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Cmbm 2 Gopi > Carbs 1 and 2 > Flashcards

Carbs 1 and 2 Flashcards

0
Q

what is the OH group’s linkage if it is below the plane of the sugar?

A

alpha

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1
Q

Do our bodies utilize D or L sugars?

A

D

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2
Q

what is the OH group’s linkage if it is above the plane of the sugar?

A

beta

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3
Q

what type of bonds link sugars?

A

glycosidic bond

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4
Q

what sort of group is found on a reducing sugar?

A

reactive carbonyl (Hemiacetals)
which can reduce metals hence the name
swaps H+ on the carbonyl group with an O

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5
Q

Anomeric carbon

A

reducing carbon on a sugar

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6
Q

Which end of a oligo or poly - saccharide has the anomeric carbon?

A

reducing end

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7
Q

A patient is found to be unable to absorb disaccharides, what could be the issue?

A

An enzyme in the gut called disaccharidases which are tethered to cells in the lumen and breakdown disaccharides into monosaccharides. this is could be the culprit because we can only absorb monosaccharides

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8
Q

what cleaves an alpha 1,6 bond?

A

Isomaltase

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9
Q

What cleaves an alpha 1,1 bond?

A

Trehalose

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10
Q

what breaks an beta 1,4 bond?

A

Lactase

Lactose = galactose and glucose

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11
Q

what pathways does G6P participate in?

A

Glycolysis
Pentose phosphate pathway
glycogen synthesis

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12
Q

what type of link bonds branches to glycogen molecules?

A

alpha 1,6

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13
Q

every polymer of glycogen is attached to _____

A

glycogenin

which is a protein

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14
Q

what enzyme is responsible for the conversion of G6P to G1P?

A

phosphoglucomutase

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15
Q

what are the building blocks of glycogen?

A

UDP-Glucose

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17
Q

What starts the seeding process for glycogen?

A

When glycogenin glycosylates itself by attaching the glucosyl residue of UDP-glucose to the hydroxyl chain of a Ser residue in the protein

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18
Q

What link connects branches to the core glycogen molecule?

A

alpha 1,6

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19
Q

glycogen degradation proceeds through a _______ rxn

A

phosphorolysis

use of phosphate to break the bond

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20
Q

Why is an ATP not required to make G6P for glycolysis ?

A

G1P and G6P are energetically equivalent

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21
Q

what is the activity of glycogen phosphorylase?

A

will cut down the glycogen chains to “limit dextrins”

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22
Q

Glycogen phosphorylase and glycogen synthase are reciprocally regulated.by…

A

phosphorylation with ATP

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23
Q

When glycogen phosphorylase B is phosphorylated then it is (active/inactive)

A

active

24
Q

Insulin secretion in response to an increase in blood sugar levels induces …

A

more GLUT4 receptors to come to the cell surface to increase uptake of glucose

25
Q

Glucagon signals to the liver result in …

A

the conversion of glycogen phosphorylase B to glycogen phosphorylase A and the inhibition of glycogen synthase

26
Q

Fructose metabolism occurs in …

A

the liver

27
Q

What does the Pentose phosphate pathway generate?

A

5 carbon sugars and NADPH

28
Q

What intermediate links the Fructose metabolism pathway to Glycolysis?

A

DHAP - dihydroxyacetone phosphate

29
Q

Name the three enzymes involved in Fructose metabolism

A

Fructokinase
Aldolase B
Triose Kinase

30
Q

Hereditary Fructose intolerance is characterized by ….

A

insufficient Aldolase B activity causing pts to accumulate very large stores of F1P
symptoms: Jaundice, vomiting and convulsions

31
Q

What does the Pentose phosphate pathway produce?

A

NADPH

Ribose 5-phosphate

32
Q

What does the first (oxidative phase)stage of the PPP generate ?

A

2 moles of NADPH per 1 mole of G6P

33
Q

What does the second (non oxidative phase)stage of the PPP generate ?

