Carbohydrate Meta Flashcards

1
Q

How quick is carbohydrate digestion and absorbtion?

A

30-90 mintes

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2
Q

How much monosaccharides can the liver remove from the portal vein

A

1/3

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3
Q

What are some sources of glucose

A
  1. Diet
  2. gluconeogenic precursors
  3. glycogen store
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4
Q

What is the fate of glucose in metabolism?

A
  • can be used to produce other carbohydrates (mammoary lactate, ribose for DNA)
  • sugar residues for other compounds (glycoproteins)
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5
Q

What cells are very dependent on glucose

A
  • brain
  • Rbc
  • Nerves
  • intestines
  • mucosa
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6
Q

What is nomal glucose levels

A

Upper end: 6mmol/L
Lower end : 4 mmol/L

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7
Q

What are the difference between glycolysis and complete oxidation of glucose?

A

Glycolysis
- Produces small amount of ATP
- Is an anaerobic process
- occurs in the cytoplasm

Complete oxidation
- occurs in the mitochandria
- Produces alot of ATP
- happens during aerobic conditions

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8
Q

What type of metabolism can occur in muscle cells and why

A

Muscles can undergo glycolysis, complete oxidation or storage of glycogen

  • muscle cells have mitochandria therefore metabolism can go all the way
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9
Q

What type of metabolism can occur is cardiac muscle

A
  • glycolysis –> cytoplasm existent
  • Completely oxidation –> yes mitochandria present
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10
Q

What type of metabolism can occur in hepatocytes?

A

-can do all types (glycolysis, complete oxidation and glycogen storage)

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11
Q

Describe the link between the muscle cells and the liver

A
  1. Glucose into the muscle –> G6P (can be converted to glycogen) –> pyruvate
  2. Pruvate has 2 fates: A. If we are reaching our VO2 max then it is converted into lactate and sent to liver B. Pyruvate can enter the mitochandria where it is converted to oxaloacetate the to citrate (this can occur more effiencient if we are well trained)
  3. A. Lactate enters the hepatocyte where it is converted into pyruvate where it can be converted into oxaloacetate then citrate –> where it can be converted to fat or CO2
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12
Q

What type of metabolism can occur in red blood

A

Glucose can only be converted to pyruvate then to lactate because they lack mitochandria

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13
Q

What type of metabolism can occur in the brain

A
  • complete oxidation of glucose BUT cannot store glycogen (big molecule)
  • can also oxidize ketones
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14
Q

What type of metabolism can occur in B-cells in pancreas

A
  • complete oxidation of glucose, very effiecient
  • High amount of mitochandria
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15
Q

What type of metabolism can occur in adipocytes

A
  • complete oxidation or synthesis of glycerol –> excess glucose to Acetyl CoA –> Fat storage
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16
Q

What organ can raise glucose level

A

the liver

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17
Q

Do skeletal, cardiac, adipose, brain tissues/cells released glucose to change blood glucose levels?

A

No, because the respond to the blood glucose changes but do not release glucose into the blood

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18
Q

Why store glycogen in a polymeric form rather than in free form?

A
  • want to store alot while keeping it readily avaible
  • Optimized degree of branching and chain length
  • more branching than amylopectin
  • uses less space and hold more water
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19
Q

What % of storage is glycogen in muscles and liver

A

muscles - 1%
Liver - 10%

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20
Q

What inhibits glycogensis

A
  • glycogenolysis and maximized glycogen stores
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21
Q

What are the 2 forms of glycogen synthase?

A

A (GYS1)
B ( GY2)

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22
Q

Describe gycogen sythase A

A
  • found everywhere in the body, RBC, brain, kidney adipose
  • more active when phosphorylated
  • Used in rapid response to an increase in blood glucose levels in fed state as well exercise
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23
Q

Describe glycogen synthase B

A
  • Only in liver
  • Less active when phosphorylated
  • ensure that large pools of glycogen avaible for blood glucose concentration
    -Lower affinity for UDP- glucose and less sensitive to allosteric activiation by G6P
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24
Q

what activate glycogen phosphorylase

A
  • glucagon
  • epinephrine
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25
Q

What is glycogenolysis

A

use of glycogen when blood glucose levels are low

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26
Q

What increases glycogensis

A

being in the fed state

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27
Q

What molecules start glycogensis

A
  • high ATP and sugar
  • Insulin triggers the increase in glucose uptake
  • Glucose enters the cells and transforms to G6P to be used for glycogen storage
  • Lactate is perferred to be used as glycogen
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28
Q

What increases glycogenolysis

A
  • fasting state
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29
Q

What triggers glycogenolysis

A
  • Liver is depleted of glycogen
  • When no dietary glucose, glycogenolysis is initiated to supply glucose
  • Glucagon stimulates in the liver
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30
Q

What is the purpose of glycogen breakdown in the liver?

