Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neurobiology of Eating > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Why do we eat?

A
  • to replenish energy
  • food also provides micronutrients, vitamins, and minerals which are essential building blocks for cellular structure and function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does energy expenditure occur?

A

cellular metabolism and physical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

When is body weight stable?

A

if the balance between energy (food) intake and energy expenditure is constant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do we maintain a stable body weight?

A

A regulatory mechanism that controls energy homeostasis (eating and body weight) needs to monitor and adjust food intake and energy expenditure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is homeostasis?

A
  • A stable internal state/maintaining a stable internal state
  • Means to keep something consistent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Who coined homeostasis?

A

Walter Bradford Cannon (physiologist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does “maintaining homeostasis” imply?

A

there must be a sort of mechanism to maintain homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is an example of a Homeostatic Regulatory Mechanism?

A

A thermostat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is negative feedback?

A

a process whereby the effect produced by an action serves to diminish or terminate the action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is eating regulated?

A

through negative feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are Components of the Homeostatic Regulatory Mechanism?

A
  • System variable
  • Set point
  • Detector
  • error correction mechanism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How have mammals evolved in relation to eating?

A

Mammals have evolved to be prevented from starving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does the process of energy homeostasis do in the body?

A

maintains a stable body weight (body fat)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the goal of eating for an organism?

A

eats to maintain a balance between used and stored energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Explain how a thermostat is a homeostatic regulatory mechanism.

A

System variable: air temp
Set point: 70 degrees
Detector: thermostat
Error correction mechanism: heat production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is an indicatior to the brain of the body state?

A
  • fat
  • it is a physiological signal
  • very important for survival
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where is the thermostat (regulatory mechanism) for body weight?

A
  • The brain! it is the detector and the correctional mechanism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Name two adiposity signals.

A

Insulin and leptin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is energy expenditure controlled?

A

Physiological signs from the body and the brain are directly related to metabolic control and maintenance of energy balance, and these determine energy expenditure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What mechanisms impact how humans actually eat?

A

anticipatory mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

WHat are anticipatory mechanisms?

A
  • We don’t want to wait till we are starving to eat

- Anticipatory mechanisms have a role in starting and stopping eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Explain the role of anticipatory mechanisms in starting eating

A
  • meals are intiated without physiological deficits
  • we eat in anticipation of future deficits
  • there are cues that predict food
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Explain the role of anticipatory mechanisms in ending eating.

A
  • Satiety mechanisms stop eating before weight is gained in anticipation of imminent replenishment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Could stability/homeostasis be achieved without a regulatory mechanism?

A

Yes if intake and outtake are exacly the same

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does levisky argue we have to achieve stability?

A
  • Believes there is a settling point/settling range instead of a set point
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is an example of a settling point/range?

A
  • sea level

- rainfall and melting ice caps vs evaporation and polar ice cap freesing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the two ways homeostasis can be achieved?

A

1) A regulatory mechanism - an active process (thermostat)
2) Settling of opposing forces - a sum of at least two independent processes
(setting a heater and a thermostat, sea level example)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What two factors primarily predetermine body weight?

A

Environment and genetic predisposition creates a range of where our body weight would be

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Is eating a good regulatory mechanism?

A

Eating is not a good homeostatic mechanism because small changes don’t cause a change in body weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What does Levitsky argue about homeostasis?

A
  • emphasizes that there is no system that regulates eating behavior
  • He is manipulating eating and he does not see a specific response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What did the Levitsky paper conclude in general? (about overfeeding?)

A
  • The studies in this review in general show that subjects increase eating for various reasons, non-homeostatic reasons
  • And they do not adjust accurately (or at all) eating to compensate for prior under/overeating
  • However, data in regard to overfeeding show changes in body weight that suggest homeostatic metabolic rate changes in response to extra energy gained
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are some of the reasons people increased their eating in the Levitsky paper?

A
  • higher calorie dense food
  • portion size
  • number of people
  • “confederate”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is a person who is part of the study but is controlled?

A

a confederate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What occurs with massive weight loss?

A
  • Metabolic slowing with massive weight loss despite preservation of fat-free mass
  • If someone suddenly loses a lot of weight there is a pushback from the body to stop weight loss (metabolic slowing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What did the biggest loser study indicate?

A
  • Only way to maintain weight loss is to exercise – exercise may prevent the metabolic slowing
  • Liver damage from sugar can be prevented by exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Where do we get energy from (general)?

A

Intake and energy stores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the two types of energy stores?

A

short-term and long term

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Where are the short term energy stores and what type of energy is stored?

A
  • liver and muscles - carbohydrates and glycogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Where are the long term energy stores?

A
  • fat (adipose tissue)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Why is it helpful to have short term and long term energy stores?

