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Medsci 312 > Lecture 21; Neuroendocrinology 1 > Flashcards

Lecture 21; Neuroendocrinology 1 Flashcards

1
Q

Which organ is a key player in energy homeostasis?

A

The brain

Detects hormonal nd neural signals regarding nutrients

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2
Q

What does the brain do regulate energy homeostasis?

A

Ø Influences energy consumption (apetite)

Ø Influences entry of nutrients into the blood and their utilisation by most tissues

Ø Overall, the brain ensures adequate circulating energy for immediate tissue needs and ensures adequate stored energy when external energy is scarce (Blood glucose regulation)

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3
Q

What is energy expenditure?

A

Physical Activity
Basal metabolic Rate
Adaptive Thermogenesis

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4
Q

How is energy balance detected?

A

Ø Peripheral signals including nutrients and fat- and gut- derived peptides act in the brain to relay the state of energy flux

Ø Brain integrates incoming information in the form of hormonal and neural signals with data on energetic and anticipated needs

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5
Q

What is an important aspect of digestion that should be noted;

A

Not all food = intake, depends on guts ability to transport nutrients

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6
Q

What is adaptive thermogenesis?

A

Body increases its temperature to aid food digestion and prevent increased food storage.

Or increase in body temperature to environment

or increase in body temperature to facilitate exercise

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7
Q

What detects the nutrient signals?

A

The median eminence neurons sense the n nutrient signals i.e Hormones, stored/released fuels and this is sensed in the hypothalamus

median eminence does this b/c this is where the BBB is thinnest

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8
Q

Describe the Relationship between peripheral signals of energy state that are sensed and integrated in the brain?

A

median eminence detects nutrient signals and stored/released fuels.

Gut; releases gut peptides regarding nutrients. Vagal nerve also relays information

Both these areas relay infortmation to;

Brainstem; Autonomic short term control (ANS response)
&
Hypothalamus; Nutrient sensing and intergration of signals
(Endocrine pituitary response)

The hypothalamus relays to the cortico-limbic system which in turn influences lifestyle environment and in turn eating. i.e apetite

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9
Q

What regulates short term appetite?

A

Satiety hormones (control frequency and size of meals)

  • Control meal size -the release of a short term regulator is affected by food intake and it regulates appetite during each meal
  • Gut peptides released in response to a meal
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10
Q

What are some satiety hormones?

A

Grhelin (Hunger hormone)

CCK (Dec)
PYY3-36 (Dec)

Short term appetite regulators

(Many more)

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11
Q

What determines the amount of CCK release?

A

Cholecystokinin

Satiety signal secreted in proportion of lipids and protein in diet

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12
Q

Whats special about CCK?

A

It can work through the vagus nerve.

Vagus nerve controls satiety normally through stretch receptors in stomach

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13
Q

What does ghrelin express?

A

Circadian rhythm in its release.

Ghrelin levels are increased by fasting and decreased by feeding = Hunger hormone

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14
Q

What are some factors that reduce apetite?

A

Leptin
Insulin
PYY3-36

CCK via vagus nerve and vagus nerve itself

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15
Q

Are satiety signals recognised solely in the brain?

A

Satiation signals are relayed to other brain areas where they are integrated with adiposity signals, hedonic and social factors and local levels of nutrients.

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16
Q

Where does this integration occur?

A

Arcuate Nucleus

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17
Q

Describe all the signals coming into the arcuate nucleus;

A
  • Nutrient hormone signals

Adiposity Signals

  • Leptin
  • Insulin

Satiety Signals

  • CCK
  • PPY3-36
  • Stomach stretch (vagus)

Neural stimuli

  • Social situation
  • Stress
  • Hedonic
  • Time of day
  • Learning
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18
Q

What is the output of the arcuate nucleus?

A

Regulation of adiposity and plasma glucose, also apetite

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19
Q

In the mouse which group of neurons were found to control body weight?

A

Lateral Hypothalamus (lesion = skinny mouse)

Venteromedial hypothalamus (lesion = obese mouse)

Therefore work together

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20
Q

What was the conclusion of the mouse brain lesion study?

A

• The hypothalamus contains 2 centers that regulate food intake:
- feeding center that is tonically active
- satiety center that stops food intake by inhibiting the
feeding center

21
Q

Of the two lesioned areas which was satiety and which was feeding?

A
  • Destroy feeding center (lateral hypothalamus): animals cease to eat - anorexic
  • Destroy satiety center (Ventromedial hypothalamus; VMH): animals overeat & become obese
22
Q

What is a molecule that the brain is careful to sense?

A

Glucose

• The brain has evolved neurons that directly sense and alter their firing rates as glucose availability changes.

23
Q

Where are the glucose sensing neurons located?

A

• These neurons are concentrated in brain areas involved in energy balance and neuroendocrine regulation, such as VMH and the brain stem.

24
Q

How does glucose regulate appetite?

A
  • Glucose utilisation by hypothalamic centers regulates food intake
  • Low blood glucose levels - satiety center is suppressed and the feeding center is dominant
  • Increased glucose utilisation - satiety center inhibits the feeding center
25
Q

What is leptin proportional to?

A

White adipose tissue

26
Q

What is lipostatic theory?

A
  • A signal from the body’s fat stores to the brain modulates eating behaviour so that the body maintains a particular weight. (Leptin)
  • Increased fat stores - decreased eating
  • Decreased fat stores - increased eating
27
Q

What is leptin production regulated by?

A

• Leptin is synthesised by adipocytes under the control of the obese (ob) gene

Leptin regulates apetite and body weight

28
Q

In the negative feedback pathway what does leptin inhibit?

