Regulation of Energy Metabolism Flashcards
(101 cards)
1
Q
Homeostasis:
A
tendency of an organism to maintain a stable internal state
2
Q
Most people maintain a ____ body weight over time.
A
stable
3
Q
Body weight regulation is directly related to….
A
energy balance
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
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
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
7
Q
The ____ of food consumed plays a major role in the amount of energy ____ and _____ each day.
A
- type
- consumed
- expended
8
Q
Under normal circumstances, _____, ______, and _____ are not easily converted to body fat.
A
- carbohydrate
- protein
- alcohol
9
Q
Oxidative hierarchy that governs the relative _____ in which fuels are selected for ____ ____ after their ingestion.
A
- order
- oxidative disposal
10
Q
Stores of alcohol:
A
none
11
Q
Stores of CHO:
A
glycogen
12
Q
Stores of protein:
A
body protein
13
Q
Stores of fat:
A
adipose tissue
14
Q
In healthy individuals, the fate of ingested alcohol is _____.
A
oxidation
15
Q
Alcohol is a ____ that must be ____ + body has no ____ capacity for it
A
- toxin
- eliminated
- storage
16
Q
_____ alcohol balance is achieved.
A
perfect
17
Q
Alcohol suppresses the _____ of other macronutrients, particularly ____.
A
- oxidation
- fat
18
Q
A chronic imbalance between alcohol intake and oxidation cannot directly cause _____, although it may indirectly influence ____ _____.
A
- obesity
- fat balance
19
Q
Carbohydrate oxidation is strongly influenced by …..
A
carbohydrate intake
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
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
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
23
Q
On a _____ basis, protein balance is achieved.
A
day to day
24
Q
Protein imbalance cannot be implicated as a direct cause of ____, but protein ____ may affect ____ ____.
A
- obesity
- intake
- fat balance
25
Excess protein consumed contribute indirectly to ___ ____ by sparing ____ ____. However, excess dietary protein is not made directly into _____ and stored as ____.
- fat storage
- dietary fat
- triacylglycerol
- fat
26
Fat intake has no or very little influence on fat ____.
oxidation
27
The oxidation rate of fat is almost totally governed by.....
the presence or absence of other macronutrients
28
There is no auto regulatory linkage between fat ___ and fat ____... as fat intake _____, fat oxidation does not ____ ____.
- intake
- oxidation
- increases
- increase proportionally
29
In conditions of spontaneous overfeeding (energy intake is ____) .......
- excessive
| - the entire excess fat intake is stored as body fat
30
Energy intake, stores, oxidation of carbs:
- intake: 1000 kcal (1500 overfeeding)
- stores: 2000 kcal
- daily oxidation % stores: 50% (70% overfeeding)
31
Energy intake, stores, oxidation of protein:
- intake: 500 kcal (750 overfeeding)
- stores: 40,000 kcal
- daily oxidation % stores: 1.3% (1.9% overfeeding)
32
Energy intake, stores, oxidation of fat:
- intake: 1000 kcal (1500 overfeeding)
- stores: 125,000 kcal
- daily oxidation % stores: < 1%
33
The amount of total body fat exerts what type of effect on fat oxidation?
small, but significant
34
This promotion of fat oxidation at higher body fat levels may represent a mechanism for ...
attenuating the rate of weight gain in response to chronic overfeeding
35
Explain getting fat on a low fat diet?
if energy intake > EE, an individual can become obese on a low fat diet
36
Most fat storage probably comes from the direct deposition of dietary fat associated with the suppression of ___ ____ caused by.....
- fat oxidation
| - excess intakes of the other macronutrients accompanying the diet
37
Fat is the only nutrient capable of causing...
- a chronic imbalance between intake and oxidation
| - directly contributing to the increase in adipose tissue
38
The regulation of feeding, ___ ____ and ____, and body weight is a ______ process.
- feeding
- energy intake
- expenditure
- body weight
- homeostatic
39
____ and ____ signals communicate information about the current state of ____ ____ to key brain regions, including the ____ and _____.
- central
- peripheral
- energy balance
- hypothalamus
- brainstem
40
The hypothalamus and brainstem receive ____ and _____ signals from the ____ that encode information about the ___ ____ and ____.
- neural
- hormonal
- periphery
- nutritional state
- adiposity
41
Key component for regulation of energy homeostasis:
hypothalamus continuously monitors signals that reflect energy status and initiates appropriate behavioural and metabolic responses
42
Energy homeostasis must be considered as resulting from an _____ process involving ...
- integrative
| - all brain areas and peripheral actors
43
Multiple _____, _____, _____ and ____ ____ were found to exert an action on energy homeostasis through their effects on energy intake and/or EE.
- substrates
- hormones
- neurotransmitters
- brain neurons
44
Most studied afferent modulators:
- adipokine (leptin)
| - gut hormones (CCK, GLP-1, PYY, ghrelin)
45
Leptin is one of the core components of the ____ system that controls ___ ___ in mammals.
- physiological
| - body weight
46
Leptin is expressed and secreted by...
exclusively by white adipose tissue adipocytes
47
Leptin provides a signal to the ____ regarding..
- brain
| - the status of fat stores
48
Leptin protects the _____ from ,,,,
- organism
| - reductions in fat mass that could threaten reproductive capacity/fertility and/or survival
49
Leptin favours ....
the preservation of body fat stores vs its reduction
50
Humans with leptin deficiency have....
obesity
51
Decrease leptin production from ____ ___ ____ has been demonstrated to contribute to....
