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B3 GI & GU > Theme 3: Metabolism: Storage, Retrieval, and Synthesis of Fats and Carbohydrates > Flashcards

Theme 3: Metabolism: Storage, Retrieval, and Synthesis of Fats and Carbohydrates Flashcards

1
Q

Normal blood glucose is?

A

under 100

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2
Q

when treating high blood glucose for T2DM, it is also important to address…

A

high cholesterol levels

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3
Q

What is the brains primary and secondary source of energy?

A

First, glucose. Then, ketones.

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4
Q

How/where are ketones produced?

A

Free fatty acid oxidation at the liver

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5
Q

Anabolism- Fed state: what hormone is high and what are the processes that are associated with it?

A

Is associated with insulin secretion; active processes of glycogenesis, protein synthesis and TG synthesis.

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6
Q

Anabolism- Fed state: what hormone is high and what are the processes that are associated with it?

A

Is associated with insulin secretion; active processes of glycogenesis, protein synthesis and TG synthesis.

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7
Q

What type of transporter and where does insulin act.

A

insulin receptors are on muscle and adipose tissue and trigger glut 4 receptors to the cell surface. This can be also triggered with exercise.

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8
Q

Drug: insulin

A

it is injected. tends to cause weight gain

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9
Q

Drug: sulfonylurea

A

ie. glucotrol, glipizide- triggers insulin secretion

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10
Q

Drug: glucatrol

A

sulfonylurea- insulin secretion by beta cells

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11
Q

Drug: glipizide

A

sulfonylurea- triggers insulin secretion by beta cells.

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12
Q

Drug: metformin

A

biguinide. inhibits gluconeogenesis by the liver and enhances glut 4 translocation

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13
Q

drug: pioglitazone

A

thiazolidines: enhances insulin receptor sensitivity and glut 4 translocation in fat cells. bu tis associated with an increased risk of MI and stroke, so it is not really used anymore.

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14
Q

exentide

A

incretin mimetic: naturally occuring homrone in response to food intake: increases the glucose dependent insulin response by the pancrease and is postitively associated with weight loss

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15
Q

sitagliptin

A

dipeptyl peptidase 4 inhbitor. aslo increases incretin availablity be decreasing degradation

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16
Q

number one risk factor for diabetes is

A

obesity

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17
Q

it is important to use what drugs in addition to insulin promoting drugs?

A

statins and aspirin, to lower lipids and decrease inflammation- to prevent cardio disease.

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18
Q

standard drugs for diabetics

A

statin with metformin/insulin

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19
Q

what is statin

A

lipid lowering drug, by partial inhibition of hmg-coa reducatase

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20
Q

checking lactate levels diabetes

A

to check for anaerobic metabolism

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21
Q

aerobic metabolism

A

pyruvate to TCA & ETC, to produce CO2 and H20

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22
Q

Insulin Independent glucose transporters: Glycolysis enzyme and location:

A

Glucokinase, at liver, pancreatic B cell, and Brain

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23
Q

Insulin DEPENDENT glucose transporters

A

at the muscle, hexokinase.

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24
Q

insulin and glucagon

A

maintain blood glucose levels. glucagon, when blood glucose is low, increases glucose release from the liver to the blood. insulin when glucos is high after a meal, decreases glucose release from the liver and actually increases glygogenesis.

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25
Q

Glucokinase/ Hexokinase

A

converts glucose to g6p in glycolysis

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26
Q

g6p phophatase

A

converts g6p to glucose in gluconeogenesis; this enzyme is key for hepatic glucose release

27
Q

PEP carboxylase

A

TCA intermediates for gluconeogenesis

28
Q

Glycogen synthase

A

glycogenesis

29
Q

Glycogen phosphatase

A

Glycogenolysis

30
Q

Energy: Muscle, what does it use?

A

It uses glucose or fatty acids, and can store glucose as glygogen

31
Q

GLUT 2 Where?

A

Liver and pancreas, glucose uptake is proportional to the plasma glucose concentration. (insulin independent)

32
Q

GLUT 3 Where?

A

Brain, glucose uptake in the brain is at a steady state over the physiological range of glucose concentration, so it is glucose and insulin independent. it has the highest affinity for glucose because it has the lowest km.

33
Q

GLUT 4 Where

A

Glut 4 is at the muscle and fat. it is translocation to the cell surface is dependent on insulin or exercise.

34
Q

Hexokinase

A

Is the type glycolysis enzyme in most cells. it is saturated at a low glucose concentration..

35
Q

Glucokinase:

A

is in the liver, and pancreatic beta cells, it as as the glucose sensor and has a very high km. because the liver is the ‘altruistic organ’ this allows it to have access to glucose after all the other organs are accounted for.

36
Q

GKRP: glucokinase regulatory protein

A

binds glucokinase in the nucleus when glucose levels are low. it is released into the cytoplasm to be active then glucose levels are higher. There is negative feedback as g6p is converted to f6p, which returns GK to the nucleus.

