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Winter 2014 > KIN 404 2 > Flashcards

KIN 404 2 Flashcards

1
Q

By how much can total daily energy expenditure vary in two adults in similar size? Why?

A

1500 kcal/day…occupation

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2
Q

What is BMR, and how is it measured?

A

Basal metabolic rate…laying awake but resting, stress free in the morning after sleep, not digesting food (post-absoprtive state) and in the absence of thermoregulatory heat production…direct or indirect calorimetry

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3
Q

What is RMR?

A

Resting Metabolic Rate…similar to BMR but not measured in the morning after sleep (usually 10% of BMR)

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4
Q

What is MMR?

A

Minimal Metabolic Rate…metabolic rate in carious conditions that cause the rate to fall below BMR (sleep decreases 10%, anesthesia, continued starvation decreases it by 10%)

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5
Q

What is FMR?

A

Field Metabolic Rate…total daily energy expenditure (TDEE) is higher than BMR due to energy requirements of feeding, cold exposure and muscle use

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6
Q

What is maximal metabolic rate?

A

Maximal steady-state metabolic rate during hard eercise (20 x BMR in trained athlete and 12 x BMR in sedentary person)

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7
Q

What are the major oxygen consuming organs of the body?

A

Skeletal muscle, liver, brain, heart, lung kidney, GI tract

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8
Q

What are the top 3 organs for body O2 % use?

A

Brain, skeletal muscle and liver

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9
Q

What us the % breakdown of metabolic pathways and cellular processes to daily energy expenditure?

A

Basal Metabolic Rate 60-70%, Physical Activity (15-30%), thermic effect of feeding (8-12%), other such as adaptive thermogenesis, growth and reproduction (2-3%)

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10
Q

What are the two components of physical activity?

A

exercise and non-exercise activity thermogenesis (NEAT)

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11
Q

What is the % of basal metabolic rate?

A

Mitochondrial Proton Leak (20%), Protein Synthesis (25-30%), Na+-K+-ATPase (19-28%), Ca2+-ATPase (4-8%), Glucogeogenesis (7-10%), Ureagenesis (3%), Actomyosin ATPase (2-8%), other (13-30%)

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12
Q

How much does Thermic Effect of Feeding stimulate the metabolic rate by 1-2 hours after a meal in humans?

A

approximately 25%

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13
Q

What are the components of the thermic effect of feeding?

A

Metabolism of ingested AA in liver for glucose, fat, urea and protein synthesis (~35-45%). Swallowing, digestion and absoprtion of food and enzyme secretion (~25-30%. SNS activation (~30-40%).

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14
Q

Steps in the overview of the acute control of brown adipose tissue (BAT)

A

1) PVN/VMN secretes MCH and CART 2) MCH and CART activate the SNS to release NE 3) Beta-3 adrenergic receptor on BAT and increases cAMP within the cell 4) Activates PKA which activates HSL 5) Lipolysis to release FFA from TG 6) FFA substrate for thermogenesis and activator of UCP-1

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15
Q

What allosterically activates UCP-1?

A

FFA

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16
Q

Thermogenesis is due to activation of?

A

UCP-1 through lipolysis

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17
Q

WHere is UCP1 found?

A

Only in the mitochondria of BROWN FAT

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18
Q

Thermogenesis in BAT at a given moment is determined by the degree of ___________ at that moment and can alter within seconds, but the ______________ for thermogenesis is determined by the degree of _______________ of the tissue (x-ais) which needs days or weeks to be significantly altered.

A

activation, capacity, recruitment

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19
Q

WHere are the sites of BAT in adult humans found by FDG PET?

A

neck, supraclavicular, medistinum, paravertebral, suprarenal

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20
Q

What is FDG PET?

A

Fluorodeoxy glucose positron emission tomography

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21
Q

How was it determined that adult humans do indeed have brown adipose tissue?

A

Gave them FDG PET scans in warm environment, and there was no BAT activation. Repeated the study with a SNS beta blocker, and again no activation…shows that adults have BAT that is activated by cold and by SNS activation

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22
Q

2 studies have shown that mice overexpressing human UCP-3 in skeletal muscle are hyperphagic and lean, and those that overexpress UCP-1 in skeletal muscle are resistant to diet-induced obesity and insulin resistance…what does this show?

