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Human Nutrition > Carbs part two > Flashcards

Carbs part two Flashcards

1
Q

The synthesis of glycogen from glucose

A

Glycogenesis

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2
Q

the breakdown of glycogen to glucose

A

Glycogenolysis

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3
Q

The breakdown of glucose

A

glycolysis

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4
Q

Cycle that breaks down acetyl coA and represents completion of glucose oxidation

A

Tricarboxylic acid (TCA) cycle

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5
Q

process wherein electrons are passed from a series of donors and acceptors, ultimately resulting in ATP production

A

Electron Transport Chain

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6
Q

the production of glucose from non-carbohydrate intermediates

A

gluconeogenesis

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7
Q

What are, arguably, the two most important tissues when discussing glucose metabolism?

A

Liver
muscle

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8
Q

what takes up approx 20% circulating glucose and regulates blood glucose by breaking down liver glycogen and also undergoing gluconeogenesis?

A

Liver

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9
Q

what takes up approx 80% of circulating glucose?

A

muscle

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10
Q

Where does glycogenesis occur?

A

predominately in muscle and liver

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11
Q

when does glycogenesis occur?

A

During periods of energy excess

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12
Q

Is glycogenesis an anabolic or catabolic reaction?

A

Anabolic

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13
Q

Is glycogenesis energy producing or energy consuming?

A

consuming

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14
Q

What happens to glucose as soon as it enters the cell in glycogenesis?

A

glucose is phosphorylated, producing glucose-6-phosphate.

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15
Q

What enzyme catalyzes glucose in the liver for step one of glycogenesis?

A

glucokinase (hexokinase IV)

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16
Q

What enzyme catalyzes glucose in the muscle for step one of glycogenesis?

A

hexokinase

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17
Q

in glycogenesis, Where does the phosphate transfer too after G-6-P is produced? what does it produce?

A

C6 to C1, producing glucose-1-phosphate

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18
Q

what state is glucose in when UDP-glucose is formed?

A

“activated”

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19
Q

In glycogenesis, what is the product of Uridine Monophosphate (UMP) coupling to G-1-P?

A

Uridine diphosphate-glucose (UDP-glucose)

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20
Q

In glycogenesis, what powers the coupling of UMP to G-1-P, forming UDP-glucose?

A

Uridine triphosphate (UTP) hydrolysis

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21
Q

In glycogenesis What protein forms a short chain of up to 8 units of glucose molecules?

A

glycogenin

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22
Q

What bond forms when UDP-Glucose molecules attach to glycogenin in step 4 of glycogenesis?

A

alpha 1-4 bonds.

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23
Q

In glycogenesis, what enzyme further extends glycogen chains over 8 units of glucose molecules?

A

glycogen synthase

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24
Q

In glycogenesis, what enzyme creates the a1,6 bonds at branching points?

A

branching enzyme

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25
Q

what is a highly branched arrangement of glucose molecules consisting of a(1-4) and a(1-6) glycosidic bonds?

A

glycogen

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26
Q

Does glycogen have more or less branch points than amylopectin?

A

more

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27
Q

What are the 3 possible fates of glucose 6 phosphate?

A
  1. Glycolysis (burn)
  2. Glycogenesis
  3. (liver exclusive) hydrolyzed by G-6-Pase and exported via GLUT transporter membrane as a free glucose molecule
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28
Q

When UDP-Glucose molecule attach to glycogen, it attaches the first _ units of glucose molecules.

What type of bond?

A

8

alpha 1-4 bonds.

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29
Q

after 8 units of glucose molecules have been attached to glycogen, what enzyme extends glycogen chains further?

A

glycogen synthase (alpha 1-4 bonds).

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30
Q

What type of response is G-6-P allosterically inhibiting hexokinase?

A

Negative Feedback Loop

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31
Q

What type of reaction does insulin have?

anabolic/catabolic

A

anabolic

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32
Q

Is glucose uptake in the liver insulin dependent?