37
Q

Glycolysis regulation

A

is by allosteric and hormonal regulation (insulin and allosteric regulation of GK, HK)

38
Q

phosphofructokinase, PFK: function and regulation:

A

Glycolysis: f6p to f1,6,bp. (+) by F2BP, AMP (-) ATP Citrate, H+

39
Q

Irreversible/ Regulated steps of Glycolysis

A

PFK and Pyruvate Kinase, allosterically regulated

40
Q

PFK -2: Function

A

PFK 2 phosporylated f6p to f26bp, which is in turn a postive allosteric regulator for the next glycolysis enzyme, PFK. it is a BIFUNCTIONAL ENZYME with kinase and phosphatase activity

41
Q

Glucagon on PFK2

A

Glucagon phosphorylates PFK2, which activates its phosphatase activity of F26BP to F6P, less F26BP means that less glycolysis is taking place (hormonal reg of glycolysis)– THIS IS IN LIVER! OPPOSITE EFFECT TO INCREASE GLYCOLYSIS IN HEART MUSCLE WHEN PHOSPHORYLATED BY ACTION OF EPI AND PKA

42
Q

Insulin on PFK2

A

Insulin, by a complicated pathway, increases F26BP, via PFK2 kinase activity, and increases glycolysis (hormonal reg of glycolysis)

43
Q

Epinephrine effect on PFK2 and glycolysis in the heart muscle

A

the PFK2 has a different isoform in heart muscle where Epi will phosphorylate it. This wil actually increase f26bp and promote glycolysis

44
Q

PFK2 effect in skeletal muscle

A

there is none, PFK 2 is not applicable in skeletal muscle.

45
Q

Pyruvate kinase regulation by glucagon

A

Glucagon phosphorylates PK to decrease its activity

46
Q

Respiration in normal vs. cancer cells.

A

In cancer cells, they only use anaerobic respiration, generating lactate, even in aerobic conditions.

47
Q

T/F: PDH is inactive when phosphorylated by kinase

A

True. Also, Ca is a strong activator of the phosphatase that dephos PDH and makes it active.

48
Q

3 Regulated steps of TCA:

A

PDH, Isocitrate dehydrogenase, a-ketoglutarate dehydrogenase

49
Q

Unique Enzymes for Gluconeogenesis:

A

6ATP per 1 glucose synthesis. Pyruvate carboxylase (Pyruvate to OAA), PEPCK (phosphoenol pyruvate carbozy kinase, OAA to PEP), F16BP, and Glucose 6 phosphatase (g6p to g)

50
Q

PEPCK regulated for what process and how

A

PEPCK transcription is regulated for gluconeogenesis, it is decreased by insulin and increased by fasting, glucocorticoids, glycogen, and thyroid homrone. (PEPCK transgenic mice can run much better)

51
Q

there is reciprocal regulation of gluconeogenesis and glycolysis. What is the corresponding enzyme to F16Bisphosphatase in glycolysis?

A

PFK

52
Q

T/F, G6p cannot be exported out of the cell, it needs to be converted to G by G6P-Phosphatase first

A

this is true. this is what allows the liver to release G to other organs.

53
Q

5 enzymes required to export glucose from the liver

A

g6p transporter, CA binding stabilizing protein, G6Pase, Glucose tranporter, Pi transporter.

54
Q

Prime function of gluconeogenesis

A

the liver provide constant glucose to the brain.

55
Q

Epi, glucagon & insulin, phos/dephos

A

Epi & Glucagon=phosphorylates, activating gluconeogenesis, glycogenolysis enzymes Insulin dephosphorylates, activating kinases/ activates glycolysis and glycogenolysis enzymes.

56
Q

substrates for gluconeogeneisis

A

lacatate, alanine, glycerol from muscle, RBC, renal medulla, and fat –> to the liver for gluconeogenesis, and then to the brain as glucose

57
Q

reciprocal regulation of glycogenesis/glycogenoslysis

A

glycogen synthase is active when dephosphorylated. this is stimulated by insulin. glycogen phosphorylase, breakdown enzymes are active when phosphorylated by epi or glucagon. This will in turn increase glycogen breakdown to form glucose

58
Q

glycogen synthase/phosphorylase are receiprocally regulated

A

Glucose 6-phoshate activates glycogen synthase, inhibits glycogen phosphorylase ATP inhibits phosphorylase Glucose inhibits phosphorylase (in liver) Ca++ and AMP activate phosphorylase (in muscle)

59
Q

Function of Actyel Coa Carboxylase (ACC)

A

for fatty acid synthesis: regulated by dephos and phos. active when dephos. opposite of hormone sensitive lipase

60
Q

Hormone sensitive lipase

A

first enzyme of lipolysis for gluconeogenesis. reciprocally reg with ACC

61
Q

Why do patients with liver failure get hypoglycemia

A

.

62
Q

Can fatty acids be converted to glucose?

A

.

63
Q

How and why is blood glucose maintained in a prolonged fast?

A

.

64
Q

Endocrine cells in the pancreas

A

islets of langerhaans

B3 GI & GU (4 decks)

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