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KIN 334 > Regulation of Energy Metabolism > Flashcards

Regulation of Energy Metabolism Flashcards

1
Q

Homeostasis:

A

tendency of an organism to maintain a stable internal state

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2
Q

Most people maintain a ____ body weight over time.

A

stable

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3
Q

Body weight regulation is directly related to….

A

energy balance

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4
Q

In normal individuals, body ___ and body ____ content are quite stable over time owing to a _____ process termed ____ ____.

A
  • weight
  • fat
  • biological
  • energy homeostasis
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5
Q

Energy homeostasis:

A

mechanism by which an organism not only fulfills its energy needs, but also reduces or induces intake when expenditure decreases or increases, respectively

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6
Q

Maintenance of body weight and body composition over time requires not only that energy ____ = energy _____, but also intakes of _____, _____, ____ and _____ = their _____ rates.

A
  • intake
  • expenditure
  • carbohydrate
  • protein
  • fat
  • alcohol
  • oxidation rates
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7
Q

The ____ of food consumed plays a major role in the amount of energy ____ and _____ each day.

A
  • type
  • consumed
  • expended
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8
Q

Under normal circumstances, _____, ______, and _____ are not easily converted to body fat.

A
  • carbohydrate
  • protein
  • alcohol
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9
Q

Oxidative hierarchy that governs the relative _____ in which fuels are selected for ____ ____ after their ingestion.

A
  • order

- oxidative disposal

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10
Q

Stores of alcohol:

A

none

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11
Q

Stores of CHO:

A

glycogen

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12
Q

Stores of protein:

A

body protein

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13
Q

Stores of fat:

A

adipose tissue

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14
Q

In healthy individuals, the fate of ingested alcohol is _____.

A

oxidation

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15
Q

Alcohol is a ____ that must be ____ + body has no ____ capacity for it

A
  • toxin
  • eliminated
  • storage
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16
Q

_____ alcohol balance is achieved.

A

perfect

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17
Q

Alcohol suppresses the _____ of other macronutrients, particularly ____.

A
  • oxidation

- fat

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18
Q

A chronic imbalance between alcohol intake and oxidation cannot directly cause _____, although it may indirectly influence ____ _____.

A
  • obesity

- fat balance

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19
Q

Carbohydrate oxidation is strongly influenced by …..

A

carbohydrate intake

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20
Q

Ingestion of excess carbs causes an _____ _____ _____ ____ in its oxidation rate with resultant _____ of fat oxidation governed by:

A
  • acute auto regulatory increase
  • suppression
  • carb small storage capacity (glycogen 500-1000g)
  • need to maintain glucose homeostasis
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21
Q

Conversion of excess dietary carbs to _____ (____) is very limited in humans and occurs only when …

A
  • triacylglyerols (de novo lipogenesis)

- large excesses of carbs are ingested

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22
Q

The protein stores increase in size only in response to ____ ____, such as….. but NOT simply from ….

A
  • growth stimuli
  • growth hormone
  • androgens
  • physical training
  • weight gain
  • increased dietary protein
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23
Q

On a _____ basis, protein balance is achieved.

A

day to day

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24
Q

Protein imbalance cannot be implicated as a direct cause of ____, but protein ____ may affect ____ ____.

A
  • obesity
  • intake
  • fat balance
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25
Q

Excess protein consumed contribute indirectly to ___ ____ by sparing ____ ____. However, excess dietary protein is not made directly into _____ and stored as ____.

A
  • fat storage
  • dietary fat
  • triacylglycerol
  • fat
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26
Q

Fat intake has no or very little influence on fat ____.

A

oxidation

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27
Q

The oxidation rate of fat is almost totally governed by…..

A

the presence or absence of other macronutrients

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28
Q

There is no auto regulatory linkage between fat ___ and fat ____… as fat intake _____, fat oxidation does not ____ ____.

A
  • intake
  • oxidation
  • increases
  • increase proportionally
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29
Q

In conditions of spontaneous overfeeding (energy intake is ____) …….

A
  • excessive

- the entire excess fat intake is stored as body fat

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30
Q

Energy intake, stores, oxidation of carbs:

A
  • intake: 1000 kcal (1500 overfeeding)
  • stores: 2000 kcal
  • daily oxidation % stores: 50% (70% overfeeding)
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31
Q

Energy intake, stores, oxidation of protein:

A
  • intake: 500 kcal (750 overfeeding)
  • stores: 40,000 kcal
  • daily oxidation % stores: 1.3% (1.9% overfeeding)
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32
Q

Energy intake, stores, oxidation of fat:

A
  • intake: 1000 kcal (1500 overfeeding)
  • stores: 125,000 kcal
  • daily oxidation % stores: < 1%
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33
Q

The amount of total body fat exerts what type of effect on fat oxidation?

