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A&P 2 > Metabolism > Flashcards

Metabolism Flashcards

1
Q

What is the first law of thermodynamics?

A

Energy can be neither created nor destroyed

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2
Q

What is energy input?

A

Ingested food

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3
Q

What is energy output?

A

External work = movement of body (use of skeletal muscles)
Internal work

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4
Q

What is internal work?

A
  1. Skeletal muscle used other than external work (e.g. shivering)
  2. Life sustaining energy requiring processes (e.g. active tpt mechanisms)
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5
Q

What is most food energy converted into?

A

Heat

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6
Q

What happens in the biochemical processing of nutrients?

A

50% of energy from food transferred to ATP
50% converted to heat

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7
Q

How much of ATP generated from food energy is lost?

A

50% is lost as heat

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8
Q

What is the net loss of heat?

A

75% of energy from food

50% direct loss from food energy + (50% x 50% of ATP lost as heat) = 75%

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9
Q

What is metabolic rate?

A

Rate at which energy is expended by the body during both external & internal work

Metabolic rate = energy expenditure/unit of time

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10
Q

What is a calorie?

A

SMALL c

Basic unit of heat energy
- Amt of heat required to raise temperature of 1g of H2O by 1°C

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11
Q

When is Kilocalorie or Calorie used?

A

Kilocalorie = kcal
Calorie = BIG c

Used when discussing human body

= 1000 calories (small c)

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12
Q

What is the basal metabolic rate (BMR)?

A

Metabolic rate under standardized basal conditions
= Metabolic activity necessary to maintain basic body functions AT REST

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13
Q

How is BMR corrected for differences in body size (usually)?

A

Skeletal muscles contribute ~20-30% of basal metabolic rate

Therefore, men usually have greater basal metabolic rate bc more skeletal muscles (65-70 Calories/hr in average 70kg man)

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14
Q

What are the standardized conditions required to find the basal metabolic rate?

A
  1. Subject X eaten for at least 12 hrs
  2. At physical rest
  3. No strenuous activity/exercise at least 30 min - 1hr before test
  4. All mental & physical factors that cause excitement must be eliminated
  5. Comfortable room temp (no shivering/sweating)
  6. After a night of restful sleep (8hrs)
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15
Q

Why can’t subject eat for at least 12 hours before the basal metabolic rate is taken?

(Standardised basal conditions for BMR)

A

To avoid diet-induced thermogenesis
- ↑ in metabolic rate due to ↑ed metabolism of processing ingested food = stomach & intestines move + secretions = all require energy

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16
Q

Why must the subject be at mental rest before basal metabolic rate is taken?

(Standardised basal conditions for BMR)

A

E.g. if stressed = skeletal muscle tone ↑ + adrenaline ↑ = ↑ metabolic rate

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17
Q

Why must the subject have enough sleep before basal metabolic rate is taken?

(Standardised basal conditions for BMR)

A

Not enough sleep = some stress hormones might be released

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18
Q

What are the methods of measuring metabolic rate?

A
  1. Direct calorimetry
  2. Indirect calorimetry
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19
Q

What is direct calorimetry?

A

Measure total quantity of heat given out by body per unit time

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20
Q

What is indirect calorimetry?

A

Food + O2 → CO2 + H2O + energy (mostly transformed into heat)
Energy equivalent of O2 (4.8 Calories/L energy liberated per litre of O2 consumed)

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21
Q

How to calculate estimated BMR (indirect calorimetry)?

A

Estimated BMR = O2 consumption (L/hr) x 4.8 Calories/L

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22
Q

What are the factors influencing metabolic rate?

A
  • Thyroid hormone = ↑ MR (impt for metabolism, growth, development)
  • Testosterone = ↑ MR
  • Growth hormone = ↑ MR (stimulates cellular metabolism)
  • Fever = ↑ MR
  • Sleep = ↓ MR (esp. during slow wave sleep)
  • Malnutrition = ↓ MR
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23
Q

What is energy balance?