A
  • To increase blood glucose levels or ATP
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31
Q

What is the purpose of glycogen breakdown in the muscle?

A

For atp for itself NOT THE BLOOD

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32
Q

What biomolecule is used for glycolysis

A

G6P

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33
Q

What organs contribute to the increase in blood glucose

A
  • liver and kidney
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34
Q

How is glycogen phosphorylase activated in the skeketal tissue

A
  • Phosphorylation control
  • Depending on the ratio of phorsphorylase a:b
  • A (more active, not sensitive to ATP) : B ( less active dephosphorylated form)
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35
Q

What activates glycogen phosphorylase in the liver?

A
  • Allosteric control
  • Glucagon and epinephrine will bind to recpetor and cAMP will induce a response
  • Activating Glycogen phosphorylase
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36
Q

How is the rate of glycogen breakdown determined by enzymes in skeletal muscles?

A

Depends on ratio of phosphorylase A and B
- Exercise can activate phosphorylase kinase that generate phosphorlyase A to stimulate breakdown of glycogen

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37
Q

Why are NAD+ and NADH important to reactions?

A

they are central for electron movement

38
Q

What activates working muscles to stimulate glycolysis

A

NADH, Pi and ADP+AMP

39
Q

What is regenerated in lactate formation

A

NAD+

40
Q

What is the rate-determining step in aerobic metabolism?

A

PDH

41
Q

How much ATP is formed during aerobic respiration?

A

34

42
Q

What does an increased rate of glycolysis mean?

A

it means there is a depletion of NAD+

43
Q

What tissue generate lactate and alanine

A

peripheral tissues

44
Q

What does lactate to pyruvate generate?

A

NADH for gluoconeogensis

45
Q

What factors impact weather pyruvate enters the CAC

A
  • availbilty of oxygen
  • Metabolic state of the cell
46
Q

How is pyruvate converted into acetyl CoA

A

via the PDC

47
Q

What tranporter carrier pyruvate across the mitochandria

A

monocarboxylate carrier

48
Q

What is the product and substrate of the CAC?

A

acteyl CoA to 2 CO2’s

49
Q

What molecules inhibit CAC

A
  • pyruvate dehydrogenase activity
  • ATP avaibility
  • Excess NADH
50
Q

Why would a cell have more mitochandria

A

to increase cellular respiration

51
Q

What cells use the pentose pathway?

A

RBC, adipocyte, liver, and mammary glands

52
Q

Where does the pentose pathway occur in the cell?

A

In cystol

53
Q

What molecule does the pentose pathway generate

A

NADPH

54
Q

How is glucose a regulator?

A

Regulated the activity of enzymes, transcription, hormone secretion, glucoregulatory neuron activity

55
Q

How is a glucose a substrate?

A

Acts a signal molecule to control glucose and energy homeostasis

56
Q

Where are some of the fates of glucose?

A

Glycogen stores, brain, adipose, muscle

57
Q

What is the post prandial fate of monosaccharides?

A
  • On the first pass most monosaccharides will be absorbed by the liver
  • insulin will initiate a response for use of monosaccharides for energy, glucose for glycogen stores

Skeletal muscle
- insulin will initiate uptake of glucose via GLUT 4 transporter
- glucose will then be used for energy and for glycogen stores
- fructose will also be absorbed

Adipose tissue
- GLUT 4 transporter will uptake, glucose will be used for energy, FA, glycerol, TG if excess glc

Cardiac muscle
- GLUT 4 transporter of glucose, glucose will be used for energy and glycogen synthesis

Other
-Glc can be up-taken (1&3) based on needs

58
Q

Where and how much is the glucose uptaken

A
  • 1/3 up-taken by the liver, high uptake due to GLUT 2 + glucokinase
  • 2/3 up-taken by peripheral tissues after insulin secretion
59
Q

Which cells are insulin dependent?

A

Skeletal muscles and adipose tissue

60
Q

Which cells are insulin independent?

A

Hepatocytes

61
Q

How glucose transported to the blood stream from GIT?

A
  • Via SGLUT transporters and GLUT transporters
62
Q

GLUT 2 ( monosaccharide substrates, sites, affinity, capacity)

A

MS: Glucose, galactose, mannose, and fructose
Sites: Small intestine, B-pancreas and liver
Affinity: low
Capacity: high

63
Q

GLUT 4 ( monosaccharide substrates, sites, affinity, capacity)

A

MS: Glucose
Site: Adipose, muscle,
Affinity: //
Capacity: high

64
Q

Where is insulin released?