A

Insulin promotes glucose uptake in liver, but not directly. Insulin indirectly promotes uptake by increasing phosphorylation (trapping) and utilization of glucose.

The liver has other glucose transporters not insulin dependent (GLUT 1,2,3)

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33
Q

What inhibits glycogen synthesis?

A

glucagon and epinephrine

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34
Q

What is the difference between glucagon and epinephrine

A

Glucagon works in the liver
epinephrine works in the muscle

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35
Q

What type of relationship does glycogen synthase and glycogen phosphorylase have?

A

Reciprocal/Inverse. The stimulation of one inhibits the other just as much.

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36
Q

What Glucose transporter provides glucose entry into the cell in the Liver?

A

Glut 2

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37
Q

What Glucose transporter provides glucose entry into the cell in the muscle?

A

GLUT 4

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38
Q

What enzyme causes glucose phosphorylation in the liver?

A

Glucokinase

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39
Q

What enzyme causes glucose phosphorylation in the Muscle?

A

Hexokinase

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40
Q

Is there negative feedback inhibition of G6P on glucokinase?

A

No

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41
Q

Is there negative feedback inhibition of G6P on hexokinase?

A

Yes

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42
Q

Is insulin needed for activation of glucokinase?

A

yes

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43
Q

Is insulin needed for activation of hexokinase?

A

yes

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44
Q

does insulin activate glycogen synthase in the liver?

A

yes

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45
Q

does insulin activate glycogen synthase in the muscle?

A

yes

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46
Q

Is Glucose 6 phosphatase present in the liver?

A

yes

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47
Q

Is Glucose 6 phosphatase present in the muscle?

A

no

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48
Q

are there glucagon receptors present in the liver?

A

yes

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49
Q

are there glucagon receptors present in the muscle?

A

no

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50
Q

Is glycogen phosphorylase present in the liver?

A

yes

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51
Q

Is glycogen phosphorylase present in the muscle?

A

yes

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52
Q

What regulates glycogen synthase and glycogen phosphorylase?

A

Insulin
glucagon in the liver
epinephrine
local factors

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53
Q

What does Glucose-6-phosphatase do?

A

Located in the liver, maintains euglycemia by converting G-6-P to free glucose

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54
Q

How does glycogenolysis maintain euglycemia?

A
  1. turns G6P into glucose molecules via G-6-Pase
  2. Glycolysis
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55
Q

What is the breaking down of glycogen to individual glucose units?

A

Glycogenolysis

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56
Q

Where does glycogenolysis primarily take place?

A

primarily in liver and muscle

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57
Q

what stimulates glycogenolysis?

A

during periods of energy deficit

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58
Q

is glycogenolysis an anabolic or catabolic reaction?

A

catabolic

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59
Q

What does glycogen produce when it is cleaved by glycogen phosphorylase at the start of the glycogenolysis process?

A

glucose-1-phosphate and the residual glycogen chain

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60
Q

What does glucose-1-phosphate convert into after it is cleaved by glycogen phosphorylase in glycogenolysis?

A

glucose-6-phosphate
(G-6-P)

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61
Q

what can glucose-6-phosphate do after being converted from G-1-P in glycogenolysis?

A
  1. glycolysis for oxidation
  2. converted to free glucose via glucose-6-phosphatase
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62
Q

Why does muscle glycogen not enter circulation?

A

muscle lacks glucose-6-phosphatase

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63
Q

What process is the breaking down of glucose to pyruvate?

A

Glycolysis

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64
Q

Where does glycolysis occur at in the cell?

A

in the cytoplasm of all cells

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65
Q

When does glycolysis occur?

A

during periods of demand

example: exercise

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66
Q

is glycolysis an anabolic or catabolic reaction?

A

catabolic

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67
Q

Is glycolysis energy yielding or energy consuming?

A

energy yielding

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68
Q

What step in the metabolic breakdown of glucose is glycolysis?

A

First step

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69
Q

What does glycolysis yield?

A
  1. 2 ATP
  2. 2 three-carbon pyruvate molecules
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70
Q

Does glycolysis function under aerobic or anaerobic activity?

