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Bloc E - GI & Metabolism > Jan29 M2-Normal and Abnormal Carbohydrate Metabolism - 1 > Flashcards

Jan29 M2-Normal and Abnormal Carbohydrate Metabolism - 1 Flashcards

1
Q

3 classes of macronutrients

A

lipids, polysaccharides, proteins

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2
Q

(EXAM) 3 stages of catabolism for macronutrients

A

1: Hydrolysis into monomers
2. conversion to acetyl coa
3. oxidative phosphorylation of acetyl coa

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3
Q

what ar the building blocks of lipids

A

glycerol and fatty acids

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4
Q

what is energy in the body exactly, what do we get out of glucose

A

ATP (high energy phosphate bonds)

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5
Q

main source of polysaccharides in our food. which polysaccharide + all its breakdown disaccharide and monosaccharides

A

potatoes, rice, pasta: starch. maltose. glucose + glucose.

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6
Q

what breaks down maltose into glucose + glucose

A

a disaccharase in the intestinal epithelium

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7
Q

lactose kind of molecule, food source and components

A

disaccharide. milk. glucose + galactose

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8
Q

sucrose kind of molecule, food source and components

A

disaccharide. plant products and sugar cane. glucose + fructose

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9
Q

basis for lactose intolerance + type of disease

A

deficiency in lactase (disaccharase). not genetic. function of bowel lost over time (mostly in early childhood). NOT genetic

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10
Q

symptoms in lactose intolerance + reason

A

flatulence and diarrhea. lactase not digested so goes to bowel and bacteria transform it to gases

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11
Q

sucrase deficiency charact.

A

rare, Inuit population, same things occur as lactase deficiency

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12
Q

where glucose is the most metabolized

A

liver

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13
Q

which monosaccharides can be transformed to glycogen (repolymerized) for storage

A

glucose and galactose

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14
Q

GLUTs: how many and why they differ

A
  1. expressed in specific cell types bc have specific properties
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15
Q

(EXAM) two GLUTs of interest + tissues

A

glut2: liver and pancreas

glut 4: muscle and adipose tissue

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16
Q

(EXAM) glut2 features and why useful to the liver

A

bidirectional transport bc livers metabolize glucose but also exports it when we’re fasting

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17
Q

(EXAM) glut2: why useful to the pancreas

A

allows beta cell to sense circulating glucose levels

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18
Q

(EXAM) 3 main insulin target tissues

A

liver, fat, muscle

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19
Q

(EXAM) glut4 in what tissue + very important property that is unique to it

A

fat and muscle.

Sensitive to insulin**

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20
Q

(EXAM) how insulin acts on glut4

A

vesicles carrying glut4 but just sitting in the cell fuse with the plasma membrane

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21
Q

2 drivers of diabetes worldwide nowadays

A

obesity (more calories intake)

sedentarity (less calories burned)

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22
Q

type 1 DM pathophgy and % of DMs

A

autoimmune destruction of insulin producing beta cells. 10%

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23
Q

type 2 DM pathophgy and % of DMs

A

insulin made but not as much glut4 is put in the membrane. 90%

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24
Q

type 2 DM: what tissue is most affected

A

skeletal muscle

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25
Q

type 2 DM first stage (Early)

A

pancreas ramps up insulin prod and glucose levels stay normal

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26
Q

type 2 DM 2nd stage (later)

A

beta cells lose ability to produce high amount of insulin (huge amount damages the cell)

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27
Q

other disorders of macronutrients metabolism and diseases that come with these disorders

A

fat metab and protein metab deregulated.

stroke, kidney failure, cognitive dysfct, muscle weakness, dementia, sarcopenia, bone more prone to fracture

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28
Q

(EXAM) first enzyme of glycolysis: 2 enzymes possible

A

hexokinase and glucokinase

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29
Q

(EXAM) hexokinase charact and what cells

A

cells other than liver and pancreas. enough activity to make enough glucose for cell to survive

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30
Q

(EXAM) glucokinase charact and what cells

A

liver and pancreas. extra activity to break down glucose.

31
Q

glucokinase advantages over hexokinase

A

more dynamic range of activity, more sensitive to glucose levels (works harder at higher glucose) and much higher max velocit

32
Q

why glucokinase does extra activity

A

also responsible for making fat in the body so breaks down glucose into metabolites then used to synthesize fats which are secreted and circulate

33
Q

(EXAM) why is the first step of glycolysis (glucose to glucose 6 P) irreversible

A

requires ATP consumption. REGULATED STEP

34
Q

2nd step (glucose 6 P to fructose 6 P) what kind of rx

A

isomerization

35
Q

(EXAM) 2nd step limiting enzyme in glycolysis and its job

A

PFK1. fructose 6 P to fructose 1-6 bisP

36
Q

what controls PFK1 activity

A

hormones and metabolites in the cell

37
Q

what happens in glycolysis after get fructose 1,6 bisP and why is it important

A

aldolase splits it into 2 metabolites. important bc results of downstream rxs must be multiplied by 2

38
Q

what does aldolase yield from fructose 1,6 bisP

A

DHAP and glyceraldehyde 3P

39
Q

link between DHAP and glyceraldehyde 3P + which is used for rest of glycolysis

A

can be converted into each other by triose phosphate isomerase. DHAP made into glyceraldehyde 3P (used for the rest of glycolysis)

40
Q

(EXAM) why glyceraldehyde 3P to product step is important

A

NADH (+ H+) is made from NAD+ + Pi.

