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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
how do cells internalize glucose?
with a glucose transporter
26
glucose transporters outside the brain
require insulin to be functional
27
when do cells outside the brain use glucose?
when there is an excess (signalled by insulin)
28
how do cells produce energy when there is no glucose?
they must break down fatty acids to create the glucose they need for energy
29
how do cells in the brain produce energy when there is no glucose?
Cells within the brain have an additional glucose transporter that works in the absence of insulin, so brain cells can always internalize sugar
30
what happens to the pancreas when there is a decrease in glucose?
it stops secreting insulin and starts secreting glucagon
31
what happens when there is an absence of glucose
most cells can no longer use glucose
32
where is glucose in the blood sent
the CNS
33
glycogen
Polysaccharide often referred to as animal starch Stored in the liver and muscle Constitutes the short-term storage of nutrients
34
insulin
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
35
glucagon
Pancreatic hormone that promotes 1) conversion of liver glycogen into glucose, and 2) conversion of adipose triglycerides into fatty acids.
36
what is the result of glucagon signalling
promotes the breakdown of trigylcerides into fatty acids
37
triglyceride
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
38
glycerol
Substance (also called glycerine) derived from the breakdown of triglycerides, along with fatty acids Can be converted by liver into glucose
39
fatty acids
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
how does an empty stomach communicate with the brain
the stomach's release of a peptide hormone called ghrelin
41
ghrelin
Peptide hormone released by an empty stomach that increases eating Also produced by neurons in the brain
42
duodenum
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
gastric factors
short-term satiety (fullness) signals are released by the stomach and duodenum immediately after eating before food is digested
44
most common gastric factors
CCK, PYY, and GLP-1, which are secreted by the duodenum in response to food ingestion in proportion to calories ingested
45
what is the result of repeated administration of CCK and PYY
decrease in meal size but increase in meal frequency
46
what is the result of GLP-1 agonists
reduce hunger and weight
47
initial satiety produced is ___
anticipatory
48
how is initial satiety produced
the liver and the pancreas, as they detect when food has been absorbed into the blood
49
liver function digestion
measures glucose and fatty acid levels in the blood
50
how does the liver signal satiety?
through the 10th cranial nerve (the vagus nerve)
51
pancreas function digestion
releases insulin as a satiety signal and measures blood-glucose levels
52
effect of insulin
detection of insulin by neurons in the hypothalamus reduces feelings of hunger
53
effect of force-feeding
people reduce food intake once permitted to choose how much to eat
54
leptin
A circulating hormone that is secreted by adipocytes (fat cells). Thought to signal the size of peripheral energy stores in the body
55
effect of fat cells on leptin
As fat cells grow and proliferate, there is an increase in leptin levels in the bloodstream
56
effect of leptin injections
decreases meal size but doesn't help weight control. but helps people with leptin deficiency
57
Glucoprivation (hypoglycemia)
Dramatic fall in the amount of glucose available to cells (detected in the liver and brainstem)
58
hypoglycemia cause
Can be caused by a lack of sugar, excess insulin signalling, or by drugs that inhibit glucose metabolism
59
lipoprivation
Dramatic fall in the level of fatty acids available to cells (detected in the liver and brain)
60
lipoprivation cause
Usually caused by drugs that inhibit fatty acid metabolism, but it can also relate to too little body fat
61
what happens when the brain detects hypoglycemia
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
what condition can be triggered by excess insulin?
hypoglycemia because it causes glucose to be stored in muscle tissue and as fat in adipose cells
63
liproprivation
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
what happens when the brain senses low leptin levels?
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
effect of leptin signalling on food intake
decreases food intake
66
effect of leptin signalling in the arcuate nucleus of the hypothalamus
inhibits AGRP/NPY neurons and activates POMC/ ɑ-MSH neurons, which both strongly regulate hunger
67
hyperglycemia
high blood sugar
68
what causes hyperglycemia
disruptions in insulin signalling because sugar is not being converted into glycogen or fat
69
effect of hyperglycemia on the body
ongoing weight loss & intense hunger
70
AGRP/NPY neurons
promote hunger. they are inhibited by leptin and activated by ghrelin
71
POMC/ ɑ-MSH neurons
inhibit hunger. They are activated by leptin and inhibited by ghrelin
72
The arcuate nucleus of the hypothalamus
Nucleus in the base of the hypothalamus that contains neurons highly sensitive to circulating levels of leptin
73
what types of neurons are found in the arcuate nucleus of the hypothalamus
AGRP/NPY neurons and POMC/α-MSH neurons, which are involved in feeding and metabolic rate
74
The paraventricular nucleus (PVN) of the hypothalamus
Nucleus of the hypothalamus that receives inputs from the arcuate nucleus.
75
what types of neurons are found in the PVN
oxytocin neurons that signal that body has adequate levels of leptin (fat)
76
what happens when PVN neurons have a low firing rate
animals will feel intense hunger
77
prader-willi syndrome
A rare chromosomal abnormality in which up to 7 genes are deleted from chromosome 15
78
effects of prader-willi syndrome
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
leptin resistance and obesity
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
hedonic aspects of hunger
The motivational and reinforcing properties of food which fluctuate in accordance with hunger and available energy
81
how are hedonic aspects of hunger regulated?
Hypothalamic neurons are thought to orchestrate these effects by releasing specific neuropeptides throughout the brain
82
function of volumetric thirst
Keeps track of extracellular fluid volume (volume of fluid in the blood)
83
where does water move in a cell
where the cell is the most concentrated
84
osmometric thirst
keeps track of intracellular fluid volume. Induced by the increase in solute outside the cell
85
effect of hypotonic solutions on red blood cells
results in a swollen red blood cell
86
effect of hypertonic solutions on red blood cells
Red blood cell shrinks
87
effect of pvn on hunger
Activity inhibits hunger
88
satiety mechanism steps
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
hunger mechanism steps
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
what happens when there are high blood glucose levels?
pancreas releases insulin => glucose is transformed and stored as glycogen => glucose can be used by CNS and outside CNS cells
91
what happens when there are low blood glucose levels?
pancreas release glucagon => glycogen is transformed into glucose => glucose is used by CNS only
92
glucagon signalling
promotes the breakdown of triglycerides into fatty acids
93
where is fat stored when you eat?
in adipose tissues in the shape of triglycerides + fatty acids are transformed into triglycerides by glucagon

PSYC 211 (23 decks)

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