A

both aerobic and anaerobic

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71
Q

What steps are the “Investment phase” of glycolysis?

A

steps 1-5

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72
Q

What steps are the “payoff” phase of glycolysis?

A

steps 6-10

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73
Q

How does the muscle differ from the liver during glycogenesis?

A
  1. G-6-P will inhibit hexokinase in the muscle, but not in glucokinase. It gets to choose how much glucose to take in.
  2. The muscle does not shuffle glucose out to the stream.
74
Q

Once G-6-P enters the cell and it’s fate is glycolysis, What does it convert into?

A

Fructose-6-P

75
Q

In glycolysis, What is the enzyme that phosphorylates F-6-P to form fructose-1,6-bisphosphate?

A

PFK - Phosphofructokinase

76
Q

Can F-1,6-BP turn back into F-6-P?

A

No

77
Q

How is glycolysis regulated?

A

Increase in AMP (cell needs energy)
Decrease in ATP and citrate (energy needs met)

78
Q

Does F-6-P catalyzed by PFK-1 use ATP when forming F-1,6-BP?

A

yes

79
Q

What has been invested in glycolysis?

A

2 ATP
two 3C molecules of G-3-P.

80
Q

In glycolysis, what is formed when an inorganic P is added to G-3-P?

A

1,3 Bis P glycerate (1,3-BPG)

81
Q

In glycolysis, what is formed when PEP donates the P to ADP in the final step?

A

ATP and Pyruvate

82
Q

What is the starting product and what is the ending product of glycolysis?

A

Started with glucose
ended with ATP and pyruvate (net 2 ATP)

83
Q

Investment or Payoff phase of glycolysis?

2 ATP are used to form 2-G3P molecules from one molecule of glucose

A

Investment Phase

84
Q

Investment or Payoff phase of glycolysis?

4ATP are formed via substrate level phosphorylation; 2NADH; 2 pyruvate

A

Payoff phase

85
Q

The disaccharide maltose, upon hydrolysis will yield:

A

2 glucose units

86
Q

Which of the following indicates high energy demand in a cell?

a. Increased AMP concentration
b. Increased ATP concentration

A

Increased AMP concentration

87
Q

Glycogenolysis in skeletal muscle occurs because of the action of the enzyme _____, which is stimulated by the hormone ______.

A

Glycogen phosphorylase, epinephrine

88
Q

After glycolysis, what is the metabolic pathway that completes the oxidation of glucose?

A

TCA cycle

89
Q

Where does the TCA cycle occur?

A

mitochondria

90
Q

What are the three fates of pyruvate created from glycolysis

A
  1. Oxidative decarboxylation
  2. Lactate- Intercellular Shuttle
  3. Lactate- Intracellular shuttle
91
Q

What shuttle operates by converting oxaloacetate into malate using NADH and the enzyme malate dehydrogenase (MDH) in the cytosol. Malate then enters the mitochondria, where MDH reverses the reaction, converting malate back to oxaloacetate and regenerating NADH. To complete the shuttle cycle, oxaloacetate is transformed into aspartate via aspartate transaminase (AST) and exits the mitochondria where it can be converted back into oxaloacetate.

A

Malate-Aspartate Shuttle

92
Q

What shuttle uses a different mechanism to transport electrons from NADH to the ETC. In the cytosol, glycerol-3-phosphate dehydrogenase uses NADH to convert DHAP into glycerol-3-phosphate. Once at the inner mitochondrial membrane, membrane-bound glycerol-3-phosphate dehydrogenase turns glycerol-3-phosphate back to DHAP, generating FADH2 in the process. FADH2 moves its electrons to the ETC via CoQ. This shuttle is less efficient

A

Glycerol-Phosphate shuttle

93
Q

What 2 shuttles can the lactate formed from pyruvate take?

A

One of two ways.
1. Intercellular
2. intracellular

94
Q

Is “cell-to-cell - the Cori cycle” Intercellular or Intracellular?

