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From Flashcardlet > Biochemistry: Carbohydrate Metabolism > Flashcards

Biochemistry: Carbohydrate Metabolism Flashcards

0
Q

Trisaccharides and disaccharides are hydrolyzed to monosaccharides by

A

Enzymes located on luminal surface of epithelial cell lining of intestine

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1
Q

Strach and glycogen are hydrolyzed by

A

a-amylase (present in saliva and pancreatic juice

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2
Q

Sucrose is hydrolyzed to ___ and __ by ___ in the ___

A

Glucose and fructose by disaccharidases in the intestine

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3
Q

D- glucose and D- galactose are taken up by

A

NA+ dependent co-transport system

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4
Q

Intestinal cells utilize ___ as a major source of energy

A

glutamine

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5
Q

Glucose usually passes into

A

Blood where it goes via portal circulation to other cells

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6
Q

First major tissue to remove glucose from peripheral blood is

A

parenchymal cells of liver

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7
Q

When concentration of glucose is high in the blood

A
  • Liver metabolizes glucose to pyruvate-lactate (glycolysis)

- or synthesizes glycogen (glycogenesis) for storage

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8
Q

D fructose is taken up by

A

NA+ independent transport system in the intestinal epithelial cells

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9
Q

When blood glucose levels are low

A

Liver breaks down stored glycogen (glycogenolysis) to yield glucose

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10
Q

24 hours after glycogen stores are depleted

A

Liver synthesizes glucose (gluconeogenesis) from non-carbohydrate precursors (lactate and alanine)

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11
Q

Blood glucose levels are regulated by

A

Hormones: glucagon and insulin which are released from the pancreatic cells

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12
Q

Glucagon

A

Hormone released in response to low blood glucose level

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13
Q

Insulin

A

Hormone released in response to high blood glucose levels

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14
Q

Uptake of glucose occurs by

A

facilitated diffusion, using glucose transporters (GLUT)

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15
Q

All glucose transporters (except ___) are present in the ___

A
  • Except GLUT 4

- located in plasma membrane

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16
Q

GLUT 1

A

Located in red blood cells and brain cells

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17
Q

GLUT 2

A

Located in intestine, liver, kidney, and pancreas

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18
Q

GLUT 3

A

Located in brain, kidney, and placenta

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19
Q

GLUT 4

A

Located in muscle, adipose, and heart

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20
Q

In the absence of insulin, GLUT 4 exists in

A
  • Intracellular vesicles
  • When insulin binds to its receptors in these tissues, GLUT-4 is translocated to plasma membrane, where it causes facilitated transport of glucose
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21
Q

Expression of ___ increases in response to exercise and hypoxia to compensate for increased utilization of glucose by tissue

A

insulin receptors

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22
Q

GLUT 5

A

Located in muscle, spermatozoa

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23
Q

Type I diabetes

A
  • Due to deficiency of secretion of insulin, glucose will not be transported to muscle tissue
  • Due to lack of translocation of GLUT-4 transporter to the plasma membrane, contributing to hyperglycemia
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24
Q

Uptake of glucose by cells in body is

A

dependent or independent of the presence of insulin in the blood

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25
Q

Uptake of glucose by ___ does not require insulin

A

RBC, brain, and liver

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26
Q

Uptake of glucose by __ requires insulin

A

Muscle, heart, and adipose tissue

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27
Q

Fate of glucose in RBCs

A
  • Because RBCs lack mitochondria, glucose metabolizes to lactic acid via glycolysis
  • Pentose phosphate pathway is used to yield NADPH
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28
Q

Fate of glucose in Brain

A
  • Undergoes glycolysis to yield pyruvate
  • Used in pentose phosphate pathway to yield NADPH for lipid biosynthesis
  • Undergoes oxidative phosphorylation of pyruvate to yield ATP
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29
Q

Fate of glucose in Muscle and Heart

A
  • Glycolysis yields pyruvate and lactate
  • Goes through pentose phosphate pathway to yield NADPH for lipid biosynthesis
  • Pyruvate undergoes oxidative phosphorylation to yield ATP
  • Glycogenesis occurs to synthesize glycogen
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30
Q

Metabolic fate of glucose in Adipose tissue

A
  • Undergoes glycolysis to yield pyruvate, which is converted to acetyl CoA, a precursor for biosynthesis of fatty acids
  • Goes through pentose phosphate pathway to yield NADPH which is essential for lipid biosynthesis
  • Goes through glycogenesis to synthesize glycogen
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31
Q