41
Q

(EXAM)glyceraldehyde-3P + product. product name and enzyme in this rx

A

GAPDH. make 1,3-biphosphoglycerate

42
Q

(EXAM) 1,3-biphosphoglycerate + product step: why important

A

makes ATP (gives one P to ADP)

43
Q

(EXAM) 2nd step in glycolysis where ATP is yielded and product of this step

A

phsophoenoylpyruvate to pyruvate (done by pyruvate kinase).

ADP to ATP

44
Q

(EXAM) 3 irreversible and regulated steps of glycolysis and why

A

1st step (GK or HK) and PFK1 step. (because consume ATP) + pyruvate kinase step (to make pyruvate)

45
Q

(EXAM) glycolysis: investments, products and end result in terms of ATP, NADH and pyruvate

A

invest: 1 glucose + 2 ATP (step 1 and 3)
product: 4 ATP + 2 NADH + 2 pyruvate
NET: 2 ATP, 2 NADH, 2 pyruvate

46
Q

(EXAM) insulin: fcts on muscle, fat and liver other than gluT insertion

A

stimulates transcription of 3 glycolysis genes: GK or HK + PFK1 + pyruvate kinase also called PK (last step)

47
Q

GK use in pancreas vs liver

A

liver: provide substrate for fat synthesis
pancreas: tell beta cell how much insulin to release

48
Q

type 2 diabetes (poor response to insulin): what enzyme is affected + treatment possible

A

glucokinase (step 1 glycolysis. liver and pancreas).

treatment: small molecule activators of GK

49
Q

(EXAM) one mutation in GK: disease name and treatment

A

MODY (maturity onset disease of the young). DON’T need insulin

50
Q

MODY often confused with what disease and diff between the two

A

often confused with type 1 diabetes. type 1 DM needs insulin.
MODY doesn’t need insulin

51
Q

(EXAM) 2 mutations in GK consequence and treatment

A

permanent neonatal DM (PNDM). Need insulin.

52
Q

enzyme breaking down sucrose + products

A

sucrase. gives glucose + fructose

53
Q

(EXAM) fructose: 2 steps diff in glycolysis and consequence

A
  1. fructose kinase makes it fructose 1P
  2. aldolase B makes it glyceraldhehyde and DHAP
    BYPASSES GK regulation/HK regulation
54
Q

what can happen to glyceraldehyde from 2nd step of fructose glycolysis

A
  1. converted to glycerol (backbone for fat synthesis(

2. phosphorylated into glyceraldehyde-3P to use it in glycolysis

55
Q

important theory on one of the many drivers of obesity

A

high consumption of fructose (ex. soft drinks) = metab rapidly by liver to make glycerol + acetylcoa to make fat

56
Q

(EXAM) fructose intolerance cause

A

genetic mutation in aldolase B

57
Q

(EXAM) 2 important implications of fructose intolerance

A
  1. fructose 1 P is an inhibitor of PFK1
  2. ATP of the cell is harvested to make fructose 1 P that won’t lead to ATP prod. (phosphate and energy deficiency, liver cells damaged)
58
Q

symptoms in fructose intolerance

A

toxicity, tissue damage (liver, kidney), hypoglycemia

59
Q

(EXAM) why hypoglycemia in fructose intolerance

A

fructose 1 P inhibits breakdown of glycogen storage. consequence: metabolites like phosphoenoylpyruvate can’t make glucose bc the more upstream pathway is blocked

60
Q

(EXAM) glycolysis: how it is changed in cancer + name of that

A

hyperactivated. Warburg effect

* *cancer cell uses glucose faster and makes lactate instead of acetyl-CoA

61
Q

(EXAM) glycolysis enzymes affected in cancer

A

HK overexpressed

HK and PK VARIANT is expressed (very active)

62
Q

basis for PET scan

A

measure hyperactivity of glycolysis by radiolabelling glucose (add radioactive 18F on a hydroxyl group)

63
Q

what happens to 18F glucose in the body

A

phosphorylated but not further metabolized and gets stocked in the cell: seen on imaging

64
Q

PET used for what

A

stage cancers and check for metastases

65
Q

what bacteria can do with pyruvate

A

ethanol

66
Q

(EXAM) what our body can do with pyruvate

A
  1. make acetyl coa to go in TCA (pyruvate dehydrogenase)
  2. reduce it to lactate (lactate dehydrogenase)
  3. make it oxaloacetate (pyruvate carboxylase) (OAA is TCA intermediate)
67
Q

why transformation of pyruvate into lactate by lactate dehydrogenase is something important

A

needs a NADH so yields NAD. NADH is a redox metabolite exchanging protons and we need a balance of NAD and NADH in the cell bc used in a lot of places. This rx consumes the NADH produced from glycolysis

68
Q

what determines if pyruvate made into acetyl coa or lactate

A

O2 amount in the cell. high O2: make acetyl coa

low O2: make lactate

69
Q

when do we have low O2 and pyruvate made into lactate

A

cardioresp exercise/high intensity sport like hockey

70
Q

why pyruvate to acetyl coa pathway works less in low O2

A

too much pyruvate to the few O2 left (O2 consumed too fast)

71
Q

lactate effect on muscle + how it is metabolized

A

muscle pain.

lactate goes in blood, reaches lier, metab by reverse rx (lactate to pyruvate)

72
Q

clinical use of lactate

A

measure in ill patients to check if severe illness bc shows something is wrong

73
Q

high lactate can be marker of what

A

O2 deficiency, MI, bleeding (not delivering O2), hypotensive states.

Bloc E - GI & Metabolism (58 decks)

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