A

small, but significant

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34
Q

This promotion of fat oxidation at higher body fat levels may represent a mechanism for …

A

attenuating the rate of weight gain in response to chronic overfeeding

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35
Q

Explain getting fat on a low fat diet?

A

if energy intake > EE, an individual can become obese on a low fat diet

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36
Q

Most fat storage probably comes from the direct deposition of dietary fat associated with the suppression of ___ ____ caused by…..

A
  • fat oxidation

- excess intakes of the other macronutrients accompanying the diet

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37
Q

Fat is the only nutrient capable of causing…

A
  • a chronic imbalance between intake and oxidation

- directly contributing to the increase in adipose tissue

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38
Q

The regulation of feeding, ___ ____ and ____, and body weight is a ______ process.

A
  • feeding
  • energy intake
  • expenditure
  • body weight
  • homeostatic
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39
Q

____ and ____ signals communicate information about the current state of ____ ____ to key brain regions, including the ____ and _____.

A
  • central
  • peripheral
  • energy balance
  • hypothalamus
  • brainstem
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40
Q

The hypothalamus and brainstem receive ____ and _____ signals from the ____ that encode information about the ___ ____ and ____.

A
  • neural
  • hormonal
  • periphery
  • nutritional state
  • adiposity
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41
Q

Key component for regulation of energy homeostasis:

A

hypothalamus continuously monitors signals that reflect energy status and initiates appropriate behavioural and metabolic responses

42
Q

Energy homeostasis must be considered as resulting from an _____ process involving …

A
  • integrative

- all brain areas and peripheral actors

43
Q

Multiple _____, _____, _____ and ____ ____ were found to exert an action on energy homeostasis through their effects on energy intake and/or EE.

A
  • substrates
  • hormones
  • neurotransmitters
  • brain neurons
44
Q

Most studied afferent modulators:

A
  • adipokine (leptin)

- gut hormones (CCK, GLP-1, PYY, ghrelin)

45
Q

Leptin is one of the core components of the ____ system that controls ___ ___ in mammals.

A
  • physiological

- body weight

46
Q

Leptin is expressed and secreted by…

A

exclusively by white adipose tissue adipocytes

47
Q

Leptin provides a signal to the ____ regarding..

A
  • brain

- the status of fat stores

48
Q

Leptin protects the _____ from ,,,,

A
  • organism

- reductions in fat mass that could threaten reproductive capacity/fertility and/or survival

49
Q

Leptin favours ….

A

the preservation of body fat stores vs its reduction

50
Q

Humans with leptin deficiency have….

A

obesity

51
Q

Decrease leptin production from ____ ___ ____ has been demonstrated to contribute to….

A
  • white adipose tissue

- a plethora of metabolic abnormalities associated with visceral obesity

52
Q

Circulating levels of leptin are proportional to ___ ____.

A

fat mass

53
Q

Leptin decreases ___ ____ and ____ ____ and increases ____ ____.

A
  • food intake
  • body weight
  • EE
54
Q

What happens with leptin resistance?

A

Despite high circulating levels and the presence of functional receptors, the expected anorexigenic effects of leptin are significantly diminished

55
Q

Exogenous leptin administration to obese or lean humans have little effect on _____ ______.

A
  • energy homeostasis

- subjects are resistant to the effects of leptin on energy balance

56
Q

Exogenous leptin could potentially assist in either _____ the period of weight loss or ______ the amount of weight lost within a certain period of time, if given along with a ____ _____ ____ that might _____ the effects of negative energy balance and leptin responsiveness.

A
  • prolonging
  • increasing
  • leptin sensitizing agent
  • overcome
57
Q

Cholecystokinin is a ___ secreted by the ____ ____ (_____ and ____).

A
  • hormone
  • upper intestine
  • duodenum
  • jejunum
58
Q

Cholecystokinin is released in bloodstream ___ min. after eating onset and peaks at ___ min, remaining elevated until ___ h.

A
  • 10 min
  • 60 min
  • 7 h
59
Q

Local regulatory effects of cholecystokinin:

A

stimulation of gallbladder contraction and inhibition of gastric emptying

60
Q

Cholecystokinin is also widely distributed within the _____.

A
  • hypothalamus

- most abundant neuropeptide in the CNS

61
Q

CCK is the first gut hormone shown to influence ____ ___.

A

food intake

62
Q

GLP-1 stands for…

A

glucagon like peptide 1

63
Q

GLP-1 belongs to the ____ family, which are….

A
  • incretins

- gut peptides that are secreted after nutrient intake and stimulate insulin secretion

64
Q

GLP-1 is released _____ by the ____ ____ and ____ in proportion to ____ ____.