A
  • Helpful to have short term to have a burst of energy

- Long term for emergencies if you cant find food for a while

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Why must glucose be in a particular (narrow) range?

A
  • Need to avoid hyper-glycemia and hypo-glycemia

- Also must ensure sufficient supply to the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What molecules are controlled by the presence/absense of glucose in the blood?

A

Hormones: insulin and glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What happens when glucose is high?

A

Glucose binds to receptors on the pancreas cells and stimulates them to release insulin -> then insulin allows cells to store extra and allows cells to use it and store some of it as glycogen (sort of like a negative feedback)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the structure of insulin?

A

polypeptide with two peptide chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What happens when glucose is low?

A
  • Not binding glucose on particular cells is allows glucagon to be released
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What can all cells in the body use for energy?

A
  • fatty acids can be metabolized directly by all cells in the body
  • Liver stores glucose, but does not use glucose for energy, it oxidizes fatty acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What does the brain use for energy?

A

The brain needs a steady supply of glucose from the blood because it does not metabolize fatty acids (In extreme conditions it can metabolize ketones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How are the cells in the body prevented from using glucose?

A
  • Insulin controls entry of glucose into muscle, adipose and other tissues
  • Glucose is non-lipid soluble and cells need glucose transporters to carry glucose across the cell membrane
  • Glucose transporters are insulin responsive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What molecule activates glucose transporters?

A

insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What occurs when glucose and insulin are both sufficiently high?

A

When glucose and insulin are both sufficiently high, insulin enables most cells in the body to use glucose as energy, by mediating entry of glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What does low insulin signal to the body?

A

Low insulin is a signal that the body is depending on lipids for energy and glucose in the blood is reserved for the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe glucose transport in the brain.

A

glucose transport is not insulin mediated in the brain

53
Q

What are the physiological effects of insulin (carbohydrate metabolism)?

A
  • Insulin stimulates the liver to store glucose in the form of glycogen
  • Insulin controls entry of glucose into muscle, adipose, and other tissues
54
Q

How much glycogen can the liver store?

A

The liver could store glycogen to up to 5% of its mass

55
Q

When the liver is saturated with glycogen and other cells in the body are utilizing glucose what happens with excess glucose?

A

Additional glucose is transferred into pathways leading to synthesis of fatty acids

56
Q

What are the physiological effects of insulin? (lipid metabolism)

A
  • Stimulates accumulation of fat in adipose tissue
  • promotes synthesis of fatty acids
  • Inhibits breakdown of fat in adipose tissue
  • Facilitate entry of glucose into adipocytes
57
Q

What type of metabolism does insulin play a role in?

A
  • Insulin promotes anabolic metabolism

- Constructive part of metabolism

58
Q

What is catabolic metabolism?

A

degradative metabolism

59
Q

What is more of a homeostatic mechanism than body weight?

A

glucose levels

60
Q

When glucose and insulin start to decrease to maintain optimal/physiological levels of glucose in the blood….

A

Glucagon is released by the pancreas and converts glycogen into glucose

61
Q

What process is activated by glucagon?

A

gluconeogenesis - Glucose synthesis from non-carbohydrates

62
Q

What diseases are associated with physiological effects of insulin?

A

type 1 and type 2 diabetes (in general diabetes mellitus - insulin malfuctioning state)

63
Q

What is type 1 diabetes and what are treatments?

A
  • Type 1: Juvenile diabetes

- insulin injections, possible transplants of insulin producing cells

64
Q

What is type 2 diabetes and what are treatments?

A
  • Type 2: is a syndrome of insulin resistance – develops later in life
  • Insulin will not help, because the cells are already resistant
65
Q

What is occuring specifically physiologically for type 2 diabetes?

A
  • Cells are not responding to insulin properly, cells are not taking up glucose
  • Receptors are missing, insulin is not binding where it is supposed to be binding
66
Q

What is glucoprivation? What does it cause?

A
  • depriving cells of glucose
  • cause hypoglycemia; insulin injections cause this
  • Under normal physiological conditions this does not occur very often – if this happens metabolic hunger will be signalled, powerful hunger signal
  • When we have a drop in glucose
67
Q

What is lipoprivation?

A

depriving cells of lipids

68
Q

How does consumption of plain sugar impact glucose blood levels and insulin?

A
  • Plain sugar causes a higher peak in glucose blood levels and insulin
  • The drop after the peak after consumption of pure sugar causes cells to experience hypoglycemia
69
Q

What does plasma insulin concentration correlate with?

A

visceral fat

70
Q

What does insulin signal to?

A

homeostatic adiposity signal to the brain

71
Q

What are the two ways signals from the body can reach the brain?

A 
humoral pathways (via blood)
neuronal pathways
72
Q

What does insulin need to do to get to the brain?

