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Human Body Systems II (BMSC 208) > Module 8: Digestive System III > Flashcards

Module 8: Digestive System III Flashcards

1
Q

How does the GI system regulate food intake?

A

It doesn’t. We rely on behavioral mechanisms.

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2
Q

The feeding state is characterizd by _____. What happens to absorbed nutrients in this state?

A

Characterized by anabolism, absorbed nutrients are converted into glycogen and triglycerides primarily.

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3
Q

The fasting state is characterised by _____. What happens to glycogen and triglycerides during this state?

A

Characterized by catabolism, glycogen and triglycerides are converted to glucose, fatty acids and ketones.

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4
Q

Neurons exclusively use _____ as a fuel source.

A

Glucose.

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5
Q

If intake = expenditure, what is the end result?

A

Normal.

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6
Q

If intake > expenditure, what is the end result?

A

Obesity.

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7
Q

If intake < expenditure, what is the end result?

A

Starvation.

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8
Q

What two structures of the brain used to the the model of the food intake centre? What were each of their roles? How has this view changed?

A
  1. Lateral hypothalamus: hunger center
  2. Ventromedial hypothalamus: satiety center

We now believe that we just cut the linkages in the satiety center, not the actual center.

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9
Q

What is the current model of the food intake centre? (1 structure hunger center, 3 structures satiety)

A

Lateral hypothalamus → hunger center

Arcuate nucleus (ARC), paraventricular nucleus (PVN), and nucleus tractus solitarii (NTS) → satiety center

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10
Q

What are two theories involved in the long term regulation of feeding behavior?

A

Glucostatic theory and lipostatic theory.

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11
Q

Define glucostatic theory. What is this phenomenon likely?

A

Glucose metabolism in the hypothalamus regulates food intake. Likely actually a short-term mechanism.

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12
Q

Define lipostatic theory. Where did evidence of this theory come from and what did it discover?

A

Signals from the body’s fat stores regulate food intake. Evidence came in the 1960’s with the identification of ob/ob (mutations in both copies of the ob gene) mice. This gene encodes a protein called leptin that tells the brain fat reserves are normal.

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13
Q

Leptin:

  1. Where is it released from?
  2. What does it do and how does it do this?
A
  1. Adipocytes (adipose tissue)
  2. Regulates body mass by acting directly on neurons of the hypothalamus that decrease appetite and increase energy expenditure.
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14
Q

Elevated leptin acts on which 2 neurons stimulating the release of what kind of peptide and causing what 2 things in the body?

A

Stimulation of aMSH/CART neurons cause the release of anorectic peptides which act on the arcuate nucleus causing:

  1. Inhibition of lateral feeding center
  2. Activation of PVN
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15
Q

Activation of the PVN causes what two responses? Describe the result of each.

A
  1. Humoral response: ↑TSH, ACTH from pituitary (increased metabolic rate throughout the body)
  2. Visceromotor response: Increased sympathetic output (↑ body temp)
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16
Q

Decreased leptin causes what 2 responses in the body?

A
  1. Reduced activation of a-MSH and CART neurons
    • Reduced activation of PVN (↓TSH and ACTH)
    • ↓ metabolic rate
    • Activation of parasympathetic output
  2. Activation of NPY and AgRP containing neurons
    • Stimulation of feeding center
    • Further inhibition PVN
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17
Q

Can leptin be used to treat obesity? Why or why not?

A

No. Likely a decreased sensitivity to leptin in obese individuals.

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18
Q

Short-term regulation of feeding behavior depends on what two factors?

A
  1. How long it has been since the last meal
  2. How much we consumed at that time
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19
Q

Short term regulation is a balance between which two signals?

A

It is a balance between satiety signals (don’t want food) that are generated during digestion and orexigenic signals (want food) that are generated during fasting.

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20
Q

The orexigenic and satiety signals are these 4 things, which compliment _____ term digestion.

A
  1. Ghrelin
  2. Gastric distension
  3. CCK
  4. Insulin/glucose concentration

Compliment long term digestion

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21
Q

What stimulates ghrelin release and how does it compliment long term digestion (what neurons does it stimulate)?

A

Released by ghrelinergic cells in the stomach in response to emptying. Stimulates NPY/AGRP containing neurons in the arcuate.

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22
Q

What will injection of ghrelin cause? Mice lacking which neurons will not respond to neurons?

A

Stimulate food intake. NPY/AgRP neurons.

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23
Q

How do gastric distension and CCK compliment long term digestion? When are both active and how are they sensed?

A

Administration inhibits meal frequency and size. Both act on the NTS to stimulate the feeling of satiety (signals via vagus nerve).

Gastric distension is sensed by mechanosensory neurons and this information is sent to the NTS which has connections to the PVN and ARC. CCK is released by I-cells in response to fats and amino acids entering the small intestine (drives bile and pancreatic enzyme secretion).

24
Q

How do insulin/glucose levels (drop and increase) compliment long term digestion?

A

During the cephalic and gastric phase increased insulin would cause a drop in blood glucose driving hunger through activation of NPY/AgRP neurons. During the intestinal phase the increased blood glucose and corresponding increase in insulin would act as a satiety signal through activation of aMSH/CART neurons in the arcuate nucleus.

25
Q

Insulin acts as both a _____ and _____ signal.

A

Satiety and orexigenic.

26
Q

Marijuana has been shown to give an increased sense of _____ in mice.

A

Smell.

27
Q

Marijuana has shown some evidence for indirect activation of _____ neurons in the _____ from CB1 receptors in the _____.

A

NPY/AgRP, ARC, lateral hypothalamus.

28
Q

We input energy 100% through our diet, and our output is divided about 50% _____ and 50% _____

A

Heat, work.

29
Q

Work in the sense of energy output refers to what 3 types?