A
  • postprandially
  • small intestine
  • colon
  • ingested calories
65
Q

Main role of GLP-1:

A
  • stimulates insulin secretion

- inhibits glucagon release

66
Q

GLP-1 reduces ___ emptying + suppresses ____ ____ secretion.

A
  • gastric

- gastric acid

67
Q

GLP-1 increases ____ + decreases ____ ____ = decreased ____ ___.

A
  • satiation
  • food intake
  • body weight
68
Q

Describe GLP-1 levels in individuals with obesity.

A

reduced circulating levels

69
Q

GLP-1 analog =

A

liraglutide

70
Q

Liraglutide has been demonstrated as a …..

A
  • well tolerated body weight reducing pharmacological agent in humans
  • improve glycemic control
71
Q

Liraglutide adverse effects:

A
  • increased nausea and vomiting
  • increased HR
  • pancreatitis risk
72
Q

Liraglutide efficacy effects:

A
  • increased insulin biosynthesis
  • increased beta cell proliferation
  • decrease beta cell apoptosis
  • increase neuroprotection
  • decrease appetite
  • decrease gastric emptying
  • increase insulin sensitivity
  • decrease glucose production
73
Q

PYY stands for…

A

peptide YY

74
Q

PYY is released into the circulation ____ a meal and is reduced by ____.

A
  • after

- fasting

75
Q

PYY is released by the ____ ____.

A
  • lower intestine
  • distal intestine
  • colon
  • rectum
76
Q

PYY appears in blood ___ min after meal onset, peaks at ____ min, high blood levels until ____ min.

A
  • 15
  • 90
  • 180
77
Q

PYY binds to areas of the ____ and ____.

A
  • hypothalamus

- brainstem

78
Q

PYY reduces ____ and ____ ____.

A
  • appetite

- food intake

79
Q

Describe circulating levels of PYY in obese people.

A

not raised

80
Q

Humans with obesity show ____ sensitivity to the anorectic effects of PYY.

A

normal

81
Q

Ghrelin is a ____ hormone released into circulation from the _____.

A
  • peptide

- stomach

82
Q

Circulating levels of ghrelin are ____ by fasting and ____ after a meal.

A
  • increased

- fall

83
Q

Ghrelin binds to the growth hormone _____ _____, which is highly expressed in the ____ and ___ ____.

A
  • secretagogue receptor
  • hypothalamus
  • brain stem
84
Q

Ghrelin stimulates ____, functions as a meal _____.

A
  • appetite

- initiator

85
Q

Ghrelin governs feelings of ____ and is called the ____ hormone

A

hunger

86
Q

Ghrelin is the only known factor to ____ appetite through the _____.

A
  • increase

- circulation

87
Q

Ghrelin decreases ____ (meal ______) and has no effect on ____ ( meal ___).

A
  • satiety
  • frequency
  • satiation
  • size
88
Q

Ghrelin also decreases fat _____ and increases fat ____ in adipose tissue.

A
  • oxidation

- storage

89
Q

In obese subjects, fasting ghrelin levels have been shown to be ____ compared with normal weight controls.

A

lower

90
Q

Ghrelin levels ____ following diet-induced weight loss.

A

rise

91
Q

The typically expected _____ fall in circulating ghrelin levels is _____ in the obese.

A
  • prandial

- attenuated (or even absent)

92
Q

Print page 45

A

-

93
Q

3 components of regulation of energy metabolism:

A
  • glucose, hormones, neural transmitters, vagal nerves
  • substrate oxidation
  • SNS
94
Q

SNS activity in energy homeostasis is ___ and heavily _____ network with several ____ areas.

A
  • dense
  • interconnected
  • brain
95
Q

SNS has effects on ____ organs such as the ____ and the _____ tissue: affecting fuel _____ and _____.

A
  • endocrine
  • pancreas
  • adipose
  • partitioning
  • mobilization
96
Q

Adipose tissue receives SNS innervation from the CNS that:

A
  • increases adipocytes lipolysis

- inhibits fat cell proliferation

97
Q

SNS activation induces ____ –> increased ______ work or increased ______.

A
  • TEE
  • cardiorespiratory
  • thermogenesis
98
Q

Obesity causes a _____ and ____ increase in sympathetic activity rather than _____ SNS activation.

A
  • selective
  • differentiated
  • generalized
99
Q

Sympathetic overactivity characterizing obesity has deleterious _____ consequences (eg. development of _____), but it is not effective in increasing ____ ____ and favouring ___ ____ as expected.

A
  • cardiovascular
  • hypertension
  • EE
  • weight loss
100
Q

Possible reason why SNS activity is increased in response to weight gain:

A

adaptive mechanism to increase resting EE and promote restoration of the antecedent weigh

101
Q

Weight loss is able to reverse ____ and ____ _____ associated with obesity.

A
  • metabolic

- SNS alterations

KIN 334 (14 decks)

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