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Medical Genetics > Genetics of Obesity > Flashcards

Genetics of Obesity Flashcards

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1
Q

How many people are obese?

A

24 in 100

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2
Q

How many people are overweight?

A

36 in 100

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3
Q

Name the two types of fat tissue

A

White Adipose tissue and Brown Adipose Tissue

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4
Q

Good fat is?

A

Subcutaneous fat

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5
Q

Bad fat is?

A

Visceral fat

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6
Q

Where is subcutaneous fat found?

A

Just under the skin

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7
Q

Where is visceral fat found?

A

Around the intra-abdominal area

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8
Q

Describe three key points on white adipose tissue?

A
  1. Energy storage
  2. Lipid droplets forming one lipid vacuole
  3. Excess calories cause lipid expansion
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9
Q

What happens to energy in brown adipose tissue?

A

It is wasted

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10
Q

Describe the lipid nature of brown adipose tissue

A

Multiple lipid droplets and numerous mitochondria essential for BAT fuel utilisation

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11
Q

What kind of tissue is brown adipose tissue?

A

Catabolic tissue = burns lipids for energy wastage in the mitochondria

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12
Q

How is energy wasted in brown adipose tissue?

A

excess calories are broken into fatty acids that enter mitochondria and undergo uncoupling

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13
Q

Name the unique protein that brown adipose tissue expresses? And where is it found?

A

Uncoupling protein 1 (UCP1) OR (THERMOGENIN)

Mitochondria’s inner membrane

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14
Q

Describe what UCP1 does?

A

UCP1 uncoupled oxidative phosphorylation from ATP synthesis. No ATP produced just H+ ions, thus producing a proton gradient. This wastes energy in the form of heat in thermogenesis.

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15
Q

What environmental factors induce thermogenesis?

A

-cold
-hypercalorie diet
-photoperiodic changes
And pharmacological stimulation of beta adrenergic receptors on BAT

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16
Q

How does UCP1 uncoupling waste energy?

A

Because it is metabolically inefficient thus burning calories

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17
Q

What does enhanced BAT thermogenesis show?

A

Prevention of diet induced obesity and promotes weight loss

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18
Q

People with less BAT tend to be?

A

Obesese/fat

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19
Q

People near to the equator in hot climates tend to have more or less BAT?

A

Less - hence asians and black tend to get obese when they move to colder climates

20
Q

Why is visceral fat dangerous?

A

Because its located around the organs and due to its lipolytic nature the lipids can readily enter the organs.

21
Q

What kind of state in obese people does visceral fat cause?

A

An inflammatory state

22
Q

Visceral fat is more readily broken down true or false?

A

TRUE

23
Q

What kind of fat is more susceptible to hypertrophy?

A

Visceral fat - cells take up adipose and get larger

24
Q

Subcutaneous fat cells are smaller or larger than visceral fat cells?

A

Smaller

25
Q

What process is subcutaneous fat cells liable to?

A

Lipolysis- break down of lipids involving hydrolysis of triglycerides to glycerol and free fatty acids

26
Q

When subcutaneous fat cells undergo hypoplasia what happens?

A

They increase in the number of cells causing it to expand. The creased blood ad nerve supply prevents inflammation

27
Q

What are th major risks of abdominal obesity?

A

Cardiovascular Disease and diabetes

28
Q

What problems arise from central obesity?

A
  • endothelial dysfunction
  • hypertension
  • insulin resistance
  • atherogenic dyslipidaemia
  • inflammatory profile
  • pro-thrombic state
29
Q

Inflammation is caused by?

A

Increased number of lipids in the muscle

30
Q

What does obesity inflammation lead to?

A

The build up of cytokines leading to increased fatty acid metabolism to remove triglycerides, producing a reactive oxygen species that effects th muscles ability to take up glucose causing type 2 diabetes

31
Q

What is Berardinelli-seip syndrome?

A

Congenital generalised lipodystrophy type 2 - complete lack of subcutaneous fat. Autosomal recessive

32
Q

What causes berardinelli-seip syndrome?

A

Mutation in the BSCL2/seipin gene

33
Q

What happens in Berardinelli-seip syndrome?

A

The person cannot produce adipose cells, thus fat cannot be stored in adipose cells, therefore fat goes into the major organs causing an insulin resistance.

34
Q

What did the genetic study of obesity in twins conclude?

A

That obesity must be a genetic predisposition, as there was little variation within twins but lots of variation between twins!

35
Q

What is leptin?

A

A hormon made by adipose cells that is used to regulate energy balance by inhibiting hunger. Its actions are opposed by ghrelin - the hunger hormone.

36
Q

What is the action of leptin?

A

It is secreted by the adipose tissue and acts on the hypothalamus where it synapses with neurones to regulate energy metabolism in the periphery.

37
Q

In 1997 what’s the disease discovered that occurred due to a mutation in leptin?

A

Congenital leptin deficiency - found to be associated with severe early onset obesity.

38
Q

What type of mutation did M.Wabitsch et.al., find?

A

A novel mutation in which leptin was still produced normally but was not functional - couldn’t bind the receptor.

39
Q

What system does leptin function in?

A

The leptin - melanocortin system - vital for energy homeostasis

40
Q

What is the name of the hormone which is a potent stimulator of appetite?

A

NPY

41
Q

List the mutation in the leptin-melanocortin system?

A 
Monogenic (non-syndromic) obesity mutations.
LEP
LEPR
POMC
MC4R
PCSK1
BDNF
NTRK2
SIM1
42
Q

monogenic obesity is…

A

…very rare

43
Q

Prader-willi is caused by?

A

paternal deletions of Ch15q11-q12

44
Q

Prader-willi causes

A

Short stature
Hyperphagia - abnormal great desire for food
Central Obesity

45
Q

What is Bardet-Biedl syndrome (BBS) caused by?

A

Several causal mutation at various loci (14t)

46
Q

BBS causes?

A

Cilipopathy
Hypogonadism
Early onset obesity
Renal Disease

Medical Genetics (1 decks)

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