A

• NPY and AGRP are two neuropeptides that leptin inhibits in a negative feedback pathway

29
Q

What are some other examples of neuropeptides and hormones that regulate eating?

A
  • Neuropeptide Y (increases feeding)
  • Pro-opiomelanocortin- derived peptides (α-MSH, ACTH) (decrease feeding) and β-endorphin (increases feeding)
  • Agouti-gene related peptide (AGRP) (increases feeding)
30
Q

What is the Melanocortin Peptidergic Axis?

A
  • Pro-opiomelanocortin (POMC) derived peptides (α- MSH) - bind to melanocortin receptors
  • melanocortin receptors (MC3-R and MC4-R associated with energy balance)
  • Agouti gene related peptide (AGRP) is an antagonist of α-MSH activating MC3-R and MC4-R
31
Q

What is the function of a-MSH acting on MCR4?

A

Inhibits apetite

AGRP antagonizes this.

Lectin balances the two molecules

32
Q

Describe how high levels of leptin have an effect?

A

POMC neurons in Arcuate Nucleus detect high levels of Leptin
= Inc. a-MSH secretion by these neurons

There are also neural projections to many places but in particular the PVN (abundance of MCR4) and Lateral hypothalamic area.

This will lead to signalling for decreased food intake.

i.e ACTH and Thyrotropin release from AP

and activating SNS to increase energy expenditure

33
Q

Describe the effects of low levels of leptin;

A

AGrP neurons in the arcute nucleus release ARRP into the VPN.

This inhibits the secretion of hypophysiotropic hormones that control the secretion of ACTH and TSH (blcoks MCR4)

AGrP in the lateral hypothalamic area stimulates feeding behaviour (blocks MCR4)

34
Q

Describe the anatomy of the structures involved in appetite etc;

A

POMC and AGrP neurons located in the arcuate nucleus at the bottom of the third ventricle (they express Leptin receptors and are therefore regulated by this)

Project to the VPN at the top of the third ventricle and the lateral hypothalamic nucleus

35
Q

What happens in a POMC knockout?

A

They become obese (no neurons producing the a-MSH)

36
Q

What other genetic mutations highlight the important aspects of these pathways?

A
  • Mice and Humans lacking the MC4-R develop obesity
  • Mice lacking the MC3-R develop obesity
  • Transgenic mice overexpressing AGRP develop obesity
37
Q

Describe how Leptin really works?

A

Direct regulation of POMC and AGrP was the historic view

but recent findings indicate that

Indirect regulation is more critical in leptin function

  • POMC neurons – catabolic
  • AgRP neurons – anabolic
38
Q

Describe AGrP and POMC interplay;

A

AGrP has inhibitory synapses onto POMC

AGrP = GABAergic

POMC =Glutamatergic or Gabaergic

39
Q

Describe the genetic mouse model that determined the action of leptin;

A
  • GABAergic inhibitory neurons (VGAT = transporter for importing GABA into synaptic vesicles) - TAGGED
  • Glutamatergic excitatory neurons (VGLUT2+ = one of three synaptic vesicle glutamate transporters) TAGGED
  • Generated mice expressing Cre in either VGAT or vGLUT2 neurons and then breed these mice with transgenic mice expressing Leprlox/lox (i.e knockout leptin receptors from gabaergic neurons)
  • Showed that majority of leptin’s anti-obesity effects mediated through GABAergic neurons (majority are not AgRP neurons)
  • Demonstrates leptin reduces inhibitory tone to POMC neurons mediated by leptin receptors on presynaptic neurons.

i.e Indirect effects

40
Q

What features of POMC and AGrP neurons allow regulation?

A

Dendritic spines which contain receptors sensitive to;

  • Leptin
  • High Fat feeding
  • Fasting (grhelin)

These are all plastic

Many peptides regulate apetite

41
Q

How are peptides regulating appetite classified?

A

Orexigenic and anorexigenic peptides

42
Q

How do arcuate nucleus neurons respond to nutrients?

A

ARC neurons respond to changes in the activity of their own intracellular metabolic processes:

43
Q

How does glucose influence ARC neurons?

A
  • Glucose-excited neurons in the ARC synthesise POMC and secrete α-MSH
  • Glucose-inhibited neurons in the ARC secrete NPY
44
Q

How do AA influence ARC neurons?

A
  • Oleic acid inhibits food intake; decreases NPY

* Leucine inhibits food intake; lowers AgRP

45
Q

What are two different psychological reasons to want food?

A

• To eat because you like food - motivation is
HEDONIC
• To eat because you want food - drive reduction - CRA VING

46
Q

What two neurotransmitters are involved in the psychological regulation of food intake?

A

Seratonin and Dopamine

47
Q

Describe dopamine related cravings

A
  • Destruction of dopamine axons passing through the lateral hypothalamus fails to reduce the hedonic responses to food even though animals stop eating. Dopamine depleted animals behave as though they like food but do not want food i.e. lacks motivation to seek food
  • Conversely, stimulation of dopamine axons in the lateral hypothalamus of normal rats induces a craving for food without increasing food’s hedonic affect

i.e Dopamine = craving

48
Q

Describe seratonin related mood / eating;

A
  • Serotonin levels in hypothalamus are low during post- absorptive period, rise in anticipation of food, and spike during a meal.
  • Drugs that elevate serotonin levels in the brain are powerful appetite suppressants – work through stimulating POMC neurons
  • Abnormalities in brain serotonin regulation are believed to be one factor that contribute to eating disorders - anorexia nervosa and bulimia nervosa

Seratonin = hedonic

49
Q

How do seratonin levels vary in the blood?

A

Serotonin is derived from dietary amino acid tryptophan, and tryptophan levels in the blood vary with the amount of carbohydrate in the diet

Medsci 312 (28 decks)

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