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Gastrointestinal System > Energy Balance and Obesity - Watford 2/18/16 > Flashcards

Energy Balance and Obesity - Watford 2/18/16 Flashcards

1
Q

energy: uses and source in the body

A
  • biological work in the body (kinetic energy)
    • mechanical energy (m contraction)
    • chemical
    • osmotic
    • electrical
  • energy sourced from food (potential energy)
    • metabolize fat, carbs, proteins
    • allows for proton gradient and ATP synth
    • HEAT
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2
Q

track energy in food to its “end” fx in body

A
  • food energy
    • lose 1-9%
    • lose some more in sweat, urine, sloughed off cells
    • ultimately end up with metabolizable energy
  • ​metabolizable energy has 3 fates
    • ​50% lost as heat (inefficient)
    • 5-10% lost as cost of digestion/abs/storage
    • 25-40% stored in high energy ATP bonds
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3
Q

energy balance eqn

[variant: during weight maintenance]

A

energy in - energy out = energy stored

during wt maintain:

energy in = energy out

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4
Q

imbalances in Ein and Eout don’t necessarily lead to massive continued weight gain.

why?

A

weight gain is accompanied by lean mass gain → increased metabolic rate

  • new equilibrium: higher Ein = higher Eout
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5
Q

Atwater table values

A

carbs: 4 kcal/g
proteins: 4 kcal/g [really 5.4, but 1.4 is urea
fats: 9 kcal/g

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6
Q

digestible energy

vs

metabolizable energy

A

digestible = energy in food - energy in feces

metabolizable = energy in food - losses in feces, urine, sweat, etc

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7
Q

ATP equivalents

and

reducing equivalents

A

creatine phosphate, GTP

and

NADH, NADPH, FADH2

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8
Q

what tasks does energy perform in the body?

A
  • pumps: Na/K ATPase (20-40% of basal egy expenditure), other transport pumps
  • thermic effect of food: 5-10%
  • inefficiency/heat: 50%
  • synthesis, needed to maintain life: 20-40%

activity causes variations in expenditure

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9
Q

describe composition and metabolic contribution of adipose tissue vs. lean mass

A
  • adipose tissue: metabolically inactive (relatively)
    • 85% lipid, 15% water
  • lean mass: where metabolism occurs
    • 20% protein, 80% water

most energy expenditure occurs in lean body mass or “fat free mass”

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10
Q

breakdown of body weight

A
  • body weight = fat + fat free mass
    • fat free mass: lean tissues + glycogen (1-2%)
    • lean tissues: 20% protein + 73% water + 7% bone
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11
Q

ways to calculate body composition and body fat

A
  • % fat vs % lean
    • bioimpedance analysis
    • hydrodensitometry
  • 2 compartment models: fat, fat-free mass
  • 4 compartment models
    • BW = water + protein + bone mineral + fat(+ glycogen - no way to measure)
    • BW = BCM (body cell mass) + fat + skeleton + ecf
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12
Q

common ways to assess body mass

A
  • BMI, CT (high radiation), dexa (low radiation),
  • skin fold thickness
  • waist circumference; waist-to-hip ratio
  • body plethysmography
  • bioimpedance
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13
Q

history of theories of energy expenditure

A
  • Santorio: weight himself, food intake, excretion for 30 years
    • “insensible perspiration”
  • Lavoisier: father of modern chem/nutrition
    • invented indirect calorimetry too

energy expenditure = thermogenesis

or

energy expenditure = oxygen consumption (ATP production)

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14
Q

direct calorimetry

vs

indirect calorimetry

A
  • direct calorimetry: measure of heat production
    • “direct” measure of egy expenditure
      • requires a closed system for approx 23 hr/day

inconvenient, usually foregone for indirect calorimetry

  • indirect calorimetry: measures oxygen consumption via respiratory quotient RQ
    • RQ = CO2 produced/O2 consumed
      • 1 = carbs, .7 = fats, in between = mixture
    • instead of lumping all expenditure over a day, allows for assessing individual components of expenditure (rest, activity, after meals)
      *
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15
Q

respiratory quotient

A

RQ, ratio of carbon dioxide produced by consumption of a fuel to oxygen used to burn that fuel

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16
Q

RQ during fat synthesis

A

synthesizing fat from glucose, RQ = 2.75

RQ >= 1.1 indicates fat synthesis

17
Q

downside/inaccuracy of calorimetry

alternatives??

A
  • issues with accuracy
  • restrictions in movement (that aren’t realistic)
  • observation (likely to change behavior)

alternative: doubly labeled water!!!

