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PSYC 211 > Lecture 15: Hunger and Thirst > Flashcards

Lecture 15: Hunger and Thirst Flashcards

1
Q

homeostasis

A

Process by which the body’s substances and characteristics (such as temperature and glucose level) are maintained at their optimal level

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2
Q

ingestive behaviour

A

Eating or drinking

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3
Q

system variable

A

Variable that is controlled by regulatory mechanisms

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4
Q

corectional mechanism

A

in the regulatory process, a mechanism that is capable of changing the value of system variable

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5
Q

negative feedback

A

Process whereby the effect produced by a correctional mechanism serves to diminish or terminate the corrective action

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6
Q

satiety mechanism

A

Brain mechanism that causes cessation of hunger or thirst, produced by adequate and available supplies of nutrients or water

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7
Q

drinking steps

A

Body loses water
Detectors signal a loss of water
Correctional mechanism (drinking)
The stomach fills with water, sending signals to the brain
The satiety mechanism inhibits further drinking

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8
Q

where is water lcoated in the body?

A

67% intracellular fluid
26% interstitial fluid
7% intravascular fluid (blood plasma)
Less than 1% cerebrospinal fluid

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9
Q

two types of thirst

A

volumetric & osmometric

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10
Q

volumetric thirst

A

Occurs when there is not enough blood circulating in the body

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11
Q

how is blood flow monitored

A

by the kidneys. Low blood flow causes the kidneys to release renin, which triggers a hormone-signalling cascade that promotes thirst, among other things.

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12
Q

what causes the feeling of thirst?

A

the activation of hypothalamic neurons near the anteroventral tip of the third ventricle (the AV3V region), where the blood-brain barrier is weak

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13
Q

tonicity

A

the relative concentration of dissolved solutes (e.g., salt) on either side of a membrane that is permeable to water.

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14
Q

isotonic solution

A

similar solute concentrations are present inside and outside the cell. The cell will neither gain nor lose water

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15
Q

hypotonic solution

A

solute is less concentrated outside the cell than in, so water will enter the cell

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16
Q

hypertonic solution

A

solute is more concentrated outside the cell than in, so water will leave the cell

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17
Q

effect of hypertonic solutions on the cell

A

causes cellular dehydration (water leaves the cell)

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18
Q

osmoreceptors

A

neurons that detect changes in cell size, which corresponds to interstitial solute concentration

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19
Q

what happens when humans ingest hypertonic solutions

A

strongly activate neurons in both the AV3V region and the anterior cingulate cortex

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20
Q

what happens when humans drink water?

A

immediately quenches thirst and reduces thirst-related activity in the anterior cingulate

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21
Q

effect of cold sensors on thirst

A

Cold sensors in the mouth and sensory fibres in the stomach are part of the rapid satiety feedback mechanism

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22
Q

3 main components of food

A

Sugars (carbohydrates)
Lipids (triglycerides)
Amino acids (proteins)

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23
Q

what happens when blood glucose levels are high?

A

the pancreas releases insulin. This causes liver and muscle cells to store glucose as glycogen

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24
Q

what happens when blood glucose levels are low?

A

the pancreas releases glucagon. This causes liver and muscle cells to convert glycogen back into glucose

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25
Q

how do cells internalize glucose?

A

with a glucose transporter

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26
Q

glucose transporters outside the brain

A

require insulin to be functional

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27
Q

when do cells outside the brain use glucose?

A

when there is an excess (signalled by insulin)

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28
Q

how do cells produce energy when there is no glucose?

A

they must break down fatty acids to create the glucose they need for energy

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29
Q

how do cells in the brain produce energy when there is no glucose?

A

Cells within the brain have an additional glucose transporter that works in the absence of insulin, so brain cells can always internalize sugar

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30
Q

what happens to the pancreas when there is a decrease in glucose?

