3. Glucose and Carbohydrate Metabolism (Part I) Flashcards

1
Q

What is glucose converted to in order to store energy?

A
  • Glycogen (short-term)

- Fat (long-term)

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2
Q

Which cells solely utilize glycolysis?

A
  • RBCs

- They do not possess organelles to utilize the TCA cycle, lipid metabolism, etc.

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3
Q

Which tissues require glucose for proper function?

A
  • Brain
  • RBCs
  • Mammary gland
  • Fetus
  • Spermatogenesis
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4
Q

What does the gut utilize as a fuel?

A

Glutamate (NOT glucose)

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5
Q

What is the consequence of advanced glycation end-products (AGEs)? Give an example.

A
  • They may damage the function of the protein

- Ex: hemoglobin A1C

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6
Q

What is the precursor of amino acids’ carbon skeleton?

A

Glucose

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7
Q

What is the most basic amino acid? What is it made of?

A
  • Alanine

- Pyruvate with an amino group

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8
Q

All of the amino acids in the body arise from ________, except for ________.

A

glucose

tyrosine

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9
Q

How is tyrosine produced? Why is it unique?

A
  • Produced from phenylalanine as it gets hydroxylated on its aromatic ring
  • Unique as it is the only amino acid that is NOT made from glucose
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10
Q

What does glucose prevent?

A

Ketosis

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11
Q

Why shouldn’t pregnant women NOT be on low-carbohydrate diets?

A

It is incredibly damaging to the fetus to lack glucose (possible ketosis could be fatal)

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12
Q

How is glucose absorbed? Where is it transported to?

A
  • Absorbed within enterocytes

- Transported to the liver through the hepatic portal vein

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13
Q

What does the liver do with glucose?

A
  • Store glucose as glycogen and/or

- Synthesize fat

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14
Q

What is the response of the pancreas to glucose?

A

Senses hyperglycemia, and produces insulin

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15
Q

What fuel sources may adipose and muscle utilize?

A

Either glucose or fat

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16
Q

What type of carbohydrate may be acquired from the diet?

A
  • Fibre
  • Starches
  • Sugars
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17
Q

How much do carbohydrates constitute the AMDR?

A

45-65%

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18
Q

What should we emphasize concerning dietary carbohydrates?

A
  • Emphasis on whole grains
  • Emphasis on more fibre
  • Emphasis of low-glycemic index carbohydrates (less simple sugars)
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19
Q

What dietary sources contain high amounts of glycogen?

A

There is no significant source of glycogen within the diet

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20
Q

Where is glycogen found?

A
  • Liver

- Muscle

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21
Q

Differentiate hexoses and pentoses.

A
  • Hexoses: 6 carbons

- Pentoses: 5 carbons (e.g. ribose)

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22
Q

What is the ratio for C:H:O in carbohydrates?

A

1:2:1

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23
Q

What is the chemical formula for hexoses? What is the formula weight?

A
  • C6H12O6

- 180 grams

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24
Q

What are the single sugar units?

A
  • Glucose
  • Galactose
  • Fructose
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25
Q

How does fructose differ from the other monosaccharides?

A

Fructose is a hexose, but it is a five-membered ring

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26
Q

How are glycosidic bonds produced? What are the different types?

A
  • Dehydration reaction (removes an H2O) between carbon 1 and carbon 4
  • Alpha bond
  • Beta bond
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27
Q

Differentiate an alpha and beta glycosidic bond.

A
  • Alpha bond: hydrogens are pointing on the same side

- Beta bond: hydrogens are pointing on opposite sides

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28
Q

What is sucrose composed of?

A

Glucose and fructose

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29
Q

What is maltose composed of?

A

Glucose and glucose

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30
Q

What is lactose composed of?

A

Galactose and glucose

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31
Q

What is the sweetness scale of monosaccharides and disaccharides (from high to low)?

A
  • Fructose (twice as sweet as sucrose)
  • Sucrose
  • Glucose
  • Maltose
  • Lactose
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32
Q

How may sugars be used as a preservative?

A

Canned fruits in a sugar syrup tie-up free water, decreasing bacterial growth

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33
Q

Starches are polymers of ________.

A

glucose

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34
Q

What chains are present in amylose?

A

a(1-4) chains

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35
Q

What chains are present in amylopectin?

A

a(1-4) chains with a(1-6) branches

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36
Q

Does amylose or amylopectin have gel-forming abilities? Why?

A
  • Amylopectin

- Due to their branching pattern, which allows them to hold more water

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37
Q

Fibre is acquired from _______.

A

plants

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38
Q

What is soluble fibre? Give examples.

A
  • Soluble fibers form GELS

- Pectins (found in fruits) and oatmeal

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39
Q

What is insoluble fibre? Give examples.