A

Energy input must equal energy output to maintain a neutral energy balance

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24
Q

What is a neutral energy balance?

A

Energy intake equals output

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25
Q

What is a positive energy balance?

A

Energy intake exceeds output
- Excess stored as adipose tissue = ↑ weight

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26
Q

What is negative energy balance?

A

Energy intake is less than immediate requirements

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27
Q

What are some short-term regulations of food intake?

A
  • Food intake from meal to meal (feeding pattern)
  • Appetite signals = sensation of hunger
  • Satiety signals = fullness, suppress desire to eat
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28
Q

Long-term regulation

A

Energy balance & body weight

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29
Q

What are some regulations of food intake?

A
  1. Short term regulation (meal to meal; feeding pattern)
  2. Long-term regulation (energy balance & body wt)
  3. Psychosocial/Environmental factors
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30
Q

What is food intake controlled by?

A

Primarily by the hypothalamus

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31
Q

What is the role of the arcuate nucleus?

A

Coordinates the release of Neuropeptide Y (NPY) and melanocortins

  • Central role in long-term control of energy balance & body weight & short-term control of food intake from meal to meal
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32
Q

What is neuropeptide Y (NPY)?

A

Potent appetite stimulator

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33
Q

What are melanocortins?

A

Group of hormones shown to play a role in energy homeostasis

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34
Q

What are the regulatory inputs to the arcuate nucleus in the long-term maintenance of energy balance?

A

Leptin & Insulin

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35
Q

What is leptin essential for?

A

Essential for normal body-weight regulation

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36
Q

What are adipokines?

A

Hormones secreted by adipose tissue that play important roles in energy balance & metabolism
- Leptin is a kind of adipokine
- If have a lot of adipose tissues, more adipokines will be secreted

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37
Q

What is insulin important for?

A

Important role in long-term control of body weight
- Indicator of glucose level in blood bc blood glucose high = insulin released

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38
Q

What is leptin an indication of?

A

Indication of amount of triglyceride fat stored in adipose tissue

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39
Q

What does leptin do?

A

Molecular satiety signal = signals fullness
- Suppress appetite = ↓ food consumption = ↑ weight loss
- Long term matching of food intake to energy expenditure

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40
Q

How does leptin act on the arcuate nucleus?

A

↓ Neuropeptide Y (NPY) production
↑ melanocortin release

41
Q

What happens if lectin gene is removed?

A

Less control in eating behaviour = weight gain

42
Q

What is Ghrelin?

A

Potent appetite stimulator

43
Q

What does PYY3-36 do?

A

Inhibits appetite-stimulating NPY secreting neurons

44
Q

What does cholecystokinin do?

A

Activates the satiety centre in brainstem
- released from duodenum during digestion

45
Q

What does stomach distension activate?

A

Activates the satiety center in brainstem

46
Q

Steps in the metabolism pathway when a meal is consumed

SLIDE 19

A

Meal =
(1) ↑ Glucose & other nutrients in blood
(2) ↑ Fat & other nutrients in duodenum
(3) ↑ Ghrelin (from stomach b4 meal)
(4) ↑ PYY3-36 (from intestines during meal)
(5) Stomach distension