18
Q

doubly labeled water

A
  • assessment of total free-living energy expenditure

water composed of “heavy” isotopes of H and O

2H218O

excretion of H has to be through water (urine, sweat, etc)

excretion of O can be either water or CO2

  • since H and O are lost at different rates due to metabolism, ratio of H to O can give you metabolic rate
19
Q

determinants of resting metabolic rate

(non-variable and variable)

A
  • fixed
    • ​age
    • gender
    • genes
  • variable
    • ​diet
    • FFM (fat free mass; lean body mass)
    • environmental temp
    • hormones (TH, SNS catecholamines)
    • drugs
    • stress
20
Q

determinants of thermic effect of food (TEF)

A

aka diet induced thermogenesis, specific dynamic action

= rise in RMR 2-5h after a meal

  • varies by type of macronutrient ingested
    • approx 25-40% of protein calories lost in this window
    • 6-8% carb calories lost
    • 3% fat calories lost
  • differences may be due to variable energy cost of storing different nutrients
21
Q

types of factors that affect food intake

A

orexigenic: increase food intake

anorexigenic: decrease food intake

22
Q

short term and long term biological signals of levels of food intake

A
  • long term
    • ​insulin and leptin levels reflect body fat
  • short term
    • ​signals from gut: Ghrelin, CCK, GLP-1 (glucagon like peptide 1), PYY, apoA IV
      • leptin modulates sensitivity to these short term signals (like CCK)
23
Q

describe some adiposity/blood glucose signals and their sources

A
  • satiation signals
    • CCK, GLP-1, gastric distention [liver, GI tract]
  • adiposity signals
    • leptin [fat]
    • insulin [pancreas]
  • nutrients

signal the brain via ARCTUATE NUCLEUS re: food intake and energy expenditure

24
Q

orexigenic signals

A
  1. Ghrelin
  2. orexin
  3. galanin
  4. MCH [melanin concentrating hormone]
  5. GABA [gamma amino butyric acid]
  6. PYY, NPY [neuropeptide Y]
25
Q

anorexigenic signals

A
  1. gastric distention
  2. CCK [chelocystikinin]
  3. GLP-1 [glucagon like peptide 1; type of incretin]
  4. insulin
  5. leptin
  6. lipids, proteins/a.a.s/glucose
26
Q

how do signals from adipose tissue set off catabolic pathways?

A

adipose tissue produces leptin, which stimulates catabolic MC4R pathway in ventromedial hypothalamus

  • leptin stimulates POMC: activates MC4R pathway
    • activate activator
  • leptin inhibits Agouti-related peptide (AgRP/NPY neurons): inhibit an inhibitor of MC4r
    • inhibit inhibitor
27
Q

how do orexigenic signals set off anabolic pathways?

A

Ghrelin/orexins set off anabolic MCH and Orexin pathways in lateral hypothalamus

increase appetite, signal body to eat more

28
Q

obesity: genetic drivers

predictors/risk factors for weight gain [Pima Indian study]

A

most human obesities likely polygenic

  • complicated interactions of multiple genes
  • risk factors [Pima]
    • low RMR/body temp
    • high RQ
    • high insulin sensitivity
    • low spontaneous physical activity
29
Q

ob db experiment and implications

A

parabiosis: linked circulation of two mice (one obese and one not) and waited to see what happened

  1. ob/ob-wt: ob lost weight
  2. db/db-wt: db gained weight and wt died of starvation
  3. ob/ob-db/db: db gained weight, ob died of starvation

leptin is produced by brain: signals to increase egy expenditure, decrease food intake

  • ob has no leptin, which is why parabiosis with a wt gave it leptin and it lost weight
  • db has faulty leptin receptors, which is why parabiosis made no change: continuous eating/weight gain

coming full circle…

  • ob-db parabiosis leads to a MASSIVE flux of leptin from db (built up due to bad receptor) to the ob, leading it to stop eating and starve to death
30
Q

leptin resistance

A

seen in many obese human beings

  • causes
    • leptin receptor polymorphisms
    • defects in leptin-R signalling?

regardless, serum leptin levels are increased in proportion to body fat in most obese people (hyperleptinemia)

31
Q

Dutch famine of Winter 1944-45

A

followup 50 years later of kids in utero during famine years saw increased

  • obesity
  • diabetes/insulin resistance
  • heart disease

worse outcomes seen when famine hit during early stages of gestation

fetal programming/metabolic programming/fetal origins of chronic disease/Barker hypothesis

  • changes to histones and DNA methylation during catch-up period of growth after an in utero insult makes you more susceptible to chronic disease like DM2
32
Q

putative contributors to obesity

A
  • sleep deprivation
  • smoking cessation
  • ambient temp
  • pharma influences
  • environmental pollutants (endocrine disruptors)
  • animal hormones/antibiotics
  • changes in food intake
33
Q

microbiota/obesity experiment

A

took feces from identical twins (one lean, one obese) and transplated into germ-free mice

  • both had same caloric intake, but began to take on lean/obese phenotype depending on which feces they got

later took obese and lean mice and put them together in same cage (mice are coprophagic - eat each others feces)

  • obese mice housed with lean mice dropped weight and their microbiota switched over
  • germ free mice housed with both obese and lean mice because lean
34
Q

brown adipose tissue

A

BAT has UCP 1 (uncoupling protein 1), which dissipates the proton gradient

  • brings protons back into mitochondria without generating ATP
    • generate a TON of heat

BAT functions as thermogenic tissue (many mitochondria, many lipid droplets, highly vascularized) - newborns, hibernation

35
Q

brown vs beige vs white adipose tissue

A

brown: dermomyotomal precursors: myogenic factor 5 (Mycf5) present - not present in others

beige (brown in white): mesodermal precursors

white: mesodermal precursors

beige and white might be able to be converted to one another

36
Q

metabolic syndrome

A
  • impaired glucose tolerance/insulin resistance
  • dyslipidemia
  • android obesity
  • HTN

Gastrointestinal System (35 decks)

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