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BSMS203 endocrinology (Theme 1) > 11. Physiology of appetite and weight > Flashcards

11. Physiology of appetite and weight Flashcards

1
Q

Obesity

A

A medical problem

Aetiology: genetic & environmental

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2
Q

Homeostasis

A

Precise matching of energy intake and energy expenditure

  • average decade of adult life
  • ~10 million kcal consumed
  • tendency towards slight average weight gain
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3
Q

Measurements

A 
BMI - kgm^2
Waist circumference
Skin-fold thicknesses
Bioelectrical impedance analysis
Ethnicity specific cut-offs
BMI:
<18.5 underweight
18.5 - 24.9 normal
25 - 29.9 overweight
30 - 39.9 obesity
>40 morbid obesity
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4
Q

Medical problems

A 
6% UK deaths attributable to obesity
Metabolic syndrome/type 2 diabetes
Cardiovascular disease
Respiratory disease
Liver
Cancer
Reproductive dysfunction
Joint problems
Psychological morbidity
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5
Q

Metabolic syndrome

A

constellation of closely associated cardiovascular risk factors:

  • visceral obesity
  • dyslipidaemia
  • hyperglycaemia
  • hypertension

Insulin resistance is the underlying pathophysiological mechanism

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6
Q

Obesity in relation to insulin resistance and metabolic syndrome

A

BMI vs body fat distribution: central vs peripheral fat distribution
Metabolic syndrome associated with central (visceral) fat, and BMI >30

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7
Q

Pathophysiology

A

Increase in free fatty acids (non-esterified):
- lipolysis of visceral fat -> gluconeogenesis, dyslipidaemia

Pro-inflammatory cytokines:

  • TNF-a, IL-6 (from overladed with white adipose tissue) -> insulin resistance.
  • Decrease in expression of GLUT-4 (insulin-sensitive glucose transporter)
  • Decrease in tyrosine kinase activity of insulin receptor
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8
Q

Role of adipocytokines

A

Regulator of food intake
vasoconstriction, endothelial dysfunction, thrombosis
Anti-atherogenic effects

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9
Q

Type 2 diabetes mellitus risk factors and targets

A

Age, obesity, family history, ethnicity

Rich people in poor countries
Poor people in rich countries - source of socioeconomic inequality in health

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10
Q

What factors contribute to increased prevalence of T2DM?

A

Increased age population
increased obesity - getting more younger obesity
Increased detection/diagnosis - 50% of cases T2DM picked up on routine examination
Increased survival with T2 DM

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11
Q

Cardiovascular disease

A

Metabolic syndrome plus:

  • increased blood volume and blood viscosity
  • increased vascular resistance
  • increased hypertension
  • increased left ventricular hypertrophy
  • increased coronary artery disease
  • increased stroke
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12
Q

Respiratory system effects of obesity

A

Obstructive sleep apnoea
Hypoxia/hypercapnia
pulmonary hypertension - due to right heart failure
Accidents - daytime somnolence

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13
Q

GI/liver effects of obesity

A 
Non-alcoholic fatty liver
Non-alcoholic steatohepatitis
May progress to cirrhosis, portal hypertension, hepatocellular cancer
Gallstones
Reflux
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14
Q

Cancer effects of obesity

A

~10% cancer deaths in non-smokers attributed to obesity
Types:
breast, endometrial, oesophagus, colon, gall bladder, renal, thyroid
Mechanisms: increased insulin, increased free IGF-I, increased oestrogen, adipo-cytokines, reflux

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15
Q

Reproductive system effects of obesity

A

Polycystic ovarian syndrome: oligomenorrhea, hirsutism, acne, subfertility, endometrial hyperplasia, insulin resistance
Male hypogonadism
Adverse pregnancy outcomes

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16
Q

Obesity effects on joints

A

osteoarthritis

gout

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17
Q

Psychological effects of obesity

A

Depression

eating disorders

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18
Q

Aetiology of obesity

A

Genetic factors
Environmental factors
Programming
Gut microbiome

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19
Q

Obesity associated syndromes

A

Rare:
Prader-Willi
Bardet-Biedi

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20
Q

Genetics in obesity

A

Commonly:
polygenic
susceptibility genes
heritability of weight is similar to the heritability of height