Fate of glucose in liver

A
  • Undergoes glycolysis to yield pyruvate and lactate
  • Pyruvate is converted to acetyl CoA (precursor for biosynthesis of fatty acids)
  • Pentose phosphate pathway to yield NADPH, which is essential for lipid biosynthesis
  • Glycogenesis to synthesize glycogen
  • Gluconeogenesis
  • Drug detoxification
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32
Q

Enzymes that play a major role in regulating the flux of glucose

A
  • Hexokinase and Glucokinase
  • Phosphofructokinase-1 and Phosphofructokinase-2 (PFK-1 and PFK-2)
  • Pyruvate kinase
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33
Q

Hexokinase

A
  • Enzyme present in most tissues of body
  • Has low Km for glucose
  • Inhibited by product (glucose-6-phosphate)
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34
Q

Hexokinase low Km is helpful

A

to brain tissue as it can utilize glucose even when blood glucose levels are extremely low

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35
Q

Glucokinase

A
  • Isozyme of hexokinase
  • Present in liver cells
  • Has high Km for glucose
  • Converts glucose to glucose-6-phosphate
  • Not inhibited by G6P
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36
Q

Liver utilizes glucose only when

A

Blood glucose levels are elevated

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37
Q

Insulin causes

A

Increased transcription of glucokinase gene

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38
Q

Person who ate a carbohydrate-rich meal will have an increased amount of ___ released. This will result in

A
  • Increased amount of insulin released for circulation
  • This will result in increased synthesis of glucokinase enzyme which accelerates the conversion of glucose to G6P leading to increased glycolysis in liver
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39
Q

Livers of type 1 diabetic patients cannot

A
  • Upregulate the synthesis of glucokinase enzyme
  • this is due to lack of secretion of insulin by pancreas
  • Glucose cannot be utilized, leading to hyperglycemia
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40
Q

Phosphofructokinase-1

A
  • Converts F6P to F-1,6 bisphosphate

- Regulated by negative allosteric inhibitors and positive allosteric effectors

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41
Q

Negative allosteric inhibitors of Phosphofructokinase 1

A
  • ATP
  • Citrate
  • low pH inside cell
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42
Q

Positive allosteric effectors of Phosphofructokinase-1

A
  • AMP

- Fructose 2,6 bisphosphate

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43
Q

Role of negative allosteric effectors on PFK 1

A
  • Affinity of PFK 1 for substrate F6P is reduced in presence of high concentration of citrate or ATP
  • ATP shuts off glycolysis at PFK1 step
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44
Q

Most tissues in body prefer to utilize ___ for ATP production and thus spare ___ to be used by the brain

A
  • Utilize fatty acids and ketone bodies for ATP production

- Spare glucose

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45
Q

How does fatty acid or ketone body oxidation spare glucose?

A
  • Oxidations of fatty acid or ketone bodies produce acetyl CoA
  • acetyl CoA condenses with oxaloacetate to generate citrate
  • Citrate acts as negative allosteric effector of PFK 1, reducing glycolysis so glucose can be used by brain
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46
Q

Effect of intracellular pH on PFK 1

A
  • low intracellular pH inhibits PFK 1 activity
    • During anaerobic glycolysis, lactic acid is produced by the cell, which ionizes to yield lactate- and H+
    • Lactate and protons move out of cell by symport transport to keep pH inside cell constant
    • Lactic acid is washed out by blood circulation
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47
Q

During aerobic exercise or an attack of angina pectorisis

A
  • Lactic acid is produced, but lactate and H+ ions cannot diffuse out rapidly due to inadequate blood flow
  • Can be reversed by:
    • Terminating exercise
    • Angina: use therapeutic agents that increase blood flow
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48
Q

Lactic Acidosis

A
  • Decrease in blood pH and bicarbonate concentrations

- Administration of bicarbonate can alleviate acidosis

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49
Q

Fructose 2,6 BP is formed from

A

F6P by PFK 2

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50
Q

When glucose levels are low in blood stream

A
  • Glucagon is released by pancreas
  • Glucagon binds to receptor on plasma membrane of liver cells which results in
  • Activation of adenylate cyclase, to form cAMP
  • cAMP binds to protein kinase, causing
  • dissocation of catalytic subunits of protein kinase
  • Phosphorylation of PFK 2 by catalytic subunits causes inactivation of PFK 2, leading to decrease in F2,6 BP levels and glycolysis is inhibited at PFK1 step
51
Q

