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LCRS Year 2 - Endocrinology > Obesity and the Endocrine Control of Food Intake > Flashcards

Obesity and the Endocrine Control of Food Intake Flashcards

1
Q

What is balanced in body weight homeostasis?

A

Food Intake
Energy Expenditure

Eat more food than you’re expending energy = rise in body weight and vice versa

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2
Q

What is the main organ which is involved in body weight homeostasis?

A

The hypothalamus

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3
Q

How does the hypothalamus regulate body weight?

A

Has many inputs from hormones and organs from around the body which all influence its regulation of food intake (via hunger sensation etc) and energy expenditure

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4
Q

What is the key area of the brain involved in the regulation of food intake?

A

Arcuate nucleus of the hypothalamus

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5
Q

What is special structurally about the arcuate nucleus, what does this allow and does it integrate peripheral or central feeding signals or both?

A

Incomplete blood-brain-barrier

  • this allows access to peripheral hormones (which regulate food intake)
  • integrates BOTH peripheral and central feeding signals
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6
Q

What are the two types of neuronal populations in the arcuate nucleus?

A

Stimulatory (NPY, Agrp neuron)

Inhibitory (POMC neuron)

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7
Q

Which neurone types increase appetite?

A

Stimulatory - NPY/Agrp neurones

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8
Q

Which neurone types decrease appetite?

A

Inhibitory - POMC neurones

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9
Q

To where do both inhibitory and stimulatory neurones extend?

A

Extend to other key parts of the hypothalamus involved in appetite regulation and extra-hypothalamic regions

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10
Q

What is the name of the receptor that reduces appetite when stimulated and where is it found?

A

MC4R

- found in the paraventricular nucleus (arcuate and paraventricular nuclei are in contact)

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11
Q

How are the arcuate nucleus, the paraventricular nucleus, and the MC4Receptor involved in regulating food intake?

A

The arcuate nucleus contains two types of neurones: POMC (appetite-decreasing) neurones and Agrp (appetite-increasing) neurones.

  • When the POMC neurones are activated, they release a peptide hormone called alpha-MSH which travels to the paraventricular nucleus, where MC4R are found. When alpha-MSH binds to MC4R, it stimulates it and MC4R reduces appetite when stimulated thus reducing food intake.
  • When the Agrp neurones are activated, they release Agrp which travels to the paraventricular nucleus. However, when it reaches the MC4R, it actually inhibits the receptor which prevents the receptor from reducing appetite, thus overall INCREASING food intake.
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12
Q

What do POMC deficiency and MC4-R mutations cause?

A

Morbid obesity

  • very rare cause of obesity but it is possible
  • if POMC and MC4-R are problematic then appetite is never reduced so continually hungry
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13
Q

Is the hypothalamus alone in regulating food intake?

A

No, quite the opposite dear Watson

  • the hypothalamus is involved with numerous other brain regions
  • also communicates with the Gut via the Vagus nerve and the brainstem, and slo communicates with adipose tissue
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14
Q

What does a recessive mutation of the Ob gene cause? (seen in mice)

A
  • Profoundly obese
  • Hyperphagia (always eating)
  • Diabetic (because of the hyperphagia)
  • Decreased body temperature
  • Decreased energy temperature
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15
Q

What is Leptin?

A

It is a peptide hormone which signals how much fat store we have in our body

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16
Q

Where is Leptin released from?

A

From fat

- white adipose tissue

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17
Q

Where are receptors for Leptin found in the body?

A

Hypothalamus

- termed Ob-R(eceptors)

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18
Q

What gene codes for the hormone Leptin?

A

The Ob gene (everything makes sense now dunnit!)

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19
Q

So what is missing in humans/mice with an Ob gene mutation?

A

Leptin!

- no communication between the fat in their body and the hypothalamus to regulate food intake so permanently hungry

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20
Q

When is Leptin high and low?

A

High when high body fat

Low when low body fat

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21
Q

What does central or peripheral administration of leptin (by injection) cause?

A

Decreases appetite and food intake
- Increases thermogenesis (way of expending energy)

Decreases food intake
Increases energy expenditure

22
Q

How does Leptin interact with the arcuate nucleus (POMC/Agrp)?

A

Activates POMC neurones (stimulates MC4-Rs which reduces appetite)
Inhibits NPY/Agrp neurones (prevents increasing appetite)

23
Q

How effective is leptin as a weight control drug and why is this?

A

Ineffective

  • leptin circulates in plasma at concentrations proportional to fat mass
  • most obese humans have very high leptin and this is mainly due to their diet of high fat, high sugar diet
  • past a certain point of obesity, the brain becomes resistant and unresponsive to leptin, so the hormone is present but doesn’t signal effectively
24
Q

What levels do insulin circulate at, where are receptors for insulin in the brain, and what does central administration of insulin cause?

A
  • Insulin circulates at levels proportional to body fat
  • receptors are in the hypothalamus (insulin is a peripheral hormone communicating centrally with the hypothalamus)
  • central administration (into the brain) reduces food intake
25
Q

What is the largest endocrine organ in the body?

A

The GI tract!

26
Q

How many different regulatory peptide hormones are released in the GI tract and what is their release regulated by?

A

More than 20

- released regulated by the content of nutrients found in the gut

27
Q

What processes are influenced by GI tract-secreted peptide hormones?

A

Gut motility
Secretion of other hormones
Appetite (important)

28
Q

What is Ghrelin also known as, what does it affect and where is it released?