A

ribose 5 phosphate

converts unused intermediates to fructose 6-P and glyceraldehyde 3-P

34
Q

What pathway do RBCs rely on to avoid oxidative damage?

A

HMP shunt

35
Q

What can not be oxidized by the electron transport chain?

A

NADPH

36
Q

What molecules does UDP glucose serve as a percursor for?

A

glycosides
lactose
glycolipids
glycoproteins

37
Q

What is the ocular consequence and mechanisms of elevated sugar in diabetes?

A

elevated glucose leads to generation of fructose in the lens of the eye. Excess will be converted to sorbitol at a faster rate then it can be cleared.
Leads to increase in osmotic pressure

38
Q

What are the functions of Glucuronides?

A

to aid in excertion of bilirubin and drugs
overall it supplys negatively charged group to couple with OH on the target molecule
More charges = increased solubility

39
Q

describe synthesis of lactose

A

Galactose is produced from conversion of UDP-glucose to UDP-galactose by epimerase
then glucose and galactose are linked by an alpha bond

40
Q

What residues on proteins are short carbohydrates attached?

A

serine
threonine
asparagine

41
Q

What are the general features of glycoproteins?

A

highly branched

no repeating disaccharide units

42
Q

what are the functions of glycoproteins?

A

most proteins in the blood - clotting enzyme, antibodies, hormones
structural components of ECM - collagen
Mucus secretions

43
Q

What is the primary component of the glycolipid, sphingosine?

A

ceramide with carbohydrate pieces

44
Q

What is a function of glycolipids?

A

cell recognition

example: ABO blood groups

45
Q

Name the enzymes that metabolize ETOH

A

liver alcohol dehydrogenase

Microsomal ethanol oxidizing system (MEOS)

46
Q

What is the side effect of the metabolism of the small alcohol, ETOH?

A

ADHs have preferences for different chain lengths of alcohols
at high concentrations, ETOH will be non specifically metabolized leading to large increase in amount of Acetaldehyde bi product which is toxic
leads to nausea and vomiting

47
Q

Where is the liver cell is the majority of ETOH metabolized?

A

Mitochondrial ALDH2

an allelic variance of ALDH2 which has very low affinity for substrate confers resistance to alcoholism

48
Q

In the liver, acetyl CoA will be used in ….

A

cholesterol and fatty acid synthesis

49
Q

What is MEOS composed of?

A

Cytochrome P 450 reductase and cytochrome P 450

oxidizes ETOH to acetaldehyde

50
Q

What enzyme shows the most activity toward ETOH?

A

CYP2E1

51
Q

Chronic ETOH consumption leads to …

A

increasing the NADH/NAD+ ratio resulting in changes to fatty acid metabolism, ketoacidosis, lactic acidosis, hyperuricemia and hypoglycemia

52
Q

What are the consequences of excessive drinking, with respect to fatty acid metabolism?

A

inhibition of oxidation of fatty acids leading to the accumulation
increases in the amount of triacylglycerols which are incorporated to VLDLs which build up in liver and enter the blood

53
Q

What conditions are the result of excess ETOH? Think about what happens metabolically

A

Hyperlipidemia

fatty liver

54
Q

What is the mechanism of Alcohol induced ketoacidosis?

A

High NADH leads to reversal of Acetyl CoA to the TCA cycle
instead Acetyl CoA is used to generate ketone bodies
build up in the blood is toxic

55
Q

What is the consequence of Lactic acidosis?

A

the altered NADH/NAD+ ratio
will shift the reaction of lactate dehydrogenase towards lactate
High lactate will lead to decreased excretion of uric acid => Gout
Lactate also inhibits gluconeogenesis so fasting blood sugar levels drop

56
Q

pt with mutation in CYP2E1 rendering protein non functional, what do expect to happen when pt consumes large amount of alcohol?

A

majority of ingested ethanol would get converted into acetaldehyde via ADH

Cmbm 2 Gopi (16 decks)

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