When levels of blood glucose are high

A

Insulin is released from pancreas which results in activation of phosphatase activity (removes phosphate from PFK2P), resulting in increase in intracellular levels of F2,6BP and stimulation of glycolysis

52
Q

In patients with type 1 diabetes who are unable to produce insulin

A

will not be able to utilize glucose or carry out glycolysis, culminating in hyperglycemia

53
Q

Pyruvate Kinase

A
  • Secondary site of regulation of glycolysis
54
Q

When intracellular levels of cAMP are high

A

Phosphorylation of pyruvate kinase occurs, causing inactivation of the enzyme and glycolysis is inhibited

55
Q

___ activates adenylate cyclase

A

Glucagon

56
Q

Fructose is converted to ___ by ___

A

Converted to fructose-1-phosphate by fructokinase

57
Q

___ converts dihydroxy acetone phosphate and glyceraldehyde

A

Aldolase B enzyme

58
Q

Glyceraldehyde is converted to ___ by ___

A

Converted to Glyceraldehyde 3 Phosphate by triose kinase

59
Q

Patients with hereditary fructose intolerance

A
  • deficient in aldolase B enzyme in liver
  • fructose 1 phosphate accumulates and ATP decreases
  • low ATP = increased PFK1 activity, increased glycolysis, and increased lactic acid formation
  • patient develops hypoglycemia and lactic acidosis
60
Q

Lactase

A

Converts lactose to glucose and galactose

61
Q

Galactose is converted to ___ by ___

A

Converted to galactose1phosphate by galactokinase

62
Q

Galatose-1-P with ___ is converted to ___ and ___ by ___

A

galactose 1P with UDP glucose is converted to glucose1P and UDP galactose with help of galactose-1-phosphate uridyl transferase

63
Q

G1P is converted to ___ by ___

A

converted to G6P by mutase

64
Q

Galactosemia

A
  • Genetic disease due to deficiency of galactose-1-phosphate uridyl transferase
  • high blood galactose levels–> galactose converted to galacitol –> cataract formation
65
Q

Excess glucose is stored in

A

Liver and skeletal muscle

66
Q

Muscle glycogen

A
  • most is cataboliized by glycolytic pathways to yield ATP
  • Small amount is converted to free glucose
  • Does not play significant role in maintaining blood glucose levels
67
Q

Glycogen in liver

A

Provides glucose to other peripheral tissues when glucose levels in blood are low

68
Q

Glucokinase vs. Hexokinase

A

Glucokinase works in liver, hexokinase works in other peripheral tissues

69
Q

Biosynthesis of all polysaccharides requires

A

Activated form of sugar in the form of UDP-glucose and UDP-galactose

70
Q

When levels of blood glucose are low ___ is released

A

Glucagon

71
Q

Glucagon causes activation of

A
  • adenylate cyclase, resulting in increased levels of cAMP.
  • cAMP activates protein kinase, which converts glycogen phosphorylase into phosphorylase a~P, which is active.
  • This causes a breakdown of glycogen to G-1-P.
  • At the same time, glycogen synthase a is phosphorylated by cAMP, resulting in its inactivation and thus glycogen synthesis does not occur
72
Q

In response to stress (liver)

A
  • epinephrine is released –> increased cAMP –> breakdown of glycogen stores in liver –> release of glucose
73
Q

When levels of blood glucose are low

A

Glucagon is released –> increased cAMP –> breakdown of glycogen and simultaneously, glycogen synthase is phosphorylated and inactivated so glycogen synthesis does not occur.