A
  • Forms the cell walls of plants, providing structure

- Cellulose, hemicellulose

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40
Q

What is functional fibre? Give an example.

A
  • Fibre that has been added in food processing

- Psyllium is added to cereals to increase fibre intake

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41
Q

What is psyllium?

A

A functional fibre

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42
Q

What is the fibre requirement for men and women?

A
  • Women: 25 grams

- Men: 38 grams

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43
Q

How much fibre does the Quebec population intake on a daily basis?

A

8 to 15 grams per day

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44
Q

What are the functions of soluble fibre?

A
  • Delays gastric emptying
  • Glycemic control
  • Binds cholesterol and bile acids
  • Fermented by colonic bacteria
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45
Q

Which type of fibre forms a viscous gel?

A

Soluble

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46
Q

How does soluble fibre increase glycemic control?

A
  • Digestion and absorption take place over a greater length of time, and a greater length of the intestine
  • Glucose is absorbed more slowly, allowing a more moderate increase in plasma glucose
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47
Q

How is soluble fibre linked to cholesterol status?

A
  • Soluble fibre binds cholesterol and bile acids, which are excreted in feces
  • This allows the body to synthesize more bile acids from cholesterol, which reduces cholesterol levels
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48
Q

How do we acquire energy from fibre, even if we don’t digest fibre?

A

Soluble fibre provides energy for the cells in the lining of the colon, as it is fermented by colonic bacteria

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49
Q

Which carbohydrate may influence the types of bacteria that populate the colon?

A

Soluble fibre

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50
Q

What are the functions of insoluble fibre?

A
  • Provides bulk (laxative, water-holding effect)
  • Delays gastric emptying (but does not form a gel)
  • Some glycemic control (not as much as soluble)
  • Binds cations
  • Minor fermentation by colonic bacteria
51
Q

What does insoluble fibre contain that binds cations? Which cations are bound? Is this a desired effect?

A
  • Phytates (anions) bind cations
  • Calcium, zinc, iron, and other positive minerals
  • NOT a desired effect given the commonality and effets of these deficiencies
52
Q

How is insoluble fibre negatively associated with iron absorption?

A
  • The phytates bind iron

- Iron is already negatively absorbed from the start (10-15%)

53
Q

How is fibre associated with softer stools?

A
  • Fibre is hydrophilic, meaning that they hold onto water
  • Fibre prevents water from being reabsorbed in the colon
  • Produces a laxative-type effect
54
Q

Where was the idea of glycemic index proposed? When?

A
  • 1980s

- University of Toronto

55
Q

Would an individual with a high-fibre intake excrete components from a meal faster than an individual with a low-fibre intake?

A
  • High-fibre intake increases the speed of excretion

- It delays gastric emptying, but fibre increases the motility of the GI tract and speeds transit time overall

56
Q

What does the glycemic index measure?

A

Measures how rapid, and how high, the blood glucose increases after consuming a standard amount of carbohydrate in food

57
Q

What is the blood glucose level in the fasted state? What should it not go above?

A
  • Fasted state: 5 mM/L

- Should not increase to over 7 mM/L

58
Q

What is the standard of the glycemic index?

A
  • Glucose

- Represents 100

59
Q

How many salivary glands do we possess? What is their function?

A
  • Six

- Moistens the food and helps us taste

60
Q

What is the function of salivary amylase?

A

Breaks the a(1-4) bonds

61
Q

Why are proteins, such as salivary amylase, no longer functional in the stomach?

A

Due to low pH, which changes the charges of the proteins

62
Q

What does the pancreas release in response to food in the small intestine?

A

Pancreatic juice through the pancreatic duct into the duodenum

63
Q

What is the function of bicarbonate in the pancreatic juice?

A

Increases pH, rising it to a slightly alkaline state

64
Q

What is contained in pancreatic juice?

A
  • Pancreatic enzymes (pancreatic amylase, glucoamylase, etc.)
  • Bicarbonate
65
Q

Where are disaccharides digested?

A

On the brush border of the small intestine (apical surface of enterocytes)

66
Q

Describe the various layers of complexity to the small intestine.

A
  • The tube itself has folds
  • Every fold has villi
  • Each villus has individual cells (columnar)
  • The cells have finger-like projections (brush-border)
67
Q

Where do surface enterocytes arise from? What is important about this process?

A
  • Arise from crypts, migrate up, and are sloughed off the top
  • The process takes three days, and is metabolically expensive
  • But, it is important for the barrier to remain intact by the renewal of these cells
68
Q

How do chylomicrons enter the lymphatic system?

A

Through the lacteal, and are dropped off to the heart for dilution

69
Q

How do water-soluble nutrients enter circulation?

