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PHAR > PHAR9 - Obesity > Flashcards

PHAR9 - Obesity Flashcards

1
Q

Define adipokine.

A

Signalling proteins secreted by adipose tissue.

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2
Q

Define amphipathic.

A

Molecules with both hydrophobic and hydrophilic regions,

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3
Q

Define anorexigenic.

A

Agents that suppress appetite .

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4
Q

Define body mass index.

A

Measurement of weight relative to height squared. Used as an indicator of underweight, overweight and obese.

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5
Q

Give a brief overview of ghrelin.

A

Hormone released by stomach and small intestine. Stimulates hunger.

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6
Q

Define hyperplasia.

A

Increase in cell number. Increases amount of organic tissue or enlarges the parent tissue.

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7
Q

Define hyper trophy.

A

Increase in size.

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8
Q

Define ionophores.

A

Molecules that bind to ions in reversible manners.

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9
Q

Give brief overview of leptin.

A

Adipokine released by adipose tissue to influence energy balance and satiety/hunger. Long term effects.

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10
Q

Define orexigenic.

A

Agent that stimulates appetite.

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11
Q

Define proton motive force.

A

Energy used to create chemiosmotic gradient across inner mitochondrial membrane, allowing for ATP synthesis.

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12
Q

Define thermogenesis.

A

Production of heat energy by biological processes e.g. exercise.

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13
Q

Define satiation.

A

Feeling full during a meal, reducing the impulse to eat more.

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14
Q

Define satiety.

A

Feeling of being full which occurs following a meal - prevents further food consumption.

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15
Q

Define a suicide inhibitor.

A

Drugs that undergo covalent binding to a target to inactive both the drug and the target. Commonly referred to as mechanism based inhibitors.

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16
Q

What other conditions does obesity increase the risk of? Give three examples.

A

CVD, diabetes and cancer.

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17
Q

What is obesity?

A

Excess adipose tissue and body mass, relative to height.

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18
Q

What is the main cause of obesity?

A

Imbalance between calorific intake and caloric expenditure.

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19
Q

How do you calculate BMI?

A

Mass in kg divided by height in metres squared.

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20
Q

What do the various ranges of BMI indicate?

A

< 18.5 - underweight
18.5-25 - normal weight
25-30 - overweight
>30 - obese

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21
Q

Why is BMI useful?

A

Easy to calculate and gives relatively good indication of an individuals health (based on height and weight solely).

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22
Q

Why can BMI be considered inaccurate? Give example.

A

Does not take into account differences within individuals e.g. body fat distributions, fat percentages, fat to muscle proportions. Individuals may have differing components.

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23
Q

Give other examples of easy obtainable alternatives to BMI.

A

Waist hip ratio.
Waist circumference.
Skin fold thickness.

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24
Q

Give an example of a difficult to obtain measurement, for evaluating healthy weight.

A

Body fat percentage - requires specific machinery.

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25
Q

What are the two locations of adipose tissue in the body? Describe each.

A

Visceral fat - stored in central locations e.g. around organs.
Peripheral fat - stores in superficial locations around the outside of the body.

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26
Q

Define comorbidity.

A

Comorbidity refers to the having multiple conditions alongside the initial condition.

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27
Q

Give three types of body shape, with description for each.

A

Ectomorph- long and thin.
Endomorph - pear shape, larger body fat amount.
Mesomorph - muscular and well built.

28
Q

What are the three main methods of body weight regulation?

A

Fat storage and energy balance.
Adipose tissue and adipokines.
Integration of gut brain axis.

29
Q

What tissue is fat stored in and how is it stored?

A

Stored in adipose tissue. Stored as triglycerides and cholesterol esters.

30
Q

Give two changes to adipocytes as a result of obesity.

A

Hypertrophy - increased size.

Hyperplasia - increased number via proliferation.

31
Q

What cells constitute the adipose tissue?

A

Adipocytes. Fibroblasts. Immmune cells.

32
Q

What are the main roles of adipokines?

A

Regulation of energy balance and eating behaviours.

33
Q

Name two key adipokines.

A

Leptin and ghrelin.

34
Q

Give the effect of leptin within mice.

A

Leptin deficiency causes obesity in mice. Treatment with leptin in these mice allows the suppression of weight gain.

35
Q

Give the effect of leptin in humans.

A

Leptin defectiveness or deficiency causes obesity in humans. Recombinant leptin administration allows for substantial weight loss.

36
Q

What is the relationship between leptin and adipose tissue?

A

Increased adipose tissue is associated increased leptin release.

37
Q

Does the release of leptin from adipose tissue have a shift term or long term effect?

A

Long term effect - amount of adipose tissue varies on a larger scale.

38
Q

Discuss the main effects of grehlin.

A

Released by the stomach to promote hunger and eating behaviours. Exhibits a short term effect with oscillatory release patterns.

39
Q

Briefly discuss the role of the gut brain axis.

A

Acts as a pathway for communication between the gut and the brain, which communicate via various hormones and signalling proteins.

