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HES Biochem > Lecture 11 - Integration of metabolism, state and regulation > Flashcards

Lecture 11 - Integration of metabolism, state and regulation Flashcards

1
Q

What 3 molecules are important key junctions in metabolism?

A

1) Glucose 6P
2) Pyruvate
3) Acetyl coA

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2
Q

List all the ways that G6P can be utilized (there are 4)

A

1) Enter glycolysis to produce pyruvate
2) Enter glycogenesis to make glycogen
3) Enter PPP to make ribose 5 P
4) Enter gluconeogenesis (make glucose)

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3
Q

List all the ways that pyruvate can be utilized (There are 4).

A

1) Made into acetyl coA via PDH
2) Made into glucose via gluconeogenesis (Pyruvate –> OAA –> PEP)
3) In anaerobic muscle, made into lactate, which is then shipped to liver and turned back into pyruvate to regenerate glucose via gluconeogenesis (cori cycle)
4) In muscle that is using its own protein for energy, made into alanine, which is then shipped to liver and turned back into pyruvate releasing NH3 (glucose alanine cycle)

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4
Q

List all the ways that acetyl coA can be utilized.

A

1) Enter CAC
2) Be used to make FAs
3) Be used to make Ketone bodies
4) Be used to make cholesterol
5) Be used to make ketogenic amino acids

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5
Q

One of the most important functions of the liver is to maintain blood glucose. What are all the ways that the liver does that?

A

1) Acts as glucose buffer - takes up and releases glucose into blood via GLUT2
2) Gluconeogenesis
3) Glycogenolysis

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6
Q

How does the liver utilize FAs?

A

Uses them for fuel via Beta oxidation

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7
Q

What organ absorbs the majority of dietary amino acids?

A

The liver, uses them for energy (if energy demand is high) or for protein synthesis (if demand is low)

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8
Q

What sources of fuel can the brain utilize?

A

Glucose

Ketone Bodies

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9
Q

What source of fuel can the muscle utilize?

A

Glucose, FAs, ketone bodies

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10
Q

For resting muscle, what is the major fuel source?

A

Fatty Acids

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11
Q

For moderately active muscle, what is the major fuel source?

A

Glucose from glycogen and FAs

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12
Q

For active muscle, what is the major fuel source?

A

Cori cycle –> pyruvate converted to lactate which is then turned back into glucose via gluconeogenesis

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13
Q

For short bursts of exercise (0-2 minutes) what is the source of energy used by muscle?

A

ATP + creatine phosphate

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14
Q

For longer bursts of exercise (2 - 6 minutes), what is the source of energy used by muscle?

A

Glycolysis of muscle glycogen

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15
Q

For longer bursts of exercise (6+ mins) what is the source of energy used by muscle?

A

Fatty acids from adipose tissue
Muscle glycogen
Plasma glucose
Liver glycogen

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16
Q

What is the main fuel source for the heart? What other sources of energy can it utilize?

A

Fatty acids

Ketone bodies, glucose, lactate, limited glycogen stores

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17
Q

What is an islet of langerhans?

A

Cluster of endocrine cells (alpha - glucagon, beta - insulin, delta - somatostatin)

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18
Q

What are the 2 priorities of the body during fasting?

A

1) provide sufficient glucose for brain and other tissues that are dependent on glucose for energy (RBCs)
2) Preserve proteins - accomplished by shifting fuels from glucose to FAs and ketone bodies

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19
Q

Starvation 0 - 4 hours

1) What is fuel source for all tissues?
2) Gluconeogenesis is active or not active?
3) What does the brain use for fuel?

A

1) Glucose
2) Not active
3) Glucose

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20
Q

Starvation 4 - 16 hours

1) What hormone is high?
2) Gluconeogenesis is active or not active?
3) What does the brain use for fuel?

A

1) Glucagon
2) Active
3) Glucose

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21
Q

Starvation 16 hours - 24 hours

1) What are the major sources of glucose?
2) What does the brain use for fuel?

A

1) Glycogen breakdown in liver and gluconeogenesis

2) Glucose

22
Q

Starvation 2 - 24 days

1) Gluconeogenesis is active or not active?
2) What does the brain use for fuel?

A

1) Active but begins to slow down and level off

2) Ketone bodies

23
Q

Starvation 24 - 40 days

1) Gluconeogenesis is active or not active?
2) Brain uses ___ for fuel

A

1) Active, but slow, occurring in liver and kidneys

2) Ketone bodies only

24
Q

How does the rate of protein degradation compare during the initial stages of starvation compared to later stages?

A

Initial degradation rate is higher, body works to conserve protein by switching to FAs and ketone body production after 3 days of starvation to preserve muscle.

25
Q

What happens to a person after ~40 days of fasting (actual # days depends on the person)

A

Their TAG stores are completely depleted, protein degradation increases and their organ function declines as they are degraded. Death ensues.

26
Q

What is AMPK?

What does it do?

A

AMP - dependent kinase

It regulates the expression and activity of proteins critical to the metabolism of lipid and carbohydrates

27
Q

How does AMPK act as a fuel sensor?

A

AMPK is responsive to AMP:ATP ratio. When ratio is high (i.e. [AMP] > [ATP]), AMP allosterically activates AMPK. This leads to phosphorylation and activation of AMPK which then phosphorylates other enzymes that turn off ATP consuming anabolic pathways and turn on ATP producing catabolic pathways.