A

They are transported to the liver through the hepatic portal vein

70
Q

What transports monomers into the enterocytes?

A

Active transporters

71
Q

Which enzymes are contained in the mouth, small intestinal lumen, and small intestinal brush-border?

A
  • Mouth: salivary amylase
  • Small intestinal lumen: pancreatic amylase, glucoamylase
  • Small intestinal brush-border: sucrase-isomaltase, lactase
72
Q

How does lactose intolerance cause flatulence and diarrhea?

A
  • Flatulence: lactose reaches the colon where it is fermented by bacteria, which produces methane, hydrogen, CO2
  • Lactose and the resulting organic acids are strongly hydrophilic, which causes osmotic diarrhea
73
Q

How may a breath hydrogen test diagnose whether an individual has lactose intolerance?

A

Hydrogen produced within the colon through bacterial fermentation may be reabsorbed back into the body and secreted in the lungs

74
Q

Which enzyme deficiency results in the inability to digest lactose in the small intestine?

A
  • B-galactosidase deficiency

- Since there are no other enzymes that can digest the B(1-4) glycosidic bond

75
Q

What are the three types of lactose intolerance?

A
  • Primary lactase non-persistence
  • Secondary lactose intolerance
  • Congenital lactose intolerance
76
Q

What percentage of adults worldwide does primary lactase non-persistance affect? What is it?

A
  • 70%

- After weaning, lactase is no longer produced

77
Q

What causes primary lactase persistence? What kind of inheritance causes it?

A
  • Mutation for lactase persistence
  • SNP in the regulatory region (intron)
  • Autosomal dominant
78
Q

What is secondary lactose intolerance?

A
  • Due to some pathology

- Ex: parasite infection, celiac disease, malnutrition

79
Q

What is congenital lactose intolerance?

A
  • Non-functioning lactase (from birth)
  • Uncommon
  • Infants must utilize lactase-free formula, and cannot drink breast milk
80
Q

How did primary lactase persistence arise?

A
  • When individuals (particularly in colder climates), in which ruminants were bred to produce milk, caused a genetic SNP
  • Allows individuals to utilize the nutrients from another specie
  • Nutrition influenced natural selection
81
Q

How may Celiac disease cause lactose intolerance and malnutrition?

A

Destroys the villus architecture in the small intestine

82
Q

Where are the SNPs for lactase persistence found?

A
  • Not in the exon (target for mRNA)
  • Found to enhance transcription from the lactase promoter
  • Related to enhanced expression of the LCT promoter
83
Q

What causes a milk allergy?

A
  • Exaggerated immune response to proteins or to peptides found in milk
  • IgE antibodies
  • Mast cell degranulation
  • Massive histamine production (anaphylaxis)
84
Q

What is the driver of glucose absorption? Where are they contained?

A
  • Na+/K+ ATPase

- Contained in large numbers on the basolateral surface of enterocytes

85
Q

What is the function of the Na+/K+ ATPase?

A
  • Transports 3 sodium ions out of the enterocyte

- Transports 2 potassium ions into the enterocyte

86
Q

What allows SGLT1 to function? What is it?

A
  • The electrochemical gradient generated by the Na+/K+ ATPase
  • SGLT1 is the Na+/Glucose co-transporter
87
Q

What kind of transport is SGLT1? What does it do?

A
  • Secondary active transport, which transports a sodium and a glucose into the enterocyte together (symport)
  • Sodium is moved down the chemical gradient
  • Glucose is moved up the chemical gradient (low to high)
88
Q

How is glucose transported from the enterocyte into the blood? What kind of transport is it?

A
  • GLUT2
  • Facilitated diffusion (uniport)
  • Moves glucose down its concentration gradient (does not require energy)
89
Q

Are enterocytes responsive to insulin?

A

No

90
Q

What prevents the flow of substrates between enterocytes?

A

Tight junctions

91
Q

Why is there no intracellular negative charge in enterocytes?

A
  • Three sodiums are pumped into the blood by the Na+/K+ ATPase, while only two potassiums are pumped in
  • A sodium ion is brought in by the sodium/glucose (SGLT1) co-transporter
92
Q

How does glucose absorption affect water absorption?

A

Glucose is hydrophilic, and allows a flux of water to enter enterocytes

93
Q

What would disfunction the GLUT2 transporter?

A

If plasma glucose concentration exceeded the concentration within enterocytes, glucose would not be able to travel through GLUT2 into the circulation (from high to low concentration)

94
Q

What does glucose and galactose utilize to enter enterocytes? What about to exit?

A
  • Enter: SGLT1 (secondary active transport)

- Exit: GLUT2 (facilitated transport)

95
Q

Galactose undergoes preferential conversion to what?