40
Q

What is the role of the hypothalamus in energy regulation?

A

Integrates various signals relating information on hunger and satiety, coordinating the specific response required.

41
Q

What are the two neuronal sets within the arcuate nucleus?

A

POMC/CART - proopiomelanocortin and cocaine and amphetamine regulated transcript. Anorexigenic - suppress appetite.

NPY/AgRP - neuropeptides Y and agouti related peptide. Orexigenic - promote appetite.

42
Q

What are give potential ways in which obesity can be target, relative to both pharmacological and lifestyle strategies?

A

Reduction in overall calorific intake - diet.

Reduction of calorific intake from specific foods - sequestering uptakes of specific nutrients.

Create natural calorific deficit - modifying physical activity.

Create artificial calorific deficit - uncoupling of calorific intake and ATP production.

Reduction in food consumption - hunger is suppressed.

43
Q

What drug is used to create an artificial calorific diet?

A

2,4-dinitrophenol. (DNP)

44
Q

Give brief overview of how DNP works.

A

DNP behaves as an ionophores. Uncoupled OXPHOS from ATP production. Protons become equilibrated across inner mitochondrial membrane. Lack of chemiosmotic gradient and proton motive force prevents ATP.

45
Q

Give a side effect of DNP use.

A

Thermogenesis - uncoupling of OXPHOS causes heart production. Can lead to hyperthermia.

46
Q

What factor of fat (being consumed via food) contributes to obesity?

A

It is an energy rich molecule. Energy is not used up therefore must be stored.

47
Q

Give two reasons why fat is required as part of the diet.

A

Absorption of fat soluble vitamins e.g. A,D,E and K.

Provision of metabolic substrates for energy production. What

48
Q

What is the role of bile acid. Give one example and how they are suitable for their role.

A

Bile acids form micelles with fat molecules, through emulsification.

Example - cholic acid.
Property - amphipathic so can bind to fat.

49
Q

Why is emulsification by bile necessary?

A

Increases surface area for liaise enzymes to hydrolyse the lipids,

50
Q

Where does triglyceride hydrolysis occur? What enzyme is required?

A

Within the intestinal lumen. Carried out by pancreatic liaise enzymes.

51
Q

Discuss the chemistry of lipid hydrolysis.

A

Ester bond is cleaved. Products are glycerol and fatty acids.

52
Q

What happens to the products of lipolysis within the intestinal lumen?

A

Glycerol and fatty acid products undergo passive diffusion across the plasma membrane into intestinal mucosal cells. Repackaged into triacylglycerols and form chylomicrons alongside apoproteins.

53
Q

Where does fat become deposited in the body?

A

Stored as adipose tissue in various organs e.g. liver.

54
Q

Discuss the mechanism of action of orlistat.

A

Orlistat inhibits lipase enzymes. Prevents triacylglycerol hydrolysis in intestinal lumen. TAGs are not absorbed (malabsorption of lipids). Eliminated from body via faeces.

55
Q

Discuss the chemistry of how orlistat inhibits lipase enzymes.

A

Binds to define amino acid residues within active site of pancreatic and gastric lipase. Acts as a suicide inhibitor - irreversible binding.

56
Q

Orlistat has a low bioavailability. Why is this not an issue in its use?

A

Does not need to be absorbed into the bloodstream to reach its target - acts on lipase enzymes within GI tract.

57
Q

Give one potential target if orlistat undergoes absorption into the bloodstream.

A

Serine hydrolyse enzyme.

58
Q

How do anorectic agents lead to weight loss?

A

Reduce food consumption.

59
Q

What is the link between cannabinoids and appetite?

A

Some cannabinoids increase appetite - referred to as the munchies.

Act on the CB1 receptor to increase appetite.

60
Q

How can the CB1 receptor be used in the treatment of obesity?

A

Activation of the receptor increases appetite. Use of an antagonist or an inverse agonist can be used to suppress appetite.

61
Q

Define an inverse agonist and what is required for its MOA?

A

Drug that binds to the target and opposes its effect. Requires a constitutive response.

62
Q

Discuss the link between drug dosage and effect of inverse agonist.

A

Increasing drug dosage further decreases the response of the target.

63
Q

Discuss the mechanism of action of rimonabant.

A

Inverse agonist of the CB1 receptor. Suppresses appetite which can be used for weight loss.

64
Q

Discuss the side effects of rimonabant.

A

Depression - reduced adenylate cyclase activity meaning cellular depressant effect. In addition, causes depression generally.

65
Q

Give example of another drug with a similar mechanism of action to rimonabant.

A

Taratabant.

66
Q

What are common exogenous and endogenous agonists for cannabinoid receptors?

A

Exogenous - anandamide.

Endogenous - 9THC

67
Q

What is epidiolex and discuss its effects?

A

It is a cannbidiol.

Used for epilepsy associated seizure treatment e.g. Lennox gastaut syndrome and dragnet syndrome.

Side effect - appetite suppression.

PHAR (9 decks)

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