A

cross the blood brain barrier

73
Q

Describe the structure of general capillaries.

A
  • have intercellular cleft passages (lots of holes in the capillaries) and things don’t have to be lipid soluble to pass through, but may pass through if they are lipid soluble
  • Endothelial cells in the capillaries are not tightly packed and form leaky junctions (garden hose with a bunch of holes)
74
Q

What are examples of beneficial and harmful things that can enter cells through general capillaries?

A
  • Beneficial: nutrients hormones

- Harmful: Toxins, viruses, and bacteria

75
Q

Describe the structure of brain capillaries.

A
  • in the brain the cells of capillaries are tightly packed

- The endothelial cells form tight junctions: this is known as the blood brain barrier

76
Q

What molecules can travel through the blood brain barrier?

A
  • Lipid soluble can travel though
  • Semi-permeable, only passage of small molecules (<500 daltons)
  • Other molecules need transporters to cross the BBB
77
Q

How does insulin reach the brain via the blood?

A
  • Insulin crosses the blood-brain barrier via receptor-mediated transport
  • Brain capillaries have insulin receptors
  • Insulin from the blood binds to its receptors on the endothelial cells, which internalize it, and release it to the brain rapidly with little to no degradation
78
Q

What two approaches can be used to test the function of insulin in the brain?

A
  • Inject insulin in the brain

- Create mouse lines without brain insulin receptors

79
Q

What is insulins overall effect in the body? The brain?

A
  • anabolic effect in the body

- adiposity signal to the brain

80
Q

What did insulin injections into the brain cause? What does this suggest about its function?

A
  • Decreased food intake
  • Decreased body weight
  • Increased energy expenditure
  • this suggests that it is a negative feedback signal in the homeostatic regulation of energy balance/BW
81
Q

What does the absense of insulin receptors in mice cause?

A

obesity

82
Q

What is the role of insulin in the brain?

A

to keep the higher limit of body weight in check

83
Q

How is insulin administered to the brain in humans?

A

intranasal is a semi-direct way to get to the brain

84
Q

Describe the result of insulin administration to the brain in humans.

A

Post-prandial: after a meal – insulin administration intensified satiety and reduced food intake

85
Q

What happened when insulin was injected for type 2 diabetes patients?

A

For Type 2: the receptors are desensitized, so injection of insulin to the brain would not suppress eating/appetite effectively

86
Q

Whar are the two strains of mice in the parabiosis study?

A
  • The ob/ob mice are a mutant strain caused by a mutation on the gene, obese (ob)
  • The db/db mice are a mutant strain caused by a mutation on the gene (db) diabetes
87
Q

What are the features/symptoms of ob/ob and db/db mice?

A

Low metabolism, overeating, morbid obesity, type 2 diabetes

88
Q

What is parabiosis?

A

surgical attachment of two animals with a shared blood supply

89
Q

What happened in the attachments in the parabiosis experiment?

A
  • OB + WT = OB mouse lost weight
  • DB + WT = diabetic mouse survived, but the wild type mouse died (WT Received signal that told it not to eat so it starved and died)
  • OB + DB = OB mouse lost weight -> suggests they received a signal that they were missing
90
Q

What did the parabiosis experiment suggest?

A
  • Db produces a satiety factor/signal in excessive amounts
  • Ob does not produce a satiety factor but has normal sensitivity to it since it responds to the satiety factor release by WT or DB
91
Q

What is leptin?

A
  • made by fat cells (adipocytes)
  • Gives the brain information about actual fat
  • The concentrations of leptin in subcutaneous WAT, and plasma correlate positively with WAT mass
  • The concentrations of leptin in plasma correlate positively with body fat
92
Q

What does the ob gene encode and what does the db gene encode?

A
  • Ob gene encodes a protein hormone (~16kDa) Leptin

- Db gene encodes Leptin-Receptor

93
Q

What is the only true effective treatment for type 2 diabetes?

A

gastric bypass surgery

94
Q

What did injecting leptin do to (+/+), (-,-), and (+,-) mice?

A

(+,+) and (+,-) no effect

(-,-) - BW decreased, food intake overall variable but consistently decreased

95
Q

In (+/+) (WT) mice adding leptin had no impact on body weight, yet when the DB and WT were attached the WT died suggesting that higher leptin caused death. Why?

A

DB mice had more than just leptin circulating and so other factors likely caused the WT to starve

96
Q

What is energy expenditure measured by?

A
  • Oxygen consumption and body temperature
97
Q

Describe metabolism of ob mice. Why is it like this?

A
  • In the OB mice the brain has no leptin, no leptin is produced
  • The Ob mice then signal to the brain that it is in starvation and the metabolic rate is decreased and the mice are cold, hypoactive
98
Q

Where is leptin acting?