(1) ↑ insulin = limits NPY-secreting neurons

47
Q

What is the :
- source of signal
- effect of signal on appetite

of Neuropeptide Y

A

Source of signal: Arcuate nucleus of hypothalamus

Effect of signal on appetite: ↑

48
Q

What is the :
- source of signal
- effect of signal on appetite

of Melanocortins

A

Source of signal: Arcuate nucleus of hypothalamus

Effect of signal on appetite: ↓

49
Q

What is the :
- source of signal
- effect of signal on appetite

of Leptin

A

Source of signal: Adipose tissue

Effect of signal on appetite: ↓

50
Q

What is the:
- source of signal
- effect of signal on appetite

of Insulin

A

Source of signal: Endocrine pancreas

Effect of signal on appetite: ↓

51
Q

What is the
- source of signal
- effect of signal on appetite

of Orexins

A

Source of signal: Lateral hypothalamus

Effect of signal on appetite: ↑

52
Q

What is the
- source of signal
- effect of signal on appetite

of Corticotropin-releasing hormone

A

Source of signal: Paraventricular nucleus of hypothalamus

Effect of signal on appetite: ↓

53
Q

What is the
- source of signal
- effect of signal on appetite

of Ghrelin

A

Source of signal: stomach

Effect of signal on appetite: ↑

54
Q

What is the
- source of signal
- effect of signal on appetite

of Peptide YY3-36

A

Source of signal: small & large intestines

Effect of signal on appetite: ↓

55
Q

What is the
- source of signal
- effect of signal on appetite

of Stomach distension

A

Source of signal: Stomach

Effect of signal on appetite: ↓

56
Q

What is the
- source of signal
- effect of signal on appetite

of Cholecystokinin

A

Source of signal: Small intestine

Effect of signal on appetite: ↓

57
Q

What regulatory signals increase appetite?

A
  • Neuropeptide Y
  • Orexins
  • Ghrelins
58
Q

What regulatory signals decrease appetite?

A
  • Melanocortins
  • Leptin
  • Insulin
  • Corticotropin-releasing hormone
  • Peptide YY3-36
  • Stomach distension
  • Cholecystokinin
59
Q

Metabolic rate vs Basal metabolic rate

A

Metabolic rate: Rate at which energy is expanded by body during external & internal work

Basal metabolic rate: Rate at which energy is expanded by body but at rest (like minimum metabolic rate)

60
Q

When does obesity occur?

A

When more kilocalories are consumed than are burned

61
Q

What is body mass index (BMI)?

A

Mathematical means of assessing the proportion of body fat (based on est. from population studies)

62
Q

How to calculate BMI?

A

Weight (kg) / Height² (meters)

63
Q

Difference between Asian BMI vs International BMI

A

Asian BMI more stringent
+ Asians have higher body fat ratio

64
Q

BMI values??

A
65
Q

What are the causes of obesity?

A

Complex ! = involves physiological, lifestyle & env. factors

  • Sedentary lifestyle
  • Abnormal feeding behaviour
  • Genetic factors
  • Leptin-signaling pathway dysfunction (leads to overeating)
  • Childhood overnutrition (linked to adult obesity bc once fat cells form, they can shrink but won’t disappear = remain the same number)
  • Hypothyroidism = deficiency of thyroid hormone
66
Q

What are some treatments for obesity?

A
  1. Lifestyle modification
    - Inc. energy output (inc activity)
    - Dec energy input (dec. food intake)
  2. Drugs
    - Dec. degree of hunger
    - Alter lipid absorption in gut (e.g. Xenical = lipase inhibitor)
  3. Surgery
    - Gastric bypass surgery
67
Q

What is metabolism?

A

Chemical processes or reactions in an organism required to sustain life

68
Q

What are the functions of metabolism?

A
  • Metabolic turnover
  • Growth & cell division
  • Special processes such as secretion, contraction & propagation of action potentials
69
Q

What is catabolism?

A

Breakdown of organic substrates
- Releases energy used to synthesize high-energy compounds (e.g. ATP)
- Releases energy

70
Q

What is anabolism?

A

Synthesis of new organic molecules (monomers)
- Uses energy (ATP) produced by mitochondria

71
Q

What happens to excess glucose?

A
  1. Lipogenesis
  2. Glycogenesis
72
Q

What is lipogenesis?

A

Excess glucose is converted to fatty acids and stored as fats

73
Q

What is glycogenesis?

A

Excess glucose converted to glycogen and stored

74
Q

What are the functions of organic compounds?

A
  • Perform structural maintenance & repairs
  • Support growth
  • Produces secretions (a lot are protein in nature)
  • Store nutrient reserves
75
Q

What is the most abundant form of storage for fats?

A

Triglycerides

76
Q

What is the most abundant form of storage for carbohydrates?

A

Glycogen

77
Q

What are proteins mainly used for?

A

For structural & functional use

78
Q

Which organic compounds mainly contribute to our energy?

A

Fatty acids & glucose

79
Q

What does carbohydrate metabolism do?

A

Generates ATP & other high-energy compounds by breaking down carbohydrates

80
Q

What is the equation of carbohydrate metabolism?

A

Glucose + Oxygen = Carbon dioxide + Water

81
Q

How many molecules of ATP are produced from the processing of one molecule?

A

30-32 ATP molecules

82
Q

Which form of carbohydrate metabolism produces the majority of energy?

A

The electron transport chain & citric acid cycle (aerobic)

Produces 30-32 ATP molecules

83
Q

How many ATP molecules does glycolysis produce?

A

2 ATP molecules (net gain)

bc
- 4 ATP produced during enzymatic rxns in cytosol
- 2 ATP used to initiate glycolysis
= 2 ATP molecules net gain to cell

Anaerobic

84
Q

What is gluconeogenesis?

A

Synthesis of glucose from noncarbohydrate precursors
- Uses Lactic acid, Glycerol, Amino acids

85
Q

What is glycogenesis?

A

Formation of glycogen from glucose
- Occurs SLOWLY

86
Q

What is glycogenolysis?

A

Breakdown of glycogen
- Occurs QUICKLY

87
Q

What happens in lipid catabolism (lipolysis)?

A

Hydrolysis splits triglyceride into components = one molecule of glycerol & 3 fatty acid molecules
- Enzymes in cytosol convert glycerol to pyruvate
- Different enzymes convert fatty acids to acetyl-CoA (beta oxidation)

88
Q

Which is the most concentrated source of energy reserve out of all the macronutrients?

A

Lipids = vv effective & efficient source of energy reserve

89
Q

How many ATP molecules does a cell gain for each 2-carbon fragment removed from fatty acid?

A

12 ATP from acetyl-CoA in citric acid cycle
5 ATP in NADH

90
Q

How many ATP molecules does a cell gain for the breakdown of one 18-carbon fatty acid molecule?

A

120 ATP molecules

Why not 153?
- Diff in calculation of yield b/w saturated & unsaturated fatty acids = due to enzyme energy requirement

91
Q

How much more efficient is fatty acid breakdown than glucose breakdown?

A

Fatty acid breakdown yields ~1.3x the energy of glucose breakdown
bc body stores excess energy as fat

92
Q

What are essential fatty acids?

A

Cannot be produced by the body = must be consumed
- Not for energy
- Linoleic acid (omega-6)
- Linolenic acid (omega-3; unsaturated 18-carbon fatty acid from plants)

93
Q

What is glycerol synthesized from?

A

Dihydroxyacetone phosphate (intermediate product of glycolysis)

94
Q

What are nonessential fatty acids & steroids synthesized form?

A

Acetyl-CoA
- Can use almost any organic substrate

95
Q

What do most lipids circulate through bloodstream as?

A

Lipoproteins

96
Q

What are free fatty acids generally bound to?

A

Albumin in blood
- Free fatty acids are a small % of total circulating lipids
- Can diffuse easily across plasma mbns

97
Q

What are lipoproteins?

A

Lipid-protein complexes
- Chylomicrons
- Very low-density lipoproteins (VLDLs)
- Intermediate-density lipoproteins (IDLs)
- Low-density lipoproteins (LDLs)
- High-density lipoproteins (HDLs)

98
Q

How to calculate LDL?

A

LDL = Total cholesterol - HDL - triglyceride/5

mg/dL

Friedewald formula

99
Q
A

A&P 2 (4 decks)

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