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21
Q

Other medical causes of obesity

A

Hypothyroidism

Cushing’s syndrome

22
Q

Environmental factors on obesity

A 
Diet:
high fat
high sufar
Coca-colanisation of developing world
Socioeconomic factors

Physical activity:
20-50% total energy expenditure
Obesity prevalence related to proxy measures of physical activity: car ownership, TV viewing
Socioeconomic factors
Social - more likely to be obese if friends are obese

23
Q

Foetal programming

A

Stimuli/insults at critical periods have persistent biological effects

Stressors in utero:
?undernutrition, ?trace elements, ?other
Crudely represented by birth weight

Mechanism: epigenetic modification of gene expression

E.g. programmed adrenal axis overactivity in adulthood, causal factor for metabolic syndrome, increased vulnerability to coronary heart disease

24
Q

Barker’s group evidence

A

Babies with lowest birth weight ended up with highest morning cortisol as adults

25
Q

Life course model

A

Factors operating at every stage of life affect health outcomes later in life
Pathway of risk between events and health outcomes
Worst outcome associated with:
- Low birth weight
- Excessive weight gain in infancy/childhood
- Adult obesity

26
Q

Gut microbiome

A

10^4 - 10^14 cells/g in colon, 10-100 times as many genes as human genome

Integral to host homeostasis (physiology):
absorption of nutrients in duodenum and jejunum
Reabsorption of bile acids in ileum
Fermentation of fibre & bile acid metabolism in colon

Influenced by diet: high fat, high fibre etc, chronic & acute (meal by meal)

Influence disease risk: obesity, T2DM etc

27
Q

Gut microbiome in obesity and T2DM vs normal

A

Differences in gut bacteria can be induced by diet e.g. high fat diet
Transplantation of faecal material alters insulin sensitivity in mice and humans

28
Q

Regulation of appetite and weight - slow acting

A

Leptin
Insulin
Signal % body fat to hypothalamus
-> decrease food intake, increase energy expenditure

29
Q

Regulation of appetite and weight - fast acting

A

Rapid-acting peptides regulate meal sizes

released from GI tract
cholecystokinin (CCK) inhibits eating
ghrelin increases eating
PYY inhibits eating up to 12 hours
Act via hypothalamus
30
Q

Hypothalamus

A

Accelerator neurons: NPY/AgRP neurons
Neuropeptide Y (NPY) encourages eating
Agouti-related peptide (AgrP) blocks melanocortin receptor

Brake neurons:
POMC neurons
Melanocortin peptides (alpha-MSH, CART)
discourage eating

31
Q

Leptin mice

A

Ob/ob mouse - leptin deficient
Db/db mouse - mutation of leptin receptor
Ob gene product = leptin
Mouse models of obesity

Leptin treatment reduces obesity in ob/ob mouse

32
Q

Leptin in humans

A

Starvation signal
Permissive effect on puberty/reproduction

Obese humans:
- very rare leptin deficiency or mutation of leptin receptor
- increased [leptin] with increased fat
? leptin resistant
? decreased CNS leptin transport
33
Q

Treatment for obesity

A

lifestyle modification
pharmacological
surgical
public health/social

34
Q

Diet modifications to treat obesity

A

500-1000kcal energy deficiency
Low energy density:
decreased saturated fat, decreased sugar
increased fruit and veg (sub for other foods)
Decrease portion sizes, decrease snacking
Structured meals/meal replacements may help promote greater weight loss

35
Q

Physical activity to treat obesity

A

Exercise 7 days a week
30 mins moderate-high intensity or 60 mins low intensity
Target 10,000 steps/day, increase 500 step increments
Regardless of weight/weight loss, exercise increases health

36
Q

Very low calorie diets (VLCD) and T2DM

A

Principle:
Primary care programme with T2DM patients diagnosed less than 6 years ago, put on a VLCD (830kcal/day) for 3-5 month

Initially, total diet replacement with formulae, then stopped food reintroduction (2-8 weeks), long-term maintenance with structured support