A

Intercellular

95
Q

Is Lactate being shuttled into mitochondria where it undergoes oxidation to pyruvate by way of mitochondrial LDH Intercellular or intracellular

A

Intracellular

96
Q

Lactate is
a. a waste product produced of metabolism
b. formed only under anaerobic conditions
c. the cause of muscle soreness
d. none of the above

A

d. none of the above

97
Q

Why can’t lactate be converted into glucose via gluconeogenesis in the muscle?

A

because the muscle doesn’t have glucose-6-phosphate

98
Q

How is lactate transported to the liver?

A

intercellular shuttle (the Cori Cycle)

99
Q

What happens to lactate when it gets to the liver?

A

converted to glucose via gluconeogenesis.

100
Q

When lactate is turned into glucose in the liver, what tissue uses it for energy when it returns to the blood stream?

A

used by the muscle as an energy source

101
Q

What cycle refers to:
movement of lactate out of the cell>to liver>convert to glucose>goes to muscle as energy source

A

the Cori Cycle

102
Q

In Intracellular transport, what transporter does pyruvate and lactate enter the mitochondria through?

A

monocarboxylate transporter (MCT)

103
Q

What is formed in the ETC that is needed for the TCA cycle and glycolysis?

A

NAD

104
Q

what is the formation of glucose from non-carbohydrate precursors

A

gluconeogenesis

105
Q

Where does gluconeogenesis occur at?

A

Liver, Kidney, Intestine

106
Q

When does gluconeogenesis occur?

A

Periods of low blood glucose

107
Q

Is gluconeogenesis energy producing or energy consuming?

A

energy consuming

108
Q

how does the body maintain blood glucose levels approximately 4 hours after a meal?

A

Glucose from that meal can no longer sustain blood glucose concentrations, so the body first starts to break down liver glycogen.

109
Q

how does the body maintain blood glucose levels approximately 12-18 hours after a meal?

A

liver glycogen stores will run low, and in order to maintain glucose levels, the body will make glucose from non carbohydrate precursors via gluconeogenesis.

110
Q

How does gluconeogenesis differ from glycolysis?

A

gluconeogenesis synthesizes glucose, consumes ATP and uses NADH. glycolysis burns glucose, produces ATP and uses NAD+.

111
Q

Substances that enter the pathway.

A

precursors

112
Q

What are three gluconeogenesis precursors?

A
  1. Pyruvate/lactate
  2. glycerol
  3. glucogenic amino acids
113
Q

How is glycerol a precursor for gluconeogenesis?

A

from mono, di, and triglycerides
-but not fatty acids

114
Q

what state does gluconeogenesis occur?

A

fasting state

115
Q

what is PEPck?

A

PEP carboxykinase

116
Q

What relationship does glycolysis and gluconeogenesis have?

A

reciprocal/inverse

117
Q

What is an alternative pathway for glucose oxidation that does not generate ATP?

A

Pentose Phosphate pathway

118
Q

What are products of the pentose phosphate pathway?

A

NADPH and ribose-5-phosphate

119
Q

what product of the pentose phosphate pathway can lead to an increase in uric acid production and used for synthesis of nucleotides and nucleic acids?

A

ribose-5-phosphate

120
Q

What product of the pentose phosphate pathway is used for various pathways including lipid synthesis?

A

NADPH

121
Q

When is the pentose phosphate pathway increased?

A

following a high carb meal

122
Q

Does the pentose phosphate pathway happen with a lot of glucogenesis or glycolysis?

A

glycolysis

123
Q

What pathway is a “detour from glycolysis”?

A

pentose phosphate pathway

124
Q

what glycogen storage disease describes:
Exercise intolerance with muscle pain and cramps

lactate levels fail to increase (and may decrease) after intense exercise

Rhabdomyolysis: breakdown of damaged muscle cells and release into blood stream; can cause renal stress and eventual failure

patients tend to feel “second wind” after approx. 10 min of exercise.

A

McArdle’s Disease (GSD-V)

125
Q

Why do patients tend to feel a “second wind” after 10 minutes of exercise?