A

Promoting inefficient metabolism in muscle represents a potential treatment for obesity and diabetes

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23
Q

2 studies have shown that mice lacking mitochondrial uncoupling protein are cold-sensitive but not obese and transgenetic mice that have BAT ablated develop obesity…what does this show?

A

UCP-1 is not the only system involved in thermogenesis even within BAT, so there may be other energy consuming processes that can be targeted for promoting inefficient metabolism.

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24
Q

What is the estimated contribution of SERCAs to daily energy expenditure?

A

~18% in skeletal muscle…60% of daily energy expenditure is from BMR. Of that 60%, 20% of it comes from skeletal muscle and muscle consumes 40-45% of that ATP at rest, therefore, ~18% of RMR comes from skeletal muscle!

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25
Q

What is BTS?

A

a drug that inhibits actin-myosin ATPase, so when muscle contracts there is no force production, but there is still Ca2+ release and change in membrane potential, so SERCA and Na+/K+ ATPase are still wokring

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26
Q

How much of the resting muscle VO2 is from SERCA?

A

40-45%

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27
Q

How is MgCl2 used to assess the contribution of SERCA activity to resting metabolic rate in isolated mouse skeletal muscles?

A

MgCl2 blocks Ca2+ leak so SERCA is not needed at rest to pump Ca2+ back into SR. So, when the calcium leak channel is blocked, the VO2 of the muscle will drop in proportion to the amount of O2 mitochondria are using at rest

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28
Q

What are some things that phyisologically reduce SR Ca2+ transport efficiency?

A

phospholamban, sarcolipin, HUFAs and cold acclimation

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29
Q

What are some things that pharmacologically reduce SR Ca2+ transport efficiency?

A

L-thyroxine (hyperthyroid), low iodine diet (hypothyroid), tamoxifen

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30
Q

What are 2 things that pharmacologically increase the efficiency of SERCA?

A

curcumin and fluoride

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31
Q

What is sarcolipin?

A

An 31 AA, integral membrane protein that ineracts with Ca2+ binding domain of SERCA to reduce its efficiency…causes calcium slippage by drastically reducing the affinity of calcium before the E2 confirmation is reached, thereby, allowing Ca2+ to slip back into the cytosol because there is a lower concentration there compared to inside the SR

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32
Q

The major energy consuming process that contributed to BMR in the G tract is?

A

Protein synthesis

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33
Q

Which of the following 2 processes combined contribute to ~50% of whole body BMR? a) actiomyosin ATPase and Na+/K+ ATPas b) mitochondrial uncoupling and ureagenesis c) actomyosin ATPase and gluconeogenesis d) Na+/K+ ATPase and protein synthesis e) digstion of food and mitochondrial uncoupling

A

d) Na+/K+ ATPase and protein synthesis (19-28% and 25-30%)

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34
Q

Which of the following is true? a) deletion of UCP-1 gene does NOT increase obesity at room temperature b) genetic ablation of BAT does not increase obesity of room temperature c) overexpression of UCP-1 reduces the efficiency of Ca2+ pumps in skeletal muscle d) a and b e) all the above

A

a) deletion of UCP-1 gene does NOT increase obesity in mice at room temperature

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35
Q

Deletion of SLN would be expected to cause… a) decrease in exercise induced thermogenesis b) decrease in BMR c) decreased efficiency of Ca2+ transport d) only a and b e) all the above

A

d) a and b only

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36
Q

Deletion of sarcolipin was shown to cause… a) decreased resting energy expenditure in ST skeletal muscle b) decreased contribution of SERCA pumps to REE in ST skeletal muscle c) decreased whole body BMR d) a and b only e) all of the above

A

b) decreased contribution of SERCA pumps to REE in ST skeletal muscle (i.e. soleus)

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37
Q

Which is true? a) SLN-null mice fed a chow diet are more glucose intolerant than age matched WT b) SLN content in BAT is increased in HF WT mice c) SLN-null mice have lower cage activity than age-matched WT mice c) SLN-null mice have lower cage activity than age-matched WT mice d) differences in diet-induced obesity between WT and SLN null mice are smaller following propanolol treatment e) none of the above

A

e) none of the above

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38
Q

How much do SERCAs contribute to daily energy expenditure?

A

~18%

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39
Q

What % of resting muscle VO2 come sfrom SERCA?

A

~40-45%

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40
Q

What is adaptive thermogenesis?

A

The energy expenditure that occurs in response to environmental temperature or diet…variable and regulated by the brain, responds to temperature and diet, occurs in brown adipocyte mitochondria

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41
Q

What does SLN ablation do to Ca2+ transport efficiency in soleus?

A

increases Ca2+ transport efficiency in the soleus

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42
Q

The relative contribution of SERCA to resting soleus VO2 is _______ in chow-fed SLN KO mice

A

lower

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43
Q

Are body weight, whole body VO2, food intake and activity different between SLN KO and WT chow fed mice?

A

NO!…Knocking out SLN will reduce the % of resting muscle VO2 that comes from SERCA, but because there is no difference in VO2 in a chow few diet at both the muscle and whole body level, some other energy wasting pathway must be upregulated in order to compensate for the lack of SLN

44
Q

SERCA contribution to resting oxygen consumption is lower in SLN-KO (35%) vs. WT (45%). This confirms that SLN reduces the efficiency of SERCAs so SLN increaes the ATP cost of maintaining Ca2+ homeostasis in resting soleus

A

afajlh

45
Q

The similar resting VO2 (soleus and whole body) and BW in chow-fed WT and SLN-KO can probably be explained by compensatory adaptations in SLN-KO mice that increases energy expenditure by other tissues/systems

A

fjalkfja

46
Q

SLN-nill mice gain __________ weight than WT mice after consuming a HFD

A

more

47
Q

SLN-null mice display _______ adiposity than WT mice after consuming a HFD

A

greater

48
Q

SLN-null mice develop severe glucose intolerance in response to a HFD

A

sfah

49
Q

Food intake is __ in SLN-KO mice than in WT mice follwoing 8 wees of a HFD

A

lower

50
Q

HFF SLN-null and WT mice have _________ activity levels in their cages

A

Similar

51
Q

Whole body daily energy expenditure is _______ in KO mice than WT mice but only after _________________

A

lower, a HFD

52
Q

In response to a HFD, SLN content in the soleus muscle of WT mice does what?

A

increased 3.8-fold…adaptive thermogenesis

53
Q

Conclusions from high fat feeding experiment in SLN-KO mice

A

1) Mice lacking SLN are more susceptible to diet induced obesity and glucose intolerance 2) Development of glucose intolerance in SLN-null mice is likely linked to increased adiposity and development of whole body insulin resistance 3) it appears that adaptive thermogenesis in responce to high fat feeding is reduced in SLN-null mice

54
Q

HFF __________ resting soleus VO2 in both WT and SLN-KO mice

A

increased

55
Q

Whole body VO2 was _________ in SLN-KO mice after HFF but not while asleep

A

lower

56
Q

VO2 during sub-maximal treadmill exercise but not VO2 max is ________ in SLN-KO mice

A

lower

57
Q

Serum catecholamine levels are ______ in HFF SLN mice only

A

increased

58
Q

What happens if SLN-KO mice are treated with a beta blocker?

A

Treatment with a beta-clocker blunts adaptive thermogenesis in soleus from SLN KO mice but not from WT mice

59
Q

Differences between WT and SLN-KO mice in whole body VO2 after HFF are ___________ by propanolol

A

enhanced

60
Q

Differences between WT and SLN-KO mice in diet induced weight gain are obesity are _____________ by propanolol

A

enhanced

61
Q

Conclusions from SLN-KO mice studies and SNS activity

A

1)Beta-adrenergc partially compensates for a lack of SLN to activate muscle-based diet-induced thermogenesis but SLN is the primary and more effective mediator 2) the effects of SLN on metabolic rate are greatest when energy demand is high 3) Induction of SLN in muscle by HFF reduces reliance on the SNS which is actiavted to a greater extent in the absence of SLN and only contributes to muscle-based DIT under those conditions 4) Our findings raise the possibility that failure to activate SLN in response to overfeeding may predispose individuals to metabolic syndrome, type 2 diabetes and CVD

62
Q

How does leptin increase energy expenditure?

A

By activating the SNS through its actions on POMC/CAR neurons and the PVN and by directly stimulating energy expenditure in skeletal muscle

63
Q

What does the increase in energy expenditure from leptin rely on in mouse soleus?

A

AMPK, PI3K and ACC activity

64
Q

What things stimulate a futile cycle of do novo lipogenesis and lipid oxidation in skeletal muscle?

A

Leptin, CH, adiponecin and catecholamines

65
Q

Explain the futile substrate cycling in skeletal muscle brought forth by leptin, CRH, adiponectin and catecholamines

A

Leptin binds to its recepto –> phosphorylates Threonine 172 on AMPK alpha catalytic subunit by CamKK (Ca2+) –> phosphorylates/inhibits ACC –> reduces malonyl-CoA levels –> iincreased fatty acid uptake due to inhibition of CPT-1 –> increased beta-oxidation –> increased in acetyl Co-A –> Kreb’s cycle overstimulated –> increase in citrate production in cytosol –> citrate lyase turns citrate back into acetyl-CoA –> by law of mass action Acetyl CoA will become malonyl CoA, this stimulating the resynthesis of the fatty acid that was just burned –> WASTING ENERGY :)

66
Q

What happens to the futile substrate cycling in skeletal muscle if citrate lyase, fatty acid synthase, CPT-1, PI3K or AMPK are blocked?

A

The futile cycle stops

67
Q

What are the possible roles of the SNS in energy expenditure on skeletal muscle?

A

futile cycles, proton uncoupling (UCP3), Ca2+ (SLN), substrate cycling

68
Q

What are the possible roles of the SNS in energy expenditure in BAT?

A

futile cycles and Ca2+/SLN?

69
Q

Are changes in leptin strongly realted to changes in NEAT?

A

NO!…changes in leptin with overfeeding are strongly correlated to changes in body fat but NOT leptin

70
Q

Does BMR increase linearly with 8 weeks of overfeeding in lean healthy subjects?

A

NO

71
Q

What is NEAT most likely regulated by in lean people that don’t gain weight in response to a HFD?

A

NEAT is likely regualted through a central mechanism that integrates NEAT with energy intake and energy stores so that NEAT is activated with over-feeding and suppressed with underfeeding

72
Q

Which of the following inhibit brown preadipocyte progression from the differentiation to the activation phase?

a. BMP7
b. Insulin
c. Wnt/PREF1
d. B/C
e. All of the above

A

c. Wnt/PREF1

73
Q
  1. Which of the following promote brown fat differentiation?
    a. BMP2
    b. BMP4
    c. BMP7
    d. B/C
    e. All of the above
A

C. BMP 7

74
Q

According to the journal article by Schlogl et al (2013), which of the following is false:

a. BAT is involved in nonshivering thermogenic response to cold in humans
b. BAT is involved in nonshivering thermogenic response to cold in rats
c. BAT ablation in mice resulted in hyperphagia and obesity
d. Cold-induced BAT activation is positively correlated with fat free mass
e. Baseline cold-induced BAT activation negatively correlated with changes in fat mass after 6 months

A

d. cold induced BAT activation is positively correlated with fat free mass

75
Q

Which of the following is not a basic component of thermogenesis based on the data collected in the UCP-1 ablation in mice study:

a. Basal metabolic rate
b. Norepinephrin induced UCP1-independent thermogenesis
c. Norepinephrin induced UCP1-dependent thermogenesis
d. Body growth
e. All of the above are basic components of thermogenesis based on the data that was obtained

A

d. body growth

76
Q

Which of the following statements is false?

a. In rodents, cold exposure and caloric excess activate BAT
b. BAT has been shown to be activated in the immediate postprandial period following a single, high-calorie, high carbohydrate meal
c. In lean males, food consumption during cold exposure showed increased BAT activation beyond that from cold exposure alone
d. Any activation of BAT following excessive caloric consumption does not last beyond 4 hours after the last meal.
e. c) and d)

A

c. In lean males, food consumption during cold exposure showed increased BAT activation beyond that from cold exposure alone

77
Q

Choose the correct statement(s):

a. Shivering and non-shivering thermogenesis are important to ensure normal cellular and physiological function under conditions of environmental challenge
b. Heat produced by diet-induced thermogenesis serves to maintain body temperature
c. Skeletal muscle is the most important organ for thermogenesis
d. a and b only
e. all of the above are true statements

A

a. shivering and non-shivering thermogenesis are important to ensure normal cellular and physiological function under conditions of environmental challenge

78
Q

Which of the following is true regarding either BAT or CIBA

a. BAT is involved in nonshivering thermogenic response in rodents but not humans
b. BAT is activated for up to 24 hours after a meal
c. BAT is transiently activated due to overeating in humans
d. CIBA is not found in individuals who live in warm climates
e. C & D only

A

c. BAT is transiently activated due to overeating in humans

79
Q

Which of the following statements in false?

a. UCP1 allows H+ in the mitochondrial intermembrane space to re-enter the mitochondrial matrix without generating ATP
b. Shivering thermogenesis is a function of skeletal muscle, while non-shivering thermogenesis is a function of brown fat
c. Diet-induced thermogenesis is not influenced by nutritional component, only by presence of food
d. Diet-induced thermogenesis and non-shivering thermogenesis are both regulated by the sympathetic nervous system (SNS)
e. Heat produced in diet-induced thermogenesis is quickly dissipated to the environment to prevent body temperature from rising

A

c. Diet-induced thermogenesis is not influenced by nutritional component, only by the presence of food

80
Q

Obligatory Thermogenesis is:

a. The regulated heat production in response to environment and diet
b. The minimal heat produced by the body systems that maintain BMR at a thermonuclear temperature
c. The rate of energy utilized by an organism in its awake but resting state
d. The temperature at which body systems are not stimulated to produce heat

A

b. the minimal heat produced by the body systems that maintain BMR at a thermoneutral temperature

81
Q

Why was a diet of 60% fat, 20% protein, and 20% carbohydrates chosen in the Overfeeding and Brown Adipose Tissue study?

a. It adds the greatest amount of fat tissue to the body
b. It increased the BMR
c. In another study it showed the greatest decrease in sleeping energy expenditure
d. In another study it showed the highest sleeping energy expenditure

A

d. in another study it showed the highest sleeping energy expenditure

82
Q

Which statement(s) regarding UCP1 are false?

a. UCP1 deficient mice are sensitive to cold temperatures
b. UCP1 is unique to brown adipose tissue
c. UCP1 functions as a proton carrier protein within the mitochondrial intermembrane space
d. In addition to UCP1 two other uncoupling proteins have been identified: UCP2 and UCP3
e. B and D are false

A

c. UCP1 functions as a proton carrier protein within the mitochondrial intermembrane space

83
Q

UCP1 ablation in which thermal stress was eliminated in mice resulted in:

a. Increase in body weight for mice fed a control diet and mice that were fed a high fat diet
b. An increase in lean and fat mass
c. A higher thermogenic response due to norepinephrine injection in UCP1 ablated mice in comparison to wildtype mice
d. all of the above

A

a. increase in body weight for mice fed a control diet and mice that were fed a high fat diet

84
Q

Which of these is not seen in UCP1 Ablated mice:

a. Diet induced thermogenesis
b. Obesity
c. Weight loss
d. A and C
e. All of the above

A

d. A and C

85
Q

Which of the following is true about cold induced brown adipose tissue activity

a. Negatively correlated with fat free mass
b. Not associated with energy expenditure regardless of diet
c. Negatively associated with changes in fat mass
d. Both a and b
e. All of the above

A

e. all of the above

86
Q

Which of the following is true?