A

body and brain, peripherally and centrally

99
Q

How does leptin cross the blood brain barrier?

A
  • via receptor mediated transport
100
Q

Describe the relationship between leptin and obesity.

A
  • Many obese people have proper Leptin release but cannot detect it properly
  • Central leptin receptors or BBB transport of leptin could be the cause in diet-induced obesity
101
Q

What occured when ob mice were administered leptin?

A
  • input (food intake decreased)
  • output (metabolic rate and physical activity increased)
  • and body weight (body weight decreased) were all impacted
102
Q

What occurred when db mice were administered leptin?

A

No change in food intake or BW - they lack leptin receptors

103
Q

What are two types of digestive system signals (gut peptides)?

A

Short term hunger signals and short term satiety signals

104
Q

Where are short term hunger and short term satiety signals produced?

A

the gut (gut peptides)

105
Q

What do short term hunger signals cause?

A

meal initiation (orexigenic)

106
Q

What do short term satiety signals cause?

A

meal termination (anorexigenic)

107
Q

What peptide is released from the gut when individuals are in the fasting phase?

A

ghrelin

108
Q

What is ghrelin?

A
  • Peptide hormone produced by the stomach
  • Binds to receptors in the hypothalamus to help stimulate eating behavior
  • Physiological meal initiator
  • Short term molecule
  • Also stimulates growth hormone secretion
109
Q

Describe blood levels of Ghrelin.

A

Blood levels of ghrelin would increase with fasting and be reduced after a meal

110
Q

What happens to ghrelin levels when rats are fasted and then fed water?

A
  • Ghrelin levels in the blood are slightly decreased, but then more and more is produced
  • It is a short-term molecule, but the rates remain high so this indicates that more and more ghrelin is produced
111
Q

What does acute and chronic ghrelin administration cause in rodents?

A
  • Acute ghrelin administration stimulates food intake

- Chronic Ghrelin administration causes weight gain and adiposity

112
Q

What happens to levels of leptin throughout the day?

A

increases slightly with meals and then are very high at night

113
Q

What is the criteria for an endogenous hunger signal?

A

1)The signal is generated prior to/at start of a meal
Increased during fasting
2)It acts within a single meal; short duration
Decreased by food (nutrients) not affected by water
3)Exogenous administration of Ghrelin should increase meal size, and be effective in physiological dose
4) Removing or antagonizing the endogenous factor should decrease meal size

114
Q

What are ObR mice vs neuronal ObR mice?

A
  • Neuronal ObR-/- mice, leptin/Ob receptors are knocked out in the brains specifically
  • In the ObR-/- All leptin receptors are knocked out
115
Q

What are the leptin levels of an underweight person?

A

If someone is underweight they overall release less leptin

116
Q

What occurred when IV ghrelin was administered to humans?

A

Intravenous Ghrelin : increase in energy consumed, analogue visual scales increased

117
Q

How was hunger compared between individuals in cases of IV ghrelin?

A

compared baseline hunger

118
Q

How was ghrelin isolated as a physiological meal initiator?

A

Plasma ghrelin levels and hunger score in humans initiating meals voluntarily without time- and food- related cues

119
Q

How does ghrelin initiate a meal?

A

Vagus nerve or via circulation/ across the BBB

120
Q

What are the two directions of communication with the brain?

A

Sensory input – anything to the brain

Motor output- output to the brain

121
Q

Describe the sensory input pathway.

A

Stomach and intestines signal to Nucleus of the Solitary Tract (NTS) (this is the first relay in the brain)

122
Q

Describe the motor output pathway.

A
  • Dorsal motor nucleus of the vagus nerve (DMX) signals to stomach from the brain
  • Vicera sensory is the sensation from the body
123
Q

How can you block peripherally administered ghrelin?

A

If a vagotomy (cut vagus nerve) or apply a neurotoxin (capsaicin) block action of peripherally administered Ghrelin

124
Q

What is capsacin?

A

Capsaicin is in spicy, food and it anesthetizes the stomach nerves – causes no communication of ghrelin

125
Q

What did Spiegel study on Bite Size, Ingestion Rate, and Meal size in Lean and obese women conclude?

A
  • Significant distance in ingestion rate with bigger bites, but no difference in the meal size with bigger bites
  • Lengthening the duration of meal did not produce satiety
126
Q

What triggers satiety?

A
  • Nutrients
  • Stomach and intestine have receptors that detect nutrients and there are GI peptides that are released in response to nutrients
127
Q

What is the most famous short term satiety signal?

A
  • Cholecystokinin (CCK)
128
Q

What is CCK?

A
  • Cholecystokinin

- GI peptide secreted from duodenal cells in response to nutrients

Neurobiology of Eating (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions