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BM3052 > Week 7- Etiology and development of Obesity > Flashcards

Week 7- Etiology and development of Obesity Flashcards

1
Q

BMI definitions

A

BMI

Status

<18.5

Underweight

18.5-25

Normal

25-30

Overweight

30-40

Obese

>40

Morbidly obese

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2
Q

is BMI a good population screening tool?

A

It is a good average population screening tool.

  • Has its disadvantages however as people with muscle mass do thus have a higher BMI
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3
Q

the trend in global prevalence of obesity and overweight status

A

The global prevalence of overweight and obesity is rapidly escalating irrespective of the amount of development a country has seen

  • Has been escalating since 1975
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4
Q

obesity is the — highest risk factor of death. what other factors that are linked to obesity and how are they ranked

A

5th

  • Diet low in fruit ranked 10th also linked to obesity
  • Diet low in nuts and seeds ranked 11th also linekd to obesity
  • Diet low in vegetables ranked 13th also linekd to obesity
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5
Q

is obesity a disease?

A

yes it is now

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6
Q

for the first time in 2 centuries….

A

CHILDREN HAVE A SHORTER EXPECTED LIFE EXPECTANCY THAN THEIR PARENTS, WHICH CONTENDS THAT THE RAPID INCREASE IN CHILDHOOD OBESITY, IF LEFT UNCHECKED, COULD SHORTEN LIFE SPANS BY AS MUCH AS 5 YEARS.

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7
Q

the effects of an increase in childhood obesity

A
  • With this increase we are also seeing an increase metabolic syndrome in children
    • Metabolic dysfunction at a young age predisposes them to the development of metabolic disease when older.
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8
Q

% of children in Aus between 2-4 who are overweight

A

30

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9
Q

is obesity more common in one sex?

A

yes, more in males- we do see sexual dimorphism here event at a young age

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10
Q

Factors that impact obesity prevalence?

A
  • Genetics/Epigenetics
    • Largely contribute to weight conformation.
  • Lifestyle eating/ exercise patterns
    • Interacts with genetics to create resistant/ susceptible phenotype
  • Socioeconomic Status
    • Increased prevalence of obesity in lower socioeconomic area
      • Linked to fact food
  • Psychological factors
  • Cultural background
  • Age
    • Endocrine changes occur as we get older make us more likely to gain weight
      • E.g. less estrogen because of menopausal transition
  • Hormonal, metabolic, physiological factors
  • Sleep disturbances
    • In shift workers there is an increased prevalence of metabolic diseases, this increases likelihood of gaining weight
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11
Q

Body composition has been seen to be —% heritable

A

~70%

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12
Q

is the determination of body compositon monogenic or polygenic ?

A

polygenic, more than 600 genes contribute

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13
Q

How heritable is BMI?

A

Reltively high, 50-90% heritable

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14
Q

Evidence seen in Genetic selectio studies for obesity

A

we do see a genetic linkage. can be seen through the creation of lineages for favourable cattle/livestock traits which shows heritbaility

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15
Q

monogenic forms of obesity are…

A

relatively rare

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16
Q

Prader-Willi Syndrome

A
  • Most known monogenic cause of syndromic obesity
    • Due to lack of expression of 15q11-q13 genes on paternal chromosome
  • Increased accumulation of adipose tissue in abdominal visceral area
  • Truncal obesity is associated with metabolic dysfunction
17
Q

% genetic causes of PWS

A
  • 65%-75% of cases are de novo
    • De novo microdeletion of 15q11-q13 genes on paternal chromosome
  • 20%-30% are because of maternal uniparental disomy
    • 2 maternal chromosomes, none from father
    • Associated with advanced maternal age
  • 2-5% are because of imprinting error
18
Q

Symptoms of PWS

A
  • Hypotonia
    • Weak muscle tone and floppiness at birth( enough for diagnosis at birth)
  • Hypogonadism
    • Immature dev of the sexual organs and other sexual characteristics
  • Obesity
    • Because of hyperphagia AND decreased caloric requirement because of lower energy expenditure
  • CNS and endocrine gland dysfucntion
    • Causing carrying degrees of learning disability
    • Short stature
    • Hyperphagia
    • Somnolence(excessive sleepiness)
    • Poor emotional and social development
19
Q

Ghrelin in PWS children

A

Children with Prader-Willi have increased ghrelin levels, significant findings.