A

it stops secreting insulin and starts secreting glucagon

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31
Q

what happens when there is an absence of glucose

A

most cells can no longer use glucose

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32
Q

where is glucose in the blood sent

A

the CNS

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33
Q

glycogen

A

Polysaccharide often referred to as animal starch
Stored in the liver and muscle
Constitutes the short-term storage of nutrients

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34
Q

insulin

A

Pancreatic hormone that facilitates 1) conversion of glucose into glycogen, 2) entry of glucose and amino acids into cells of the body, and 3) transport of fats into adipose tissue

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35
Q

glucagon

A

Pancreatic hormone that promotes 1) conversion of liver glycogen into glucose, and 2) conversion of adipose triglycerides into fatty acids.

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36
Q

what is the result of glucagon signalling

A

promotes the breakdown of trigylcerides into fatty acids

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37
Q

triglyceride

A

Form of fat storage in adipose cells (fat cells). Constitutes the long-term storage of nutrients
Consists of a molecule of glycerol joined with three fatty acids

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38
Q

glycerol

A

Substance (also called glycerine) derived from the breakdown of triglycerides, along with fatty acids
Can be converted by liver into glucose

39
Q

fatty acids

A

Substance derived from the breakdown of triglycerides, along with glycerol
Can be metabolized into sugars by most cells of the body except for the brain

40
Q

how does an empty stomach communicate with the brain

A

the stomach’s release of a peptide hormone called ghrelin

41
Q

ghrelin

A

Peptide hormone released by an empty stomach that increases eating
Also produced by neurons in the brain

42
Q

duodenum

A

First portion of the small intestine, attached directly to the stomach. The presence or absence of food in the duodenum regulates the release of ghrelin from the stomach

43
Q

gastric factors

A

short-term satiety (fullness) signals are released by the stomach and duodenum immediately after eating before food is digested

44
Q

most common gastric factors

A

CCK, PYY, and GLP-1, which are secreted by the duodenum in response to food ingestion in proportion to calories ingested

45
Q

what is the result of repeated administration of CCK and PYY

A

decrease in meal size but increase in meal frequency

46
Q

what is the result of GLP-1 agonists

A

reduce hunger and weight

47
Q

initial satiety produced is ___

A

anticipatory

48
Q

how is initial satiety produced

A

the liver and the pancreas, as they detect when food has been absorbed into the blood

49
Q

liver function digestion

A

measures glucose and fatty acid levels in the blood

50
Q

how does the liver signal satiety?

A

through the 10th cranial nerve (the vagus nerve)

51
Q

pancreas function digestion

A

releases insulin as a satiety signal and measures blood-glucose levels

52
Q

effect of insulin

A

detection of insulin by neurons in the hypothalamus reduces feelings of hunger

53
Q

effect of force-feeding

A

people reduce food intake once permitted to choose how much to eat

54
Q

leptin

A

A circulating hormone that is secreted by adipocytes (fat cells). Thought to signal the size of peripheral energy stores in the body

55
Q

effect of fat cells on leptin

A

As fat cells grow and proliferate, there is an increase in leptin levels in the bloodstream

56
Q

effect of leptin injections

A

decreases meal size but doesn’t help weight control. but helps people with leptin deficiency

57
Q

Glucoprivation (hypoglycemia)

A

Dramatic fall in the amount of glucose available to cells (detected in the liver and brainstem)

58
Q

hypoglycemia cause

A

Can be caused by a lack of sugar, excess insulin signalling, or by drugs that inhibit glucose metabolism

59
Q

lipoprivation

A

Dramatic fall in the level of fatty acids available to cells (detected in the liver and brain)

60
Q

lipoprivation cause

A

Usually caused by drugs that inhibit fatty acid metabolism, but it can also relate to too little body fat

61
Q

what happens when the brain detects hypoglycemia

A

it launches an emergency cascade of effects via glucose-sensing neurons in various regions of the brain. these include 1) insulin suppresion 2) glucose production 3) decrease energy expenditure 4) promotes feeling of hunger

62
Q

what condition can be triggered by excess insulin?

A

hypoglycemia because it causes glucose to be stored in muscle tissue and as fat in adipose cells

63
Q

liproprivation

A

When the brain senses low leptin levels, it believes the body has no fat to support the energy homeostasis system. results in feelings of hunger

64
Q

what happens when the brain senses low leptin levels?