a. humans do not exhibit CIBA
b. lean males, already exposed to the cold, increases BAT activation
c. activation of BAT from overfeeding lasts more than 4 hours
d. all of the above
e. none of the above

A

e. none of the above

87
Q

In adult humans, the most common location for metabolically active deposits of brown adipose tissue is:

a. Supra-cranial
b. Inter-peritoneal
c. Cervical-supraclavicular
d. Axillary-humeral
e. Both A) and B) above

A

c. cervical-supraclavicular

88
Q
  1. With normal diets, UCP-1 ablation induces obesity:
    a. Only in thermoneutral environments
    b. Only in cool living environments
    c. In both thermoneutral and cool environments
    d. UCP-1 ablation did not cause obesity in any test conditions
A

a. only in thermoneutral environments

89
Q
  1. Which of the following statement is true?
    a. Accumulation of brown adipose tissue is only found in human newborn
    b. Alternative adaptive adrenergic thermogenesis is mediated by UCP1
    c. Basal metabolic rate was unaffected by the amount of UCP1 but in response to norepinephrine
    d. Only A &C
    e. All of the above
A

c. basal metabolic rate was unaffected by the amount of UCP1 but in response to NE

90
Q
  1. Which of the following doesn’t belong in the three components of thermogenesis?
    a. adaptive adrenergic thermogenesis
    b. UCP1-independent norepinephrine-induced thermogenesis
    c. basal metabolic rate
    d. UCP1-dependent norepinephrine-induced thermogenesis
A

a. adaptive adrenergic thermogenesis

91
Q
  1. According to the “UCP1 Ablation Induces Obesity and Abolishes Diet-Induced Thermogenesis in Mice Exempt from Thermal Stress by Living at Thermoneutrality” article, which of the following is/are true?
    a. Response to norepinephrine injection was higher in UCP1-ablated mice
    b. Response to norepinephrine was lower in UCP1-ablated mice
    c. Response to norepinephrine was higher in high-fat-fed wild-type mice
    d. A and C
    e. B and C
A

e. b and c

92
Q
  1. BMP7 expression in mice leads to:
    a. Increases in brown fat mass but not to white fat mass
    b. Increases in white adipose tissue differentiation
    c. A scarcity of brown adipose tissue in the body
    d. An absence of UPC-1 expression
    e. None of the Above
A

increases in brown fat, but not white fat

93
Q
  1. What are the effects on BAT activation following consumption of a high caloric meal?
    a. The effects are seen beyond 4 hours but not up to 24 hours
    b. Activation of BAT will last for at least 24 hours
    c. There is no activation of BAT
    d. No effect of BAT is seen beyond 4 hours
    e. The effects are seen postprandial and disappear within the first hour
A

d. No effect of BAT is seen beyond 4 hours

94
Q
  1. Which of the following is/are false?
    a. CIBA is evident in individuals from warm southern countries.
    b. BAT is activated immediately after a meal with high caloric content.
    c. Food consumption during cold exposure failed to show an increase in BAT activation beyond cold exposure itself.
    d. Prolonged BAT activation in humans occurs after 24 hours of overfeeding.
    e. Both C and D are false
A

d. Prolonged BAT activation in humans occurs after 24 hours of overfeeding

95
Q
  1. Normal animal housing conditions (18 to 22 degree Celsius) is a chronic thermal stressor to mice?
    a. True
    b. False
    c. Unrelated to the articles
A

true

96
Q
  1. Which of the following is FALSE regarding UPC1?
    a. It is an inner mitochondrial transmembrane protein
    b. It is expressed only in Brown Adipose Tissue
    c. Allows proteins in the inner mitochondrial space to re-enter mitochondrial matrix without generating ATP
    d. UPC1 deficient mice exhibit a decreased sensitivity to diet-induced obesity
    e. Mediates Brown Adipose tissue thermogenesis
A

c. allows PROTEINS in the immer mitochondrial membrane space to re-enter mitochondrial matrix without generating ATP

