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Nutrition and Metabolism > Energy Balance > Flashcards

Energy Balance Flashcards

1
Q

How Is Body Composition Measured?

A

Body = Fat + fat free mass

  • Body density (More fat=more dense)
  • Body water
  • Total body K (potassium)
  • Methyl histidine or creatinine excretion
    Skinfold measurements
  • Biceps, triceps, supra iliac, sub scapular
  • can get rough estimate of percentage of body fat
  • Mid-arm circumference
  • leg may hhave edema so arm used
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2
Q

How is body composition measured with Bioelectrical Impedance?

A
  1. electrical signal is sent through the body
  2. travels quickly through lean tissue (high % water, therefore good conductor of electricity
  3. more slowly through fat lower % water , poor conductor of electricity.

Bioelectrical Impedance devices use the information from this signal to work out body fat percentage.

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3
Q

How is body compostition measured with The bod pod?

A

**Air Displacement Plethysmography **
* Measure volume of chamber with and without subject
* From subject wieght and volume can calculate body density and fat and fat free mass

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4
Q

How do we get energy from food?

A

Total energy : Heat of combustion
Digestible energy : Absorbed
Metabolisable: Digestible minus energy that lost in urine sweat and skin
50% lost as heat. Less than 50% used for ‘work’

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5
Q

What are our energy requirements?

A

**Energy requirement = energy expenditure **

Oxygen consumption proportional to Energy expenditure
1 litre oxygen : 20 kjoules

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6
Q

What does the Energy requirements depend on?

A
  1. Basal metabolic rate
    - kj/hour/kg body weight
    - when doing nothing
  2. Diet induced thermogenesis
    - when eat, heat relased in metabolism
    - different for everyone
  3. Physical Activity
    sitting = 1.7BMR
    football = 7BMR
  4. Environmental temperature
    - eat less
    - but dont include this when calculating
  5. Growth, pregnancy, lactation
    -0.8 MJ or 200 kcal/day in trimester 3
    -2 MJ or 500 kcal /day in lactation
    infant year one, requirement 2x adult /kg bw
  6. Age
    decrease in BMR and activity
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7
Q

How does Intake v Expenditure of energy have significance?

A

If balanced = maintain weight
Most people maintain relatively constant body weight.

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8
Q

Regulation of Energy Intake

A

Hypothalamus
1. hunger centre
2. satiety centre

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9
Q

Regulation of Energy Intake with satiety (full)?

A

Long term signals: SATIETY

Leptin and insulin - Reducing apatite

  • leptin signals the state of the fat stores
  • plasma concentration reflects size of fat stores
  • insulin signals the fullness of carbohydrate stores
  • act in the hypothalamus through variety of neurotransmitters and neuropeptides.Both
    * Inhibit hunger pathways
    stimulate satiety pathways    *
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10
Q

Regulation of Energy Intake with Hunger?

A

leptin and insulin low

  • signal need for energy
    BOTH
    hunger pathways stimulated
    satiety pathways suppressed

Neuropeptide Y (NPY) is hunger signal
Ghrelin (stomach and hypothalamus) hunger signal - it means gut is empty and u need to eat
Pro-opiomelanocortin (POMC) related peptides, PYY 3-36 suppresses appetite

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11
Q

Regulation of Energy Intake with Hunger and satiety?

A

Integration of hunger and satiety signals by the hypothalamus

Signaling molecules are released by:
* stomach, intestine, adipocytes, pancreas.
* signals integrated in the arcuate nucleus of the brain generating the feeling of hunger or satiety

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12
Q

Appetite control via hypothalamic neurons?

A
  • Stomach empty - ghrelin produced
  • ghrelin strimulates NPY/AgRP producing neurons
  • And NPY and AgRP stimulate hunger
  • PYY3-36 (from intestine) inhibits NPY/AgRP producing neurons
  • Inhibits feeling of hunger
  • Leptin and insulin produced
  • stimulates pomc neurons
  • inhinit hunger and give stimulate feeling of satiaty
indicates stimulation = + indicates inhibition = -
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13
Q

Where do short term signals come from?

A
  • the GI tract
  • the hepatic portal vein
  • the liver

They bring about the feeling of satiety through vagus nerve and circulation

long term - better
short term - bad

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14
Q

Trend of obesity?

A
  • about two-thirds (66 per cent) of adults are now overweight or obese.
  • obesity has tripled in the past 20 years and is still rising.
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15
Q

Causes for obesity?