74
Q

When levels of blood glucose are high

A
  • insulin is released –> glycogen breakdown is shut off and simultaneously, glycogen synthase b is dephosphorylated and converted to glycogen synthase~a which promotes glycogen synthesis
75
Q

In response to stress (in muscle)

A

Epinephrine binds to adrenergic receptors –> breakdown of glycogen –> G6P formed and utilized by ATP synthesis by either glycolytic or oxidative phosphorylation pathways

76
Q

Muscle cells lack

A

Glucagon receptor

77
Q

In muscle, G6P is not hydrolyzed to free glucose because

A

Muscle tissue lacks the glucose-6-phosphatase enzyme

78
Q

Causes of hypoglycemia

A
  • Hereditary fructose intolerance (deficient in aldolase B enzyme in liver)
  • Deficiency in enzymes of glycogen breakdown (i.e. enzymes involved in glycogenolysis)
  • Von Geirke’s disease (malfunctioning/lack of glucose-6-phosphatase)
  • No gluconeogenesis
  • Affected enzymes:
    • Liver-glycogen phosphorylase
    • Muscle glycogen phosphorylase
  • Chronic alcohol consumption
  • Hypoglycemia is low blood glucose levels
79
Q

Causes of hyperglycemia

A
  • Type I diabetes: deficiency of secretion of insulin, inability to upregulate synthesis of glucokinase
  • Hyperglycemia is high blood glucose
80
Q

Von Geirke’s Disease

A
  • Ineffective glucose-6-phosphatase
  • Affects the liver
  • Leads to enlarged liver and kidney, growth failure, fasting, hypoglycemia, acidosis, and lipemia
81
Q

Effects of fasting in liver

A
  • Glucagon levels in blood are high, Tissue cAMP increases, glycogen breakdown increases, glycogen synthesis decreases
82
Q

Effect of high-carbohydrate meal in liver

A
  • Insulin in blood is high, tissue cAMP levels decrease, glycogen breakdown decreases, glycogen synthesis increases
83
Q

Effects of exercise and stress in liver

A
  • Levels of epinephrine in blood increase, tissue cAMP levels increase, glycogen breakdown increases, glycogen synthesis decreases
84
Q

Effect of fasting in muscle

A
  • Levels of insulin in blood are low, glycogen synthesis decreases (no effect on tissue cAMP or glycogen breakdown)
85
Q

Effect of high-carb meal in muscle

A

Insulin levels in blood are high, glycogen synthesis increases (no effect on tissue cAMP or glycogen breakdown)

86
Q

Gluconeogenesis

A
  • synthesis of glucose from non-carbohydrate precursors (i.e. from lactate, alanine, and glycerol)
  • Pathway maintains blood glucose during fasting or starvation to supply energy needs of the brain
87
Q

Malfunctioning liver-glycogen phophorylase leads to

A
  • Heptaomegaly

- Hypoglycemia

88
Q

Malfunctioning muscle-glycogen phosphorylase leads to

A
  • Exercise-induced muscular pain
  • Cramps
  • Progressive hypoglycemia
89
Q

Why does lactic acidemia (acidosis) occur

A

-Lactate is not converted to glucose via Gluconeogenesis

90
Q

Why does hyperlipemia occur?

A
  • Increased amounts of lactate –> lactate is converted to pyruvate –> pyruvate is converted to acteyl CoA which is a precursor for lipid biosynthesis
91
Q

High glucagon levels promotes

A

Lipolysis in adipose tissue, contributing to lipemia

92
Q

Organs where gluconeogenesis occurs

A
  • Liver

- Under extreme starvation, can occur in kidney

93
Q

Precursors for gluconeogenesis

A
  • Lactate
  • Gluconeogenic amino acids (alanine)
  • Glycerol
94
Q

Lactate is produced by

A

Anaerobic glycolysis in tissues such as RBCs or exercising muscle

95
Q

Amino acids for gluconeogenesis come from

A
  • protein in the diet
  • breakdown of proteins in skeletal muscle during starvation
  • Alanine is generated in the muscle from other amino acids
96
Q

Glycerol for gluconeogenesis is released from

A
  • Adipose tissue whenever the levels of glucagon or insulin or cortisol (stress hormones) are elevated
97
Q

___ cannot be utilized for the net synthesis of glucose

A
  • Fatty acid carbon atoms
98
Q

Differences in enzymes between glycolysis and gluconeogenesis

A
  • Glycolysis
    • Hexokinase/glucokinase
    • Phosphofructokinase
    • Pyruvate kinase
  • Gluconeogenesis
    • Glucose-6-phosphatase
    • Fructose 1,6 bisphosphatase
    • Pyruvate carboxylase
    • Phosphoenol pyruvate carboxykinase
99
Q