A

B-cells in the pancreas

65
Q

Where is glucagon released?

A

A- cells in the pancreas

66
Q

What does insulin do?

A

Stimulate hepatic uptake and storage

67
Q

What response does glucagon have on the liver?

A

Increase liver output of glucose but can be catabolic

68
Q

Where are the A and B cells found ?

A

Islet of langerhans

69
Q

Explain how glucagon raises blood sugar

A
  • decrease in bloods glucose
  • breakdown glycogen into glucose in the liver
  • breakdown fats to fatty acids and ketones in the liver (ketogenesis)
  • breakdown non carbohydrates to produce glucose (gluconeogensis)
    Increases blood glucose concentration
70
Q

Explain how insulin promotes energy storage?

A

Raising blood glucose levels
Anabolic effects
- uptake of skeletal muscles and adipose tissue for energy
- convert glucose to glycogen for storage
-promote synthesis of muscle
- promote synthesis of fat

71
Q

How is GLUT 4 impacted by insulin?

A

Once insulin binds to its receptor, it send a response to the transporter to move to the membrane of the cell and to bring the extra cellular glucose into the cytoplasm

72
Q

What does the rate of glucose transport depend on in muscle and adipose tissue?

A

How long glut 4 is on cell surface and amount

73
Q

Explain the process of how insulin is secreted.

A
  • glucose enters the cells via GLUT 2 and gets phosphoryl aged by glucokinase
  • Pyruvate is made and undergoes the transformation inside the mitochondria (PDH -> A CoA -> CAC)
  • the increase of ATP: ADP ratio cause depolarization, which opens up the CA+ channels. Ca2+ fusion of insulin vesicle to be released via exocytosis
74
Q

How is insulin production coupled with glucose

A

Via ATP production

75
Q

What can stimulate insulin production?

A

GLUCOSE
-certain aa
-Parasympathetic stimulation
-incretin hormones

76
Q

Does fructose cause an insulin response, why or why not?

A

Fructose enters cells via GLUT 5 which not present in the pancreas therefore I’ll not initiate a response

77
Q

What enzymes/transporters senses blood glucose levels?

A

GLUT 2 and glucokinase/ rate of glycolysis

78
Q

Explain glucose homeostasis during the fed state

A
  • pancreas will increase insulin production and decrease glucagon production
  • increased glucose utilization (glycogenesis and lipogenesis ) and decrease glucose production (gluconeogensis and glycogenolysis )
  • muscle will uptake glucose and utilize
79
Q

Explain glucose homeostasis during the fasted state

A
  • Pancreas will produce glucagon and decrease insulin production
  • liver will increase glucose production (lipogenesis and glycogenesis ) and decrease glucose utilization ( gluconeogenesis and glycogenolysis )
  • muscle will decrease uptake and utilization
80
Q

What are normal glucose ranges

A

4-6mmol/l
70-110 mg/dl

81
Q

What is insulin resistance?

A

Increase insulin secretion for the same response in GLUT 4 transporters

82
Q

What does insulin resistance lead to?

A

Hyperglycaemia and hyperinsulimeia

83
Q

What are Catecholamines effect on glucose levels?

A

Increased glycogenolysis and gluconeogenesis

84
Q

What are Glucocorticoids effect on glucose levels?

A

Increased hepatic glucose output & expression of gluconeogenic genes

85
Q

What are the effects of Tri-iodothyronine (T3) on glucose levels?

A

Can modulate or amplify many other hormones & actions, increases gene expression for enzymes to regulate metabolism (both anabolic & catabolic systems; INCR BMR)

86
Q

What happens to glucose metabolism during starvation

A
  • Increased glucagon secretion
  • increase glycogenolysis and gluconeogensis
  • decreased up p take of glucose by muscles and adipose, switches to fat oxidation
87
Q

What is glycemic index?

A

The incremental area under the blood glucose response curve of a 50 g carbohydrate portion of a test food expressed as a percent of the response to the same amount of carbohydrate from a standard food taken by the same subject

88
Q

What’s the difference between a high glycemic response and a low glycemic response?

A

Low glycemic response has a smaller more controlled increase in blood glucose but high glycemic response and a high spike in blood glucose filled by a dip which leads to a drop. High glycemic response put pressure on the pancreas to produce more insulin

89
Q

What is glycemic load?

A

takes into account BOTH GI and the amount of food in a given serving

GL=GI/100x(gofCHO/serving)

90
Q

What is the glucose sparing effect?

A

Glucose uptake by muscle and adipose tissue decreases and switches to lipid fuels