- white adipose tissue
| - a plethora of metabolic abnormalities associated with visceral obesity
52
Circulating levels of leptin are proportional to ___ ____.
fat mass
53
Leptin decreases ___ ____ and ____ ____ and increases ____ ____.
- food intake
- body weight
- EE
54
What happens with leptin resistance?
Despite high circulating levels and the presence of functional receptors, the expected anorexigenic effects of leptin are significantly diminished
55
Exogenous leptin administration to obese or lean humans have little effect on _____ ______.
- energy homeostasis
| - subjects are resistant to the effects of leptin on energy balance
56
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.
- prolonging
- increasing
- leptin sensitizing agent
- overcome
57
Cholecystokinin is a ___ secreted by the ____ ____ (_____ and ____).
- hormone
- upper intestine
- duodenum
- jejunum
58
Cholecystokinin is released in bloodstream ___ min. after eating onset and peaks at ___ min, remaining elevated until ___ h.
- 10 min
- 60 min
- 7 h
59
Local regulatory effects of cholecystokinin:
stimulation of gallbladder contraction and inhibition of gastric emptying
60
Cholecystokinin is also widely distributed within the _____.
- hypothalamus
| - most abundant neuropeptide in the CNS
61
CCK is the first gut hormone shown to influence ____ ___.
food intake
62
GLP-1 stands for...
glucagon like peptide 1
63
GLP-1 belongs to the ____ family, which are....
- incretins
| - gut peptides that are secreted after nutrient intake and stimulate insulin secretion
64
GLP-1 is released _____ by the ____ ____ and ____ in proportion to ____ ____.
- postprandially
- small intestine
- colon
- ingested calories
65
Main role of GLP-1:
- stimulates insulin secretion
| - inhibits glucagon release
66
GLP-1 reduces ___ emptying + suppresses ____ ____ secretion.
- gastric
| - gastric acid
67
GLP-1 increases ____ + decreases ____ ____ = decreased ____ ___.
- satiation
- food intake
- body weight
68
Describe GLP-1 levels in individuals with obesity.
reduced circulating levels
69
GLP-1 analog =
liraglutide
70
Liraglutide has been demonstrated as a .....
- well tolerated body weight reducing pharmacological agent in humans
- improve glycemic control
71
Liraglutide adverse effects:
- increased nausea and vomiting
- increased HR
- pancreatitis risk
72
Liraglutide efficacy effects:
- 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
PYY stands for...
peptide YY
74
PYY is released into the circulation ____ a meal and is reduced by ____.
- after
| - fasting
75
PYY is released by the ____ ____.
- lower intestine
- distal intestine
- colon
- rectum
76
PYY appears in blood ___ min after meal onset, peaks at ____ min, high blood levels until ____ min.
- 15
- 90
- 180
77
PYY binds to areas of the ____ and ____.
- hypothalamus
| - brainstem
78
PYY reduces ____ and ____ ____.
- appetite
| - food intake
79
Describe circulating levels of PYY in obese people.
not raised
80
Humans with obesity show ____ sensitivity to the anorectic effects of PYY.
normal
81
Ghrelin is a ____ hormone released into circulation from the _____.
- peptide
| - stomach
82
Circulating levels of ghrelin are ____ by fasting and ____ after a meal.
- increased
| - fall
83
Ghrelin binds to the growth hormone _____ _____, which is highly expressed in the ____ and ___ ____.
- secretagogue receptor
- hypothalamus
- brain stem
84
Ghrelin stimulates ____, functions as a meal _____.
- appetite
| - initiator
85
Ghrelin governs feelings of ____ and is called the ____ hormone
hunger
86
Ghrelin is the only known factor to ____ appetite through the _____.
- increase
| - circulation
87
Ghrelin decreases ____ (meal ______) and has no effect on ____ ( meal ___).
- satiety
- frequency
- satiation
- size
88
Ghrelin also decreases fat _____ and increases fat ____ in adipose tissue.
- oxidation
| - storage
89
In obese subjects, fasting ghrelin levels have been shown to be ____ compared with normal weight controls.
lower
90
Ghrelin levels ____ following diet-induced weight loss.
rise
91
The typically expected _____ fall in circulating ghrelin levels is _____ in the obese.
- prandial
| - attenuated (or even absent)
92
Print page 45
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93
3 components of regulation of energy metabolism:
- glucose, hormones, neural transmitters, vagal nerves
- substrate oxidation
- SNS
94
SNS activity in energy homeostasis is ___ and heavily _____ network with several ____ areas.
- dense
- interconnected
- brain
95
SNS has effects on ____ organs such as the ____ and the _____ tissue: affecting fuel _____ and _____.
- endocrine
- pancreas
- adipose
- partitioning
- mobilization
96
Adipose tissue receives SNS innervation from the CNS that:
- increases adipocytes lipolysis
| - inhibits fat cell proliferation
97
SNS activation induces ____ --> increased ______ work or increased ______.
- TEE
- cardiorespiratory
- thermogenesis
98
Obesity causes a _____ and ____ increase in sympathetic activity rather than _____ SNS activation.
- selective
- differentiated
- generalized
99
Sympathetic overactivity characterizing obesity has deleterious _____ consequences (eg. development of _____), but it is not effective in increasing ____ ____ and favouring ___ ____ as expected.
- cardiovascular
- hypertension
- EE
- weight loss
100
Possible reason why SNS activity is increased in response to weight gain:
adaptive mechanism to increase resting EE and promote restoration of the antecedent weigh
101
Weight loss is able to reverse ____ and ____ _____ associated with obesity.
- metabolic
| - SNS alterations