A

they lack glycogen-phosphorylase. after 10 minutes, the fat starts to breakdown to provide energy.

126
Q

What nutritional intervientions help exercise tolerance for McArdle’s Disease?

A

Ketogenic diet

127
Q

What glycogen storage disease describes:
Most common of all glycogen storage diseases (~1 in 50,000 births)

severe hypoglycemia, increased glycogen in liver and kidney

hepatomegaly (enlarged liver) develops in childhood

A

Van Gierke’s Disease (GSD I)

128
Q

What is a:
mixture of fructose and glucose
55-65% fructose (35-45% glucose)
a major sweetener in most food products

A

High fructose corn syrup
(HFCS)

129
Q

Fructose is cheaper and sweeter (g for g) than _____ or ______.

A

sucrose or glucose

130
Q

what are two major dietary sources of fructose?

A
  1. sucrose
  2. High fructose corn syrup
131
Q

how much of fructose taken up by the liver in the first pass?

A

~75%

132
Q

Why is Fructose dangerous?

A

contributes to Fatty Liver and Very Low Density Lipoproteins (VLDLs)

133
Q

How does overconsumption of fructose contribute to ATP depletion? what is a product?

A

ATP is used to phosphorylate fructose. when you can’t remake ATP fast enough, there starts to be ATP depletion; resulting in uric acid.

134
Q

what major regulatory step in glycolysis does fructose skip resulting in an increase in acetyl CoA?

A

Phosphofructokinase

135
Q

What is a result of fructose bypassing PFK and increasing acetyl CoA?

A

some acetyl CoA is converted to fat. an increase of acetyl CoA increase risk of obesity and fatty liver, and increased VLDL secretion from liver

136
Q

What describes a group of diseases marked by a high level of glucose?

A

Diabetes

137
Q

What group of diseases is a result from defects in insulin production, insulin action, or both?

A

diabetes

138
Q

Auto-immune disorder in which the body’s immune system destroys the pancreatic beta cell, where insulin is produced

A

Type I Diabetes

139
Q

Is Type I diabetes typified by insulin deficiency or insulin resistance?

A

Insulin deficiency

140
Q

what rapidly breaks down when there is lack of insulin?

A

fat and muscle

141
Q

lack of what hormone causes fat and protein breakdown in the muscle cell?

A

insulin

142
Q

What is a disorder in which the body does not adequately utilize the insulin produced by the pancreas?

A

Type II diabetes

143
Q

What term describes the inability to adequately use insulin?

A

Insulin resistance

144
Q

What diabetes accounts for 95% of diabetes cases in adults?

A

Type II diabetes

145
Q

What is a systemic consequence of insulin resistance in fat cells?

A

Increase in lipolysis (breakdown of fat)

146
Q

What is a systemic consequence of insulin resistance in the liver?

A

Increase in hepatic glucose output (gluconeogenesis)
Increase in VLDL production

147
Q

What is a systemic consequence of insulin resistance in muscle?

A

Decrease in glucose uptake due to inability to bind to GLUT4

decrease in glycogen synthesis due to lack of glycogen synthase

148
Q

What is a systemic consequence of insulin resistance in blood vessel?

A

decrease in vasodilation ability (vessel constriction)

149
Q

For the A1C test what is the diagnostic criteria percentage for diagnosing diabetes?

A

at or above 6.5% with a positive test

150
Q

For the Fasting plasma glucose test what is the diagnostic criteria for diagnosing diabetes?

A

at or above 126 mg/dL with a positive test (no caloric intake for atleast 8 hours)

151
Q

For the 2-hour plasma glucose test what is the diagnostic criteria for diagnosing diabetes?

A

at or above 200 mg/dL after 75 g of glucose in water

And positive test

152
Q

For the random plasma glucose test what is the diagnostic criteria for diagnosing diabetes?

A

at or above 200 mg/dL in a patient with symptoms of hyperglycemia

153
Q

What are the three tests used to diagnose diabetes?