A
  1. Genetic
  2. Socio-economic, cultural
  3. Endocrinological
  4. Physical activity
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16
Q

Genetic causes for obesity

A

Rare
1. leptin
very few cases of severe obesity due to leptin deficiency or MC receptor deficiency or other single gene defect (and they act through increased appetite)

Leptin concentrations usually higher in obese people and they do not lose weight with leptin injections
Usually Leptin is proportial but obese people develop Leptin resistance

17
Q

Metabolic Rate in obese people

A

Basal Metabolic Rate is usually higher in obese as you are increasing both body fat mass as well as lean muscle mass

18
Q

What is the socio-economic, cultural cause of obesity?

A
  • obesity higher in lower socio-economic class in the UK and the Western world
  • in affluent classes in poorer areas of the world - lifestyle and eating habits and different perception of desirable size and status
19
Q

What is the Endocrinological cause of obesity?

A
  • rarely
  • adrenal hyperactivity (hypothroritism)
  • hypothyroidism
  • type 2 diabetes is a result of, not a cause of obesity
20
Q

How is Physical activity a cause of obesity?

A

Physical activity

  • children spend** 65% less energy **than 25 years ago.
  • food intake has not decreased proportionally
21
Q

Link between Microbota and obesity?

A

Evidence that GI tract of lean subjects has more diverse microbiota than obese
Faecal transplants from obese to lean have resulted in obesity and vice versa (e.g sterile gut from antibiotic treatment)

  • Some gut microbes digest components of fibre
  • Produce butyrate , colonic cell proliferation and maintenance of healthy gut barrier
  • Produce propionate, stimulates PYY production by colonic cells and decrease appetite
22
Q

FTO gene link to obesity?

A

FTO gene codes for 2 oxoglutarate dependent dioxygenase

Subjects with 1 copy of the FTO gene - 1.5 kg heavier
2 copies of the genes - 3 kg heavier

NIH
People with “high-risk” FTO genotypes exhibit preference for high-fat foods, reduced satiety responsiveness, andgreater food intake consistent with impaired satiety.

23
Q

Risk factors for obesity?

A
  • low level of education
  • chronic disease
  • little physical activity
  • heavy alcohol consumption
  • getting married
  • giving up smoking
24
Q

Conditions caused by or associated with obesity?

A

Cardiovascular disease
* relative risk MI x1.9 as likely tp develop with obesity

  • angina x2.5
  • stroke x3.1
  • venous thrombosis x1.5
  • Diabetes mellitus type 2 . Insulin resistance (2.9)
  • Hypertension (2.9)
  • respiratory problems
  • gall bladder stones (2)
  • osteoarthritis in weight bearing joints (11.8)
  • reduced fertility in men (decreased androgens)
  • polycystic ovary syndrome
  • breast, endometrial, colon & prostate cancers
25
Q

What diets work best?
How do diets work?

A

** All diets work if energy intake is restricted if adhered to.**

  • Fad diets are at best harmless and often metabolically undesirable
  • > 80-% of dieters regain weight
  • MR decreases in starvation by 15-30%
  • Intake has to decrease accordingly rats after 4 days without food need 60% of normal intake to maintain their weight
    *
26
Q

What is keto diet? Benefits? Dreawbacks?

A

Keto diet

  • Primarily used to reduce frequency of epileptic seizures in children
  • As a weight loss regime (Harvard and Mayo advice:) High saturated fat content in most keto diets may be of concern.
  • Protein should be very limited to allow the liver to produce ketones

Initially water loss and some fat loss but no more successful than other e restricted diets after one year

27
Q

What is Intermittent fasting diet? Benefits? Dreawbacks?

A
  • Improve thinking
  • Heart
  • Type 2 diabetes and obesity

Most studies on animals
Human studies show no benefit compared to continuous restriction of calories

NIH: Many diet and exercise trends have origins in legitimate science, though the facts tend to get distorted by the time they achieve mainstream popularity. Benefits are exaggerated. Risks are downplayed. Science takes a back seat to marketing.

28
Q

What are some pharmacological therepy for obesity?

A
  1. Uncouplers and thyroid hormone treatment
    - dangerous and have been lethal (withdrawn)
  2. Sibutramine
    increases conc of serotonin and tends to reduce appetite (now withdrawn)
  3. Orlistat*
    decreases fat absorption
  4. leptin
    modest effect at high doses but obese have leptin resistance
  • = licenced in the UK
29
Q

Surgical options for obesity?

A
  • Liposuction (removes fat locally)
  • Resection of intestine
  • Stomach stapling
  • Stomach banding

Complications common, maintenance difficult

30
Q

How stomach banding surgery takes place?

A
31
Q

How does the stomach banding outcome affect obesity?

A

Food passes slowly
only little food comes into stomach
Reverisible

Nutrition and Metabolism (14 decks)

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