28
Q

What is the effect of AMPK on the hypothalamus? (2)

A

1) Increases secretion of hormones that signal to increase food intake
2) Decrease energy expenditure

29
Q

What is the effect of AMPK on adipose tissue?

A

Decrease TAG breakdown into free FA

30
Q

What is the effect of AMPK on Muscle tissue?

A

Increased FA oxidation and increased glucose uptake

31
Q

What is the effect of APMK on liver tissue?

A

Decreased FA synthesis

Decreased gluconeogenesis

32
Q

What is PPAR?

What do they do?

A

Peroxisome Proliferator Activated Receptors

Nuclear receptor involved in transcriptional regulation of fat metabolism (lipid sensors)

33
Q

What is the mechanism of PPAR?

A

Ligand (FA and FA derivatives) cross plasma membrane. Ligand binds with PPAR in cytosol. RXR binds with PPAR + Ligand complex in cytosol. Whole complex enters nucleus where it binds to DNA and acts as transcription factor.

34
Q

What are the 3 kinds of PPAR and what do they do in general?

A

PPAR alpha (starvation response)

PPAR gamma (regulates adipogenesis)

PPAR delta (senses dietary lipids)

35
Q

Knowing that PPAR alpha regulates the starvation response, what effect will PPAR alpha have in the liver, muscle and adipose?

A

Liver: Increase FA oxidation, increase formation of ketone bodies

Muscle: increase FA oxidation

36
Q

Knowing that PPAR gamma regulates adipogenesis, what effect will PPAR gamma have on the liver, muscle and adipose tissue?

A

Liver: increase fat synthesis and storage

Muscle: increase insulin sensitivity

Adipose: increase FA uptake and storage, increase adipocyte differentiation an d survival

37
Q

Knowing that PPAR delta senses dietary lipids, what effect with PPAR delta have on the liver, muscle and adipose tissue?

A

Liver: no effect
Muscle: Increase FA oxidation
Adipose: Increase FA oxidation, Increase energy expenditure (thermogenesis)

38
Q

PPAR alpha and PPAR delta both have similar goals. What is different bout these 2 receptors?

A

PPAR alpha acts under starvation or fasting conditions, PPAR delta acts when fat stores are high.

PPAR alpha provides acetyl coA for energy and ketone bodies, PPAR delta controls the amount of stored fat and revs up thermogenesis.

39
Q

What is the relationship between BAT and thermogenesis?

A

BAT contains more uncoupling protein so it is a potent producer of thermogenesis. Also, as BAT mass increases, BMI decreases.

40
Q

What is the “set point” theory for body weight?

A

There is a control system built into every person dictating how much fat he or she should carry. BF% and BW are matters of internal controls that are set differently in different people.

41
Q

What is the purpose of the hypothalamus as it relates to body weight?

A

Serves as regulator of energy balance, releases hormones associated with feeding and hunger

42
Q

What are adipokines?

A

Peptide hormones produced by adipose tissue that carry information about energy reserves stored in adipose tissue and that produce changes in fuel metabolism and feeding behavior that reestablish adequate fuel reserves and maintain body mass

43
Q

Leptin

1) When is this released and by what tissue?
2) What organ does it act on? What effect does it produce?
3) What 2 things does leptin promote?

A

1) Released by adipose tissue in response to increased adipose mass
2) Acts on hypothalamus to suppress appetite
3) a) Decreased fuel intake, signals to brain to increase release of alpha MSH which is a neuronal signal to eat less and decrease release of NPY which is a neuronal signal to eat more
b) Promotes increased expenditure of energy

44
Q

ob/ob mice have been produced which are completely deficient in leptin. What behavior do these mice exhibit?

A

Always hungry, behave as if starved, will overeat when given unlimited amounts of food (high levels of NPY)

45
Q

Why doesn’t leptin injection work for humans to correct overeating and obesity?

A

Obesity in humans isn’t due to lack of leptin but rather to leptin resistance at the receptor level. Leptin levels increase as body fat increases and this leads to impaired transport of leptin across blood brain barrier and also impaired neuronal leptin signaling in target neurons.

46
Q

What is a parabiosis experiment?

A

2 animals are cut and sewn together and their blood supplies merge after a couple days, effects are observed in the animals.

THIS IS HORRIBLE, FUCK THE PEOPLE WHO DO THIS.

47
Q

What effect does adiponectin have on metabolism of FAs and carbohydrates?

A

Adiponectin acts through AMPK, so it is going to increase catabolism and reduce anabolism.

  • Increases FA oxidation in muscle
  • Decreases FA synthesis in liver
  • Decreases gluconeogenesis in liver
  • Increases glucose uptake in muscle
  • Increases insulin sensitivity
48
Q

What does the absence of adiponectin cause?

A

Desensitization to insulin

49
Q

Leptin exerts control on the level of the ___, while adiponetcin acts on the level of the ___

A

CNS

Tissues

50
Q

Leptin levels are ___ in obese people, adiponectin levels are ___ in obese people

A

Higher

Lower

51
Q

Ghrelin

1) Where is it secreted from
2) Where does it act?
3) What are its effects?

A

1) Produced by cells that line stomach
2) Acts on hypothalamus
3) apetite stimulant, stimulates release of NPY

52
Q

PYY

1) Where is it secreted?
2) where does it act?
3) What are its effects?

A

1) Peptide hormone produced by cells that line small intestines
2) Acts on hypothalamus
3) Appetite suppressant, inhibits release of NPY

HES Biochem (11 decks)

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