is missing in the ob/ob mouse?

A

Leptin

They have only got two mutated versions of the Ob gene

Recessive mutation

People with this mutation are:

  • profoundly obese
  • hyperphagic
  • sometimes diabetic (due to obesity)
  • have decreased body temperature
  • have decreased energy expenditure
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22
Q

What two conditions cause extreme hyperphagia?

A

Leptin deficiency

Prader-Willi Syndrome

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23
Q

Which people would have a high leptin level?

A

People with high amounts of body fat

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24
Q

What does central administration of leptin do to animals?

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A

Decrease food intake

Increases thermogenesis

25
How does leptin act on the hypothalamus?
Activates POMC Inhibits NPY/AgrP Therefore, MC4Rs are activated by alpha-MSH, leading to decreased food intake
26
Where does leptin circulate?
Leptin circulates in plasma Circulates in concentrations proportional to fat mass
27
What happens to leptin sensitivity in obese people?
Obesity often causes leptin resistance Leptin is present in high amounts, but doesn't signal effectively Therefore, leptin is ineffective as a weight control drug.
28
What kind of graphs are these?
Centile growth charts e.g.98th centile = child is in the higher bracket for weight for his age group but still in the normal range
29
What does the top graph show?
Child has higher weight gain compared to other children of their age until the age of 10 Due to leptin deficiency and therefore no suppression of appetite Leptin administration at age of 10 Weight decreases Weight begins to increase at age of 12, as sometimes in peptide hormone administraion, antibodies can be developed against the hormone
30
What is the role of insulin in food intake?
Insulin circulates at levels proportional to body fat Receptors for insulin in the hypothalamus Central administration of insulin reduces food intake by co-ordinating with glucose and energy homeostasis
31
What is the largest endocrine organ in the body?
GI tract * enteroendocrine/L cells
32
How many hormones are released by the gut and what is their release regulated by?
Releases more than 20 different regulatory peptide hormones Release regulates by gut nutrient content
33
What general functions do some of the hormones released by the GI tract have?
gut motility secretion of other hormones appetite
34
What is the colloquial name for Ghrelin?
"Hunger Hormone"
35
What does this graph show?
Healthy individuals had their ghrelin levels measured throughout a day Ate breakfast at 08:00, lunch at 12:00 and dinner at 16:00 Before each food intake, rise in ghrelin After each food intake, fall in ghrelin
36
How does ghrelin carry out its function?
Directly modulates neurons in the arcuate nucleus of the hypothalamus * Stimulates NPY/Agrp neurons * Inhibits POMC neurons * Therefore, it increases appetite
37
How does ghrelin communicate with the arcuate nucleus?
Arcuate nucleus has an incomplete BBB Therefore, ghrelin in the systemic circulation can reach it
38
What cells in the gut release hormones?
Enteroendocrine cells
39
What type of appetite control hormone is PYY (Peptide YY)?
A satiety hormone
40
Explain how hormone PYY3-36 functions
Inhibits NPY release Stimulates POMC neurons Decreases appetite
41
What gut hormone has the opposite effect to ghrelin?
PYY3-36 Reduces food intake by 1/3
42
What is GLP-1?
Glucagon-like Peptide-1 Gut hormone Coded for by the preglucagon gene and released post-prandially
43
Other than GLP-1, what other well-known hormone is coded for by the preproglucagon gene?
Glucagon
44
Where does processing of the preproglucagon gene occur?
Intenstinal L-cells
45
What are the effects of GLP-1?
* Well characterised incretin role * Also reduces food intake
46
What are incretins and name an example of an incretin?
Incretins are hormones that: * are released after eating * augment insulin secretion from ß islet cells An example is GLP-1
47
What is synthetic GLP-1 used to treat?
Type 2 Diabetes Mellitus They are injectable only
48
What are DPP-4 inhibitors used for?
These slow down the metabolism of GLP-1 Therefore, for people who don't like the idea of injecting GLP-1 for treatment for T2DM, they can take DPP-4 inhbitors to slow the breakdown of their endogenous GLP-1
49
What is the problem with administration with peptide hormones?
They have short half-lives in circulation
50
What is Liraglutide?
Long acting GLP-1 receptor agonist (liraglutide) Longer half-life than endogenous GLP-1 From Novo Nordisk * They augment insulin secretion * Reduce appetite
51
What is Saxenda?
GLP-1 analogue Licensed for obesity Double dose needed for diabetics
52
Why is PYY not used to treat obesity?
Narrow therapeutic index Above a certain plasma level of PYY, patients experience extreme nausea
53
What must you warn patients about before prescribing GLP-1 analogues as obesity treatment?
That the patients may experience some nausea as a side effect of the drugs
54
What comorbidities are associated with obesity?
Depression Sleep Apnoea Stroke Myocardial Infarction Bowel Cancer Osteoarthiritis Gout Peripheral Vascular Disease Diabetes Hypertension
55
What is the Thrifty Gene Hypothesis?
**James Neel, 1962** Specific genes selected for to increase metabolic efficiency and fat storage In the context of plentiful food and little exercise, these genes predispose their carriers to obesity and diabetes Evolutionarily sensible to gain weight Thin humans did not survive famines, so didn't [ass their genes on [lean people selected against as reproduction was not possible for them]
56
What evidence supports the Thrifty Gene Hypothesis?
Populations historically prone to starvation become the most obese when exposed to the Western diet and sedentary life-style e.g. * Pima Indians * Pacific Islanders
57
What is the Adaptive Drift (Drifty Gene) Hypothesis?
Normal distribution of body weight * extremely fat are eaten * extremely thin don't reproduce and starve Leaves the majority average people HOWEVER 10-20,000 years ago, humans learned to defend against predators Thus obesity not selected against Putting on fat then a neutral change (genetic drift) In current context, inheritors of thse genes become obese
58
What does this graph show?
Drifty Gene Hypothesis In healthy environment, everyone remains fairly slim In toxic environment where people are exposed to high fat foods and sedentary lifestyle, inheritors of the genes to put on weight become obese

Yr 2 LCRS - Endo (28 decks)

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