A
  1. Transport across membranes
  2. Mechanical work (movement)
  3. Chemical work
    • Synthesis
    • Energy storage
      • High energy phosphate bonds
      • Chemical bonds
30
Q

How do we measure energy input? How is it off at times?

A

​Bomb calorimeter: heat released from burned food is measured

  • One kilocalorie is the amount of heat needed to raise the temperature of 1 L of water by 1oC

Slight over estimation because we do not completely digest and absorb most foods.

31
Q

What two methods do we use to measure energy output?

A
  1. Direct calorimetry
    • Most accurate, but more complicated
  2. Indirect calorimetry
    • Measures O2 consumption or CO2 production
    • More common, only requires a small device
32
Q

What is the basal metabolic rate (BMR)?

A

An individual’s lowest metabolic rate (just sitting and breathing).

33
Q

What 6 factors affect overall metabolic rate? Which is the most important? (HAG LAD)

A
  1. Age and sex (males have faster metabolism)
  2. Amount of lean muscle mass (increased LMM = increased BMR)
  3. Activity level: metabolic activity above BMR
  4. Diet, diet induced thermogenesis: energetic cost of food digestion and storage differs between different food components (greater cost for protein rather than fat)
  5. Hormones: thyroid hormones considered single most important determinant of BMR, influence oxygen consumption and heat production of most tissues in the body (increased carbohydrate and lipid metabolism)
  6. Genetics
34
Q

What is metabolism? What are the three purposes?

A

The sum of all metabolic reactions.

  1. Extract energy from nutrients
  2. Use energy for work (transport, mechanical, synthesis)
  3. Store excess energy for later use
35
Q

How does the fed state affect the skeletal muscles handling of glucose and amino acids?

A

Takes up large portion of glucose for energy usage and stores glucose as glycogen (70% of body storage). AA’s primarily taken up for natural protein turnover.

36
Q

How does the fed state affect the liver’s handling of glucose and amino acids?

A

Coverts glucose to glycogen (24% of body stores) or to fatty acids (transported to adipocytes). AAs used for synthesis and converted to keto acids (energy or fatty acid synthesis).

37
Q

How does the fed state affect the adipocytes’ handling of fats and glucose?

A

Take up dietary triglycerides from chylomicrons. Excess glucose taken up and converted to triglycerides. Store triglycerides synthesized in liver.

38
Q

_____ and _____ storage limited, _____ storage unlimited.

A

Glucose, protein, fat.

39
Q

How long do glycogen, protein and fat stores last?

A
  • Glycogen stores can sustain quiet activity for only a few hours
  • Proteins potentially for long periods of time but decreased protein levels eventually compromise cellular function
  • Fats for approximately two months
40
Q

How does the fasted state affect skeletal muscle’s handling of glycogen?

A

Can convert glycogen to glucose-6-P (glycogenolysis) for its own use. Form pyruvate and lactate.

41
Q

How does the fasted state affect liver’s handling of glycogen and fatty acids?

A

Glycogen can be converted to glucose (glycogenolysis) and transported throughout the body, producing new glucose from pyruvate, lactate, glycerol and certain amino acids (gluconeogenesis). Converts FA to ketone bodies for energy usage.

42
Q

How does the fasted state affect adipocytes’ handling of fats?

A

Lipolysis occurs, fatty acids and glycerol enter bloodstream to be used as energy in most cell

43
Q

Fed vs fasted state is primarily dependent on _____ concentration, which is balanced by _____ and _____ levels.

A

Glucose, insulin, glucagon.

44
Q

Fed State vs Fasted State:

Which molecule is primarily used for energy?

A

Fed: glucose

Fasted: fatty acids

45
Q

Fed State vs Fasted State:

Does glycogenesis or glycogenolysis occur?

A

Fed: glycogenesis

Fasted: glycogenolysis

46
Q

Fed State vs Fasted State:

Synthesis using which molecule is performed?

A

Fed: AA uptake and protein synthesis (muscle)

Fasted: gluconeogenesis

47
Q

Fed State vs Fasted State:

For which does ketogenesis occur?

A

Fasted.

48
Q

Fed State vs Fasted State:

Which does protein degradation primarily occur?

A

Fasted.

49
Q

In the fed state, which hormone is in primary control? What does this hormone promote (anabolism/catabolism)?

A

Insulin. Promotes anabolism.

50
Q

What are the 4 stimuli for insulin release?

A
  1. Increases in plasma glucose
  2. Amino acids
  3. GIP
  4. Parasympathetic activity
51
Q

Insulin is released by _____ cells. Describe this 5 step process.

A

Beta.

  1. High glucose causes the opening of GLUT receptors, allowing glucose into the cell
  2. Glucose is then converted to pyruvate and enters glycolysis
  3. Oxidative phosphorylation occurs releasing ATP into the cytosol
  4. ATP binds ATP-selective K+ channels, locking them which depolarizes the cell
  5. VG-Ca2+ channels trigger insulin release
52
Q

Describe insulin’s cellular mechanism of action.

A
53
Q

In the fasted state, which hormone is primary? What does it promote? What organ is it’s primary target?

A

Glucagon. It promotes catabolism, and it’s primary target is the liver.

54
Q

What 2 things stimulate glucagon release?

A
  1. Decreased plasma glucose
  2. Sympathetic activity
55
Q

Glucagon acts on the _____ receptor, triggering the _____ pathway that causes changes in enzymatic activity.

A

G-protein coupled receptor, adenylate cyclase pathway.

56
Q

Glucagon acts in almost total _____ to insulin.

A

Opposition.

57
Q

_____ stores most of the glycogen and proteins, while _____ stores most of the triglycerides

A

Skeletal muscle, adipose tissue

Human Body Systems II (BMSC 208) (11 decks)

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