A
  1. A1C test
    2.a fasting plasma glucose test
  2. an oral glucose tolerance test
154
Q

What happens to glycogen in the liver during exercise?

A

glycogenolysis. want glucose to travel to muscle.

155
Q

What happens to blood glucose in the muscle during exercise?

A

glycogenolysis. want glucose to make ATP to use in the muscle

156
Q

How is blood glucose regulated during exercise?

A

As it goes from liver to blood blood glucose concentration is increased

goes from blood to muscle - decrease

157
Q

When doing high intensity exercise, does blood glucose increase or decrease?

A

decrease because demand is so high

158
Q

Type 2 diabetes progresses from _____ to ______.

A

insulin resistance

diabetes

159
Q

Type 2 diabetes progresses from insulin resistance to diabetes over

a. weeks
b. years
c. decades
d. both b and c

A

d. both b and c

160
Q

With type 2 diabetes progression, what does the pancreatic beta cell do to normalize glucose levels?

A

compensates by increasing insulin secretion

161
Q

In type 2 diabetes progression, What results in the beta cells beginning to fail thus insulin secretion failing?

A

hyperglycemia

162
Q

In type 2 diabetes progression, what is required to maintain blood glucose after the pancreatic beta cells begin to fail?

A

exogenous insulin

163
Q

What is a limitation of the hbA1C diagnostic test?

A

Can’t use it for pregnant women because 3 months (the turnover rate of blood) will be drastically changing.

164
Q

What is a limitation of the fasting plasma glucose test?

A

You can have insulin resistance, but because of increased insulin production blood glucose may look normal.

165
Q

What is a limitation of an oral glucose tolerance test?

A

the load of glucose will be metabolized differently in varying body weight/sizes.

166
Q

Regarding Progression of Diabetes, what does this line represent?
a. Insulin Resistance
b. Insulin Production
c. Fasting Blood Sugar

A

a. Insulin resistance

167
Q

Regarding Progression of Diabetes, what does this line represent?
a. Insulin Resistance
b. Insulin Production
c. Fasting Blood Sugar

A

b. Insulin Production

168
Q

Regarding Progression of Diabetes, what does this line represent?
a. Insulin Resistance
b. Insulin Production
c. Fasting Blood Sugar

A

c. Fasting blood sugar

169
Q

Does this graph represent someone with or without diabetes after a normal meal?

A

without diabetes

starts below 126 mg/dl
low after 2 hours

170
Q

Does this graph represent someone with or without diabetes after a normal meal?

A

with diabetes

starts above 126 mg/dL
high after 2 hours

171
Q

What does glucagon stimulate?

A

glycogenolysis and gluconeogenesis
the breakdown pathways

172
Q

How can glucagon make diabetes worse?

A

both glycogenolysis and gluconeogenesis puts sugar in the blood.

173
Q

Is T1D and T2D associated with hyper or hypoglucagonemia?

A

hyperglucagonemia

174
Q

Condition in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy, especially in 3rd timester?

A

gestational diabetes

175
Q

How many pregnancies are affected by gestational diabetes?

A

3-10%

176
Q

is gestational diabetes symptomatic or asymptomatic?

A

asymptomatic

177
Q

How is gestational diabetes diagnosed?

A

Either OGTT or FGT.

Never A1C

178
Q

Do gestational diabetes symptoms resolve?

A

Symptoms resolve following pregnancy

179
Q

What are gestational diabetes risks the baby may have?

A

excessive birth weight
initial low blood sugar
childhood obesity
type 2 diabetes later in life

180
Q

What are gestational diabetes risks the mother may have?

A

Pre-eclampsia during pregnancy
difficult delivery
Increased risk of type 2 diabetes especially if GD required exogenous insulin

181
Q

How is gestational diabetes thought to be a natural phenomenon?

A

Placental hormones thought to mediate the insulin resistance

Most women become insulin resistant during pregnancy, which is thought to secure glucose supply to the growing fetus

Human Nutrition (5 decks)

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