97
Q
  1. Which of the following statements is false?
    a. In a thermoneutral environment, UPC1 ablation induces obesity in chow fed mice
    b. In a thermoneutral environment, UPC1 ablation induces obesity in mice fed a high-fat diet
    c. UPC1 ablation prevents diet-induced thermogenesis in chow fed mice
    d. UPC1 ablation increases diet-induced thermogenesis in mice fed a high-fat diet
    e. UPC1 ablation has no effect on lean mass
A

d. UCP-1 ablation increasese diet-induced thermogenesis in mice fed a high fat diet

98
Q
  1. Which of the following statements regarding Brown Adipose Tissue (BAT) is true?
    a. BAT is involved in the nonshivering thermogenic response to cold
    b. BAT is activated in the immediate postprandial period after a high-calorie meal
    c. BAT is not activated after 24hr of overfeeding
    d. A and B only
    e. All of the above
A

e. all of the above

99
Q
  1. Which of the following regarding Adaptive Thermogenesis is true?
    a. It is regulated primarily by brown adipose tissue (BAT) activity
    b. Heat produced by responses by the body to cold temperature and diet are not referred to as adaptive thermogenesis.
    c. Energy is dissipated in mitochondria of brown fat and skeletal muscle in the form of heat in response to external stimuli.
    d. A & B
    e. A & C
A

a. it is regualted primarily by BAT

100
Q
  1. Which of the following regarding UCP1 ablated mice is true?
    a. Inability to recruit diet induced thermogenesis
    b. The metabolic efficiency is lower in UCP1 ablated mice than Wild type mice.
    c. The increase in body weight and fat depot size is only caused by an increase in food intake.
    d. All of the above
    e. None of the above
A

a. inability to recruit diet induced thermogenesis

101
Q
  1. Which of the following can activate brown adipose tissue in humans?
    a. overfeeding
    b. cold exposure
    c. increased energy expenditure
    d. a and b
    e. a, b and c
A

d. a and b

102
Q
  1. Why was a diet of 60% fat, 20% protein, and 20% carbohydrates chosen in the Overfeeding and Brown Adipose Tissue study?
    a. It adds the greatest amount of fat tissue to the body
    b. It increased the BMR
    c. In another study it showed the greatest decrease in sleeping energy expenditure
    d. In another study it showed the highest sleeping energy expenditure
A

d. in another study it showed that highest sleeping energy expenditure

103
Q
  1. Adaptive thermogenesis is the physiological process whereby….
    a. Energy is dissipated in mitochondria of white fat and cardiac muscle in the form of heat in response to external stimuli.
    b. Energy is dissipated in the mitochondria of brown fat and skeletal muscle in the form of heat in response to external stimuli.
    c. Energy is dissipated in the mitochondria of brown fat and cardiac muscle in the form of heat in response to external stimuli.
    d. None of the above.
A

d. none of the above

104
Q
  1. In rodents, cold exposure activates ______ and caloric excess may also stimulate this activity as an adaptation to _______.
    a. Brown adipose tissue; increase body weight gain.
    b. Brown adipose tissue; limit body weight gain.
    c. Diet-induced thermogenesis; increase body weight gain.
    d. Diet-induced thermogenesis; limit body weight gain.
    e. Diet-induced thermogenesis; maintain body weight.
A

b. BAT; limit body weight gain

105
Q
  1. The phenotype of UCP1-ablated mice consists of all of the following except:
    a. The mice should be less susceptible to cold
    b. The mice have to rely on shivering for thermoregulatory thermogenesis
    c. The mice lack the ability to recruit adrenergic thermogenesis during acclimation to cold
    d. The mice should become obese
    e. All of the above are true
A

a. the mice should be less susceptible to cold

106
Q
  1. Choose the true statement(s):
    a. UCP1 is found in all mitochondria
    b. UCP1 in mitochondria regulate thermogenesis by causing shivering
    c. Temperatures of thermoneutrality for mice are similar to that of humans
    d. UCP1 ablation can induce obesity in mice exempt from thermal stress
    e. All of the above are false
A

d. UCP-1 ablation can induce obesity in mice exempt from thermal stress

Winter 2014 (5 decks)

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