Outcomes:
12 month outcomes reported
24% of participants lost 15kg or more
46% induced remission of T2DM: normal HbA1c off all medication for 2 months, >10kg weight loss: 73% remission

37
Q

Lifestyle modifications

A

USUAL TARGETS
• 10% weight loss (doesn’t equal ideal weight)
• 1-2 lb (0.5 – 1 kg) per week
• Some evidence that ‘ambitious’ goals promote more weight loss
PROBLEMS
• Most patients can achieve ~ 5-10 % weight loss / 1 year
• ‘Yo-yo’ dieting / regaining weight lost
• ‘Obesogenic environment’
• Weight loss results in increased hunger, decreased satiety, decreased metabolic rate

BEST HOPE
• Sustainable lifestyle changes
• Diet combined with exercise / physical activity
• Ongoing management is required to maintain weight loss

38
Q

Pharmacological therapy for obesity

A

25 years research many products, only orlistat

39
Q

Orlistat mechanism

A

Binds & inhibits lipases in lumen of gut, stops fat absorption
Prevents the hydrolysis of dietary fat into absorbable free fatty acids/glycerol
Excrete 1/3rd dietary fat

40
Q

Orlistat adverse effects

A

Flatulence, oily faecal leakage, diarrhoea

stops absorption of fat soluble vitamins (ADEK), but can take supplement

41
Q

Metformin

A

best 1st line agent for overweight/obese patients with type 2 diabetes
All other oral hypoglycaemic agents and insulin cause weight gain
used to prevent diabetes but not licensed for this use
NICE recommended in preventing type 2 DM in adults at high risk

42
Q

Pharmacological therapy problems

A

Can only increase by 3-4 fold the proportion who achieve a 5% weight loss in a year
Weight re-gained after treatment stopped

43
Q

Pharmacological therapy future

A

All identified gut peptides/neuropeptides/their receptors are potential therapeutic targets/options
Gut hormones in combination most likely way forwards

44
Q

Surgical treatment for obesity

A

Laparoscopic adjustable banding

Roux-en-Y gastric bypass

45
Q

Laparoscopic adjustable banding

A

restrictive only

Inject/withdraw saline to adjust the diameter of the band

46
Q

Roux-en-Y gastric bypass

A

Restrictive, malabsorptive, alterations in gut hormones and bile acid flow contribute to weight loss

Endocrine factors important in effects: plasma from operated rats to sham-operated rates - ate 1/3rd less

Increased satiety seems to be key, shown by F-MRI studies

47
Q

Roux-en-Y bypass complications

A

Micronutrient deficiencies - supplement with iron, B12, folate, calcium vitamin D

Dumping syndrome - GI & vasomotor symptoms

48
Q

Advantages of surgical treatment

A

Weight loss 25-30%
Resolve or improve co-morbidities
Brings cost savings

49
Q

Disadvantages of surgical treatment

A

Perioperative mortality / morbidity
-Depends on procedure and experience of surgeon

Long-term follow-up
- Micronutrient deficiencies

Some weight re-gain
- Patients will still be obese

Expense
- Though cost effective by 2 - 5 years, depending on co-morbidities and weight

50
Q

Swedish obesity subjects (SOS) study

A

Ongoing, non-randomised, prospective, controlled study
2010 obese subjects who had bariatric surgery vs 2037 matched obesity controls
Banding & bypass operations
Outcomes were improved through bariatric surgery

51
Q

UK position on bariatric surgery

A 
NICE 2006
	• After failure of other options if
		○ BMI >40 kg/m^2
		○ BMI > 35 with co-morbid conditions
	• Or first line
		○ BMI >50 kg/m^2
NICE 2014
	• Recent onset T2DM:
	• Expedite bariatric surgery if BMI >35
	• Consider surgery if BMI >30

UK position bariatric surgery: NHS guidelines
NHS England 2013
• As per NICE but…..
• Must have been obese for at least 5 years
• Must engage with non-surgical weight-loss programme for 12-24 months first

52
Q

Public health/societal approaches to overcoming obesity

A 
• Schools
		○ PE, lunches, vending machines
	• Urban design
	• Marketing/media/social media
		○ Food labelling, food advertisements

BSMS203 endocrinology (Theme 1) (26 decks)

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