A

‘The Hunger Hormone’

  • increases appetite
  • released by the stomach
29
Q

When is Ghrelin high and low around meals?

A

High before meals (increases appetite)

Low after meals (appetite is ‘satiated’)

30
Q

How does Ghrelin affect neurones in the arcuate nucleus?

A

Directly modulates neurones in the arcuate nucleus

  • Stimulates NPY/Agrp neurones
  • Inhibits POMC neurones

Overall increases appetite

31
Q

What interesting research did Imperial conduct on Ghrelin’s effects?

A

Gave participants infusion of saline or ghrelin and assessed food intake after both.

  • both participant and instructor blinded
  • every single participant ate more on the day they were give Ghrelin compared with the day they were given Saline
32
Q

What hormones do L cells secrete and where are L cells found?

A

PYY
GLP-1
- L cells are endocrine hormone-secreting cells found in the gut

33
Q

What is PYY also known as and what does it do?

A

Peptide-YY - the ‘satiety hormone’

  • reduces appetite after we’ve eaten
  • induces the feeling of ‘fullness’
34
Q

How does PYY work?

A

OPPOSITE OF GHRELIN
Directly modulates neurones in the arcuate nucleus
- inhibits NPY/Agrp neurones
- stimulates POMC neurones

Overall decreases appetite

35
Q

What did the results in a study assessing the effect of PYY show?

A

Opposite effect to ghrelin

  • all 12 volunteers ate less food after PYY injection compared with the control
  • reduced food intake by 36%
36
Q

What is GLP-1, where is it released, what is it coded for and when is it released?

A

Glucagon-like Peptide-1

  • Released in the gut
  • coded for by the PREPROGLUCAGON gene (some of which codes for glucagon itself)
  • released post-prandially (after eating)
37
Q

What type of hormone is GLP-1 and what effect does it have on appetite?

A 
An Incretin (has good incretin characteristics, augments insulin secretion well)
- Reduces appeitite
38
Q

What are Incretins?

A

Hormones that

  • are released after eating
  • augment insulin secretion from beta islet cells
39
Q

Thinking on the effects of incretins, what can GLP-1 be used to treat?

A

Diabetes!

- pharmacological mimicry of GLP-1 enhances insulin release which helps treat the diabetes

40
Q

What is DPP-4?

A

DPP-4 is a peptide enzyme which breaks down GLP-1

41
Q

What is the purpose of DPP-4 inhibitors and what is the main benefit to the patient of these drugs over GLP-1 agonist injection?

A

Inhibit DPP-4 enzymes preventing breakdown of endogenous GLP-1 (boosts GLP-1 effect)
- main benefit is they can be given orally whereas GLP-1 agonists must be injected, sometimes multiple times a day which is unpalatable enough to some patients that they can’t follow the treatment plan

42
Q

Why must GLP-1 agonist analogues be developed to be resistant to breakdown?

A

Endogenous GLP-1 only has a half-life of around 1 minute before it is inactivated by DPP-4
- any drugs that mimic GLP-1 must be resistant to breakdown in order to have enough of an effect that the patient doesn’t constantly have to inject it

43
Q

What is Saxenda?

A

Saxenda (liraglutide) is a long-acting glucagon-like peptide-1 receptor AGONIST

  • reduces appetite
  • enhances insulin release close to the degree of effect of endogenous GLP-1
44
Q

Why is PYY not a good drug target?

A

In studies, when levels of PYY goes too high, it can induce strong nausea and vomiting
- even with GLP-1 analogues, which are FDA licensed for treatment of diabetes, patients have to be warned of nausea that should usually settle over the first couple weeks

45
Q

Why is obesity a problem, from a medical perspective?

A

Obesity is associated with numerous severe co-morbidities (predisposition to severe clinical problems)

46
Q

What is one major appearing clinical problem associated with obesity?

A

Depression

- both due to their own views on their body and societies pressures and ideals

47
Q

What is the ‘thrifty gene hypothesis’?

A

Hypothesis that when we were cavemen, specific genes were selected for to increase metabolic efficiency and fat storage. In the context of plentiful and easily available food and little exercise, these genes predispose their carriers to obesity and diabetes

  • evolutionary sensible to put on weight and store energy as fat in case of no dinner
  • thin humans didn’t survive famines so didn’t pass on their genes to modern humans
48
Q

Where is the evidence for the ‘thrifty gene hypothesis’?

A

Populations historically prone to starvation become the most obese when exposed to Western diet and sedentary life-style (e.g. Pima Indians, pacific islanders)

49
Q

What is the question that highlights the problem with the ‘thrifty gene hypothesis’?

A

Why aren’t we all overweight if we all have these genes?

50
Q

What is the alternate hypothesis to the ‘thrifty gene hypothesis’?

A 
Adaptive drift ('drifty gene') hypothesis
- idea is that there is a normal distribution of body weight where the most obese can't run away so are eaten and the leanest die during famine

(SEE THE SLIDES IN NIAMH’S PRESENTATION WHICH EXPLAIN THIS FULLY)

51
Q

As a general consensus between the two hypotheses, what drives obesity?

A

The effects of the environment on the genetic background
- everyone is affected different due to genetic variation but some will be affected more than others as their background both promotes this directly (large availability of unhealthy food and sedentary lifestyle) or indirectly (genetically predisposes people to becoming obese when exposed to the correct environment)

LCRS Year 2 - Endocrinology (21 decks)

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