A

it believes the body has no fat to support the energy homeostasis system, so it launches an emergency cascade of effects via glucose-sensing neurons in various regions of the brain. these include 1) insulin suppresion 2) glucose production 3) decrease energy expenditure 4) promotes feeling of hunger

65
Q

effect of leptin signalling on food intake

A

decreases food intake

66
Q

effect of leptin signalling in the arcuate nucleus of the hypothalamus

A

inhibits AGRP/NPY neurons and activates POMC/ ɑ-MSH neurons, which both strongly regulate hunger

67
Q

hyperglycemia

A

high blood sugar

68
Q

what causes hyperglycemia

A

disruptions in insulin signalling because sugar is not being converted into glycogen or fat

69
Q

effect of hyperglycemia on the body

A

ongoing weight loss & intense hunger

70
Q

AGRP/NPY neurons

A

promote hunger. they are inhibited by leptin and activated by ghrelin

71
Q

POMC/ ɑ-MSH neurons

A

inhibit hunger. They are activated by leptin and inhibited by ghrelin

72
Q

The arcuate nucleus of the hypothalamus

A

Nucleus in the base of the hypothalamus that contains neurons highly sensitive to circulating levels of leptin

73
Q

what types of neurons are found in the arcuate nucleus of the hypothalamus

A

AGRP/NPY neurons and POMC/α-MSH neurons, which are involved in feeding and metabolic rate

74
Q

The paraventricular nucleus (PVN) of the hypothalamus

A

Nucleus of the hypothalamus that receives inputs from the arcuate nucleus.

75
Q

what types of neurons are found in the PVN

A

oxytocin neurons that signal that body has adequate levels of leptin (fat)

76
Q

what happens when PVN neurons have a low firing rate

A

animals will feel intense hunger

77
Q

prader-willi syndrome

A

A rare chromosomal abnormality in which up to 7 genes are deleted from chromosome 15

78
Q

effects of prader-willi syndrome

A

People with this syndrome are born with very low muscle mass and have little interest in eating. But, between 2-8 years old, they develop a sense of starvation and eat until they rupture their stomach

79
Q

leptin resistance and obesity

A

leptin resistance is a possible cause of obesity, in some populations of obese people, there is a reduction of leptin’s ability to cross the BBB, a reduction in the neuronal response to leptin signalling, and a reduction in the downstream consequence of leptin-signalling neurons

80
Q

hedonic aspects of hunger

A

The motivational and reinforcing properties of food which fluctuate in accordance with hunger and available energy

81
Q

how are hedonic aspects of hunger regulated?

A

Hypothalamic neurons are thought to orchestrate these effects by releasing specific neuropeptides throughout the brain

82
Q

function of volumetric thirst

A

Keeps track of extracellular fluid volume (volume of fluid in the blood)

83
Q

where does water move in a cell

A

where the cell is the most concentrated

84
Q

osmometric thirst

A

keeps track of intracellular fluid volume. Induced by the increase in solute outside the cell

85
Q

effect of hypotonic solutions on red blood cells

A

results in a swollen red blood cell

86
Q

effect of hypertonic solutions on red blood cells

A

Red blood cell shrinks

87
Q

effect of pvn on hunger

A

Activity inhibits hunger

88
Q

satiety mechanism steps

A

Leptin -> stimulates the POMC/Alpha-MSH neurons in the arcuate nucleus of the hypothalamus -> stimulate oxytocin neurons in the paraventricular nucleus of the hypothalamus -> inhibits hunger

89
Q

hunger mechanism steps

A

Ghrelin -> stimulates ARGP/NPY Neurons in the arcuate nucleus of the hypothalamus -> inhibit oxytocin neurons in the paraventricular nucleus of the hypothalamus -> signals hunger

90
Q

what happens when there are high blood glucose levels?

A

pancreas releases insulin => glucose is transformed and stored as glycogen => glucose can be used by CNS and outside CNS cells

91
Q

what happens when there are low blood glucose levels?

A

pancreas release glucagon => glycogen is transformed into glucose => glucose is used by CNS only

92
Q

glucagon signalling

A

promotes the breakdown of triglycerides into fatty acids

93
Q

where is fat stored when you eat?

A

in adipose tissues in the shape of triglycerides + fatty acids are transformed into triglycerides by glucagon

PSYC 211 (23 decks)

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