Hunger And Thirst Flashcards

(23 cards)

1
Q

What is Osmometric & Volumetric thirst?

A

Volumetric thirst
▪ Caused by low extracellular fluid volume
(hypovolemia – low blood flow).

▪ Signalled by renin (hormone released by kidney).

▪ Renin causes the release of Angiotensinogen
Angiotensin I and Angiotensin II

Osmometric thirst
▪ Keep track of intracellular fluid volume. Induced
by increase in solute outside cell.

▪ Signalled by osmoreceptors (detect changes in cell size)

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2
Q

How do we induce thirst and satiate thirst?

A

▪ Neurons in the AV3V region of the hypothalamus can be sensitive to angiotensin/osmoreceptors/both

▪ Drinking hypertonic saline (inducing thirst) => activate AV3V + anterior cingulate cortex

▪ Anterior cingulate cortex + cold sensors in mouth and stomach => rapid mechanism, responsible for the conscious sensation of thirst

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3
Q

What is our short term reservoir of energy?

A

Glucose
▪ Simple sugar
▪ Fuel for cells
▪ In Blood

High glucose level
➡️ use insulin to put glucose in storage

Glycogen
▪ Polysaccharide (chains of sugar)
▪ stored in liver and muscles
▪ short term storage of energy

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4
Q

What happens when you have a low glucose level?

A

increase glucose levels by turning the Glucagonin storage back to glucose!

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5
Q

Does the CNS use the same glucose as the rest of the body?

A

CNS+ cells outside CNS can use glucose:
-Cells outside the CNS can only use glucose transporter when insulin is present (meaning when there is excess glucose)

CNS only can use glucose
-When glucose is rare (there is no insulin), glucose goes in priority to the brain

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6
Q

What does the body do with High glucose level?

A

put glucose in storage
▪ Pancreas releases insulin
▪ Insulin transforms glucose into glycogen to be stored in liver and muscles
▪ The excess glucose can be used to both cells in the CNS and outside of the CNS

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7
Q

What does the body do with Low glucose level?

A

increase glucose levels
▪ Pancreas releases glucagon
▪ Glucagon transforms glycogen
into glucose
▪ Glucose can only be used by cells in the CNS

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8
Q

What happens to the fat you eat?

A

When you eat food
▪ Fat is stored in adipose tissues in the shape of triglycerides.
▪ Fatty acids are transformed into triglycerides by insulin

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9
Q

What happens when When digestive system is empty (low blood glucose level)?

A

Pancreas releases glucagon => glucagon breaks triglycerides into fatty acids => fatty acids are used by the cells outside the CNS

Livers breaks triglycerides into glycerol => glycerol is transformed into glucose => glucose is used by cells inside the CNS

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10
Q

What happens when food is in the digestive system

A

▪ High blood glucose = release of insulin by pancreas
▪ Glucose is stored as glycogen in the livers by insulin
▪ Fatty acids are stored in adipose tissue as triglycerides
▪ Glucose is used as a source of energy by the brain + cells outside CNS

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11
Q

What happens when empty digestive system?

A

Empty digestive system
▪ Low blood glucose = release of glucagon by pancreas
▪ Glycogen is transformed into glucose by glucagon and used as a source of energy by the brain
▪ Triglycerides are broken down into glycerol and fatty acids. Glycerol are transformed into glucose which is used by the brain only. Fatty Acids are used as a source of energy for cells outside the CNS

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12
Q

How does the empty Empty Duodenum (tummy) cause hunger? (Chemical)

A

Ghrelin

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13
Q

What does the Duodenum(tummy) do Post-Eating?

A

Cholecystokinin (CCK) GLP-1 to make you feel satisfied and full.

▪ CCK and PYY are anticipatory (happens after you eat, but before food is digested)
▪ Increasing CCK does not lead to weight loss -> will reduce meal length but people compensate by eating more often
▪ GLP-1 agonist can lead to weight loss

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14
Q

What happens when High blood-glucose level?

A

• Pancreas release insulin.
• Insulin crosses the blood/brain barrier
• Neurons in the hypothalamus detects it and
inhibits hunger

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15
Q

What happens when High levels of glucose and fatty acids?

A

liver signals satiety through the 10th cranial nerve (vagus nerve)

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16
Q

People tend to think animals have a set weight, why?

A

The body weight of most people and animals is regulated over a long-term basis
▪ If an animal is force-fed, it will reduce its food intake once it is permitted to choose how much to eat to go back to a set point
▪ This indicates the presence of a long-term satiety mechanism

17
Q

What does leptin do?

A

Decrease hunger

Increase sensitivity of hypothalamic neurons to
short term satiety signals

18
Q

What happens when Leptin Deficiency?

A

• Cannot produce leptin => body think it’s starving
• Leads to obesity
• Treated with Leptin injection

19
Q

What does Ghrelin do?

A

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

20
Q

What is Prader Willi Syndrome?

A

Loss of PVN Oxytocin neurons due to deletion of genes on chromosomes 15 => no sensation
of satiety
▪ Born without interest in eating, low muscle mass
▪ Between 2-8 years old: permanent sensation of starving to death
▪ Have no satiety signal to stop eating/throw up => eat until they rupture their stomach
• Average life expectancy = 30 yrs

21
Q

What is Hypoglycaemia

A

Lack of sugar, excess insulin, drugs that inhibit glucose metabolism ➡️ Low Glucose Level

22
Q

Hyperglycaemia

A

Caused by problem in insulin signalling
▪ Glucose is not taken from blood to fat cells/muscle
▪ Lead to a loss of fat -> decrease in leptin signalling -> intense
hunger (even if there is high glucose levels !)

High glucose but can’t use it!

23
Q

How does obesity happen using the previously discussed concepts?

A

▪ Elevated levels of fat
▪ Leptin resistance
▪ Reduction in leptin’s ability to cross the blood/brain barrier
▪ Reduction in neuronal response to leptin
▪ Reduction in the downstream consequences of leptin-signalling neuron
▪ Harder to feel satiated -> need more leptin (meaning more fat cells) to be satiated