Energy required for gluconeogenesis

A
  • 6 moles of ATP required from lactate in liver

- Comes from breakdown of fat and concomitant oxidation of fatty acids

100
Q

Effects of chronic alcohol consumption

A
  • Hypoglycemia and lactic acidosis because:
    • Ethanol –> acetylaldehyde in liver by alcohol dehydrogenase, NAD+ –> NADH
    • Ratio of NADH/NAD+ increases, preventing conversion of lactate to pyruvate so gluconeogenesis stops, leading to hypoglycemia and lactic acidosis
101
Q

Glucose-6-phosphatase is present in ___ and absent in ___

A

Present in liver- therefore G6P is converted to glucose which is released into blood
Absent in muscle- therefore G6P undergoes catabolism for energy production

102
Q

Pentose phosphate pathway

A
  • Converts G6P to R5P (ribose-5-phosphate) and generates NADPH.
  • It utilizes glucose-6-phosphate dehydrogenase enzyme
103
Q

R-5-P is a precursor for

A
  • RNA
  • DNA
  • ATP
  • NAD
  • FAD
104
Q

Glucose 6 Phosphatase deficiency leads to

A
  • Hypoglycemia
  • Hyperuremia
  • Increased lactate
  • Increased cholesterol
  • Increased triglycerides
105
Q

Why does hyperuremia occur if patient has glucose-6-phosphotase deficiency?

A

More G6P is shunted into the pentose phosphate pathway, leading to more formation of R5P and uric acid

106
Q

Purpose of NADPH in pentose phosphate pathway

A
  • Utilized for biosynthesis of lipids
  • If generated in cell or tissue, it keeps glutathione in reduced state, which keeps proteins from forming S-S crosslinks, which prevents RBCs from becoming rigid/susceptible to hemolysis
107
Q

Patient with deficiency of glucose-6-P dehydrogenase- symptoms:

A
  • RBCs show signs of hemolytic anemia
    • Low NADPH levels causes S-S cross-linking in proteins, which leads to rigidity of membrane, which makes RBCs more susceptible to hemolysis
108
Q

Non-enzymatic glycosylation

A
  • Occurs when glucose binds to protein in the absense of enzyme
109
Q

Measurement of HbA1c is a diagnostic tool to assess

A
  • Metabolic control in diabetics

- Is independent of variables such as prior ingestion of food

110
Q

AGE Molecules

A
  • Advanced Glycation End Products
  • Accumlate in increased amounts in hyperglycemia and can cause cellular signaling
  • Cause deleterious effects in blood vessels, kidney, and retina
111
Q

High glucose levels in plasma leads to

A

Diabetes

112
Q

Deficiency of lactase enzyme leads to

A

Accumulation of lactose, resulting in diarrhea and cramps

113
Q

Deficiency of pyruvate kinase in RBCs leads to

A

Hemolytic anemia

114
Q

Deficiency of glucose-6-phosphatase leads to

A

Hypoglycemia

115
Q

Excess consumption of alcohol leads to

A

Hypoglycemic state, which can cause irreversible brain damage

116
Q

Deficiency of glucose-6-phosphatase can lead to

A
  • accumulation of glycogen in liver and hypoglycemia

- can be overcome by eating carbohydrate meal

117
Q

Deficiency of glycogen debrancher enzyme causes

A

Accumulation of glycogen (Cori’s Disease)

118
Q

Deficiency of muscle phosphorylase causes

A

Accumulation of glycogen (McCardle’s disease)

119
Q

Deficiency of glucose-6-phosphate dehydrogenase in RBCs leads to

A

hemolytic anemia

120
Q

Deficiency of galactokinase causes

A

Accumulation of galactose in tissues, leading to cataract formation, mental retardation, and liver damage

121
Q

Role of galactokinase

A

Converts galactose to galactose-1-phosphate

122
Q

Deficiency of galactose-1-phosphate uridyltransferase results in

A
  • Galactosemia (accumulation of galactose) which causes severe damage to tissues if it is not converted to glucose .
  • Results in cataract formation, growth failure, and mental retardation
123
Q

Main hormone that regulates gluconeogenesis

A

Glucagon

124
Q

Major source of energy for the survival of intestinal epithelial cells:

A

-Intestine does not metabolize glucose, so intestine uses glutamine as a source of energy

125
Q

Increase of ___ enzyme activity in liver leads to increased formation of F 2,6 BP

A

Phosphotase activity

126
Q

Only ___ pathway is affected by deficiency in glucose-6-phosphate dehydrogenase

A

Pentose Phosphate pathway

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