A

Glycogen and glucose

96
Q

Which transporter is responsible for fructose entry into the enterocyte?

A

GLUT5

97
Q

Which transporters are responsible for fructose exit out of the enterocyte?

A

GLUT5 or GLUT2

98
Q

What is the control point for glycolysis?

A

Phosphoglucokinase and fructose-1,6-bisphosphate

99
Q

What is fructose preferentially converted to?

A
  • Oxidized rapidly

- Or, if there is no need for energy, fructose undergoes de novo lipogenesis (conversion to FAs and TGs)

100
Q

Why isn’t fructose metabolized to glucose?

A

Since it enters glycolysis downstream of the control point

101
Q

Why may potential health complications occur from consuming a large quantity of fructose?

A

As it is preferentially converted to FAs or TGs, if there is no need for energy

102
Q

What is stimulated as blood glucose increases?

A

Stimulates the B-cells of the pancreas to secrete insulin

103
Q

Which glucose transporter is sensitive to insulin? Which tissues is it present in?

A
  • GLUT4

- Muscle, adipose, heart

104
Q

What does insulin stimulate as an anabolic hormone?

A
  • Glucose oxidation
  • Storage and conversion to fat
  • Use of glucose as a fuel
  • Glycogen synthesis
  • Protein synthesis
105
Q

What does insulin inhibit?

A

If there is an abundance of glucose entering the system, there is no need to synthesize more glucose (decreased gluconeogenesis)

106
Q

What is the glycemic response to a high glycemic index food?

A
  • Rapid increase and subsequent decrease of plasma glucose to below normal levels (rebound hypoglycemia)
  • High insulin response
107
Q

What is the glycemic response to a low glycemic index food?

A
  • Moderate increase of blood glucose and insulin response

- Aid in the maintenance of a regular insulin response

108
Q

How is glycogen related to water storage?

A

Glycogen is highly hydrophilic, allowing it to hold a large quantity of water

109
Q

How is glucose activated for the synthesis of glycogen?

A
  • Addition of a phosphate group on carbon-1

- Enzyme: UDP-glucose pyrophosphorylase

110
Q

What does glucose-1-phosphate form for glycogen synthesis?

A
  • Glucose-1-phosphate and UTP forms UDP-glucose and two inorganic phosphate groups
  • Glycogen synthase catalyzes the elongation
111
Q

Why does the increased storage of glycogen cause an increase in liver mass?

A

Because glycogen stores water as it is highly hydrophilic

112
Q

Which enzymes catalyze glycogenesis and glycogenolysis? How does their activity fluctuate based on the addition of glucose?

A
  • Glycogenesis (glycogen synthase): increases with the addition of glucose
  • Glycogenolysis (glycogen phosphorylase): decreases with the addition of glucose
113
Q

When ATP is unnecessary, what is the Acetyl-CoA generated from glucose utilized for?

A
  • Lipogenesis

- May also be converted to cholesterol

114
Q

Which fatty acids may be synthesized de novo? Which must be ingested?

A
  • De novo: saturated and oleic fatty acids

- Ingested: polyunsaturated fatty acids

115
Q

What are the consequences of fat accumulating within the liver?

A
  • Causes the liver to increase in size

- Becomes paler in colour due to excess lipids

116
Q

What may cause fatty liver?

A

Alcohol consumption or obesity

117
Q

How is non-alcoholic fatty liver disease (NAFL) screened?

A
  • Analyzing liver enzymes within the blood

- If there is damage to liver cells, liver enzymes leak out into the blood, allowing for diagnosis

118
Q

What is non-alcoholic steatohepatitis (NASH)?

A
  • Extends from NAFL

- Causes cirrhosis, in which scarring prevents the liver to function properly

119
Q

What does the control point of glycolysis respond to?

A
  • Insulin and glucagon
  • Insulin: promotes flux through glycolysis
  • Glucagon: limits flux through glycolysis
120
Q

What is fructose converted to following ingestion?

A

Three-carbon intermediate (dihydroxyacetone phosphate), which lies beyond the control point

121
Q

What is the primary hormone during a fast?

A

Glucagon

122
Q

What is the effect of glucagon on glycogen stored in the liver?

A

Glycogen is degraded to glucose to feed peripheral tissues and the brain

123
Q

What is the effect of glucagon on glycogen stored in muscles?

A
  • Degraded to glucose to feed muscle tissues
  • Glycogen from muscle stores are NOT exported in the plasma, and remains in muscle to feed exercising muscle in the fasted state
124
Q

What are the primary effects of glucagon?

A
  • Releases glucose from stores
  • Degradation of glycogen in liver and muscle
  • Degradation of triglycerides from adipose tissue