  • Ghrelin is the only bodily hormone that increases food intake
20
Q

Mutations in the ob gene lead to…

  • lack of function leptin
A

lack of functional leptin.

  • This causes…
    • Profound obesity
    • Glucose intolerance/ insulin resistance
      • T2DM
    • Infertility
    • Cold intolerance
      • Because leptin is involved in energy expenditure
    • Immune dysfunction
    • No circulating leptin levels
21
Q

Leptin

A
  • 16kDa encoded by ob gene
  • Produced by fat cells
  • Directly proportional to the total amount of fat in the body
  • Informs the brain how much fat is contained in the body
22
Q

Why is leptin not a good weight loss agent?

A

When individuals become obese, they lose the ability to respond to leptin and become resistant. This is why leptin is not an effective weight loss agent.

23
Q
A
24
Q

Congenital leptin deficiency in humans( effects ans treatments)

A
  • Leads to a rapid gain in body weight early in life
  • Treatment: human recombinant leptin treatment.
    • Can restore body weight to normal with therapy
25
Q

The effects of a leptin deficiency

A

Without leptin the body believes it is constantly in a state of starvation or there is an absence of fat stores. This signals to the brain to increase food intake and reduce energy expenditure

  • No satiation leads to patients eating uncontrollably
  • Leads to profound morbid obesity
  • Body weight can be restored with leptin replacement
26
Q

Mutations in Leptin Receptor

A

Mutations in the LepR often result in early onset of obesity

  • Marked increase in body weight even in childhood
  • Treatment: can place on weight loss therapy
    • Works for a bit but very hard to sustain
  • Causes increasing levels of leptin
    • The brain continues to produce it despite not responding
  • Individuals DO NOT respond to exogenous leptin therapy
27
Q

What to do about patients with typical idiopathic obesity?

A

We think there is a gene and environemnt interaction that causes obesity

  • There is a bodily set point determined by our environemnt and genetics
  • it has been found that when we eat too little or too much there is compensatory chnages in energy expenditure which occur to remain at the set point
    • Eat too much: increase in EE, temporary
    • Eat too little: reduction in EE, lasts longer as we are wired to prevent weight loss
28
Q

is set point plastic?

A

Set point occurs in adults and cannot be changed in adulthood but it is not present in adolescents

  • In pre pubertal children we can re-establish and rest the set point
29
Q

How do we identify susceptibility genes?

A
  • Through genome wide association studies/ GWAS
  • Examination of a genome wide set of genetic variants in different individuals to see if nay variant is associated with the trait
  • Primarily investigates SNPs and how they are related to the phenotype of obesity
  • From this the first gene known to contribute to common obesity was found(FTO)
30
Q

what is FTO and how was it found?

A
  • FTO gene “fat mass and obesity associated gene”
  • First screening study was done in…
    • 4000 individuals
    • Identified FTO gene in all samples
    • A variant was found when a single nucleotide changes
    • When the individual has 2 copies of the variant FTO they were 1.67 x more likely to be obese
31
Q

Overexpression of FTO in mice lead to

A
  • Increased body weight
  • Drastically increased fat mass
  • Increased food intake
  • Increased preference of higher calorie foods
  • Reduced physical activity and energy expenditure
  • Impaired browning of WAT
32
Q

Several different variants in FTO have been linked to…

A

obesity onset, ghrelin and impaired food-cure responsivity

BM3052 (25 decks)

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