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NUTR 301 - nutritional BIOCH and Metabolism > Carbohydrates > Flashcards

Carbohydrates Flashcards

1
Q

what reaction is the hydration of a carb?

A

Photosynthesis

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2
Q

what is the minimal recommended intake of carbs for men and women? how does this number change for pregnant and lactating women?

A

130g/day minimum
175 for pregnant women
210 for lactating women

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3
Q

what is the DRI for carbs?

A

45 - 65% of energy intake

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4
Q

How are carbs classified?

A

simple vs complex

Simple: mono and disaccharides

complex: oligosaccharides and polysaccharides

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5
Q

what are 3 most common monosaccharides?

A

glucose, fructose galactose

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6
Q

what are 3 most comon disaccharides?

A

lactose, maltose, sucrose

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7
Q

what are oligosaccharides? give me 2 most common examples?

A

3-10 sugar units
-raffinose and stachyose

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8
Q

what are polysaccharides? give me 3 most common examples?

A

starch, glycogen and dietary fiber

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9
Q

what is the structure of monosaccharides?

A

1 sugar unit with 6 carbon atoms
-glucose and fructose are 6-sided ring structure while galactose is a 5-sided ring structure

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10
Q

how do glucose and galactose differ in structure?

A

their hydroxyl groups face opposite directions

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11
Q

how are glycosidic bonds formed? what types of bonds does it form?

A

through a condensation reaction of sugar molecules
-alpha and beta forms

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12
Q

what is the difference between a beta and alpha glycosidic bond? how does this change in structure affect the function?

A

beta- bond is facing up (OH on C1 of the first glucose is above the plane of the ring)

alpha- bond is facing down (OH on C1 of the first glucose is below the ring)

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13
Q

how are monosaccharides named? and how is their chirality differentiated?

A

aldose or ketose
-D or L

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14
Q

how is sucrose made?

A

fructose and glucose

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15
Q

how is lactose made?

A

glucose and galactose

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16
Q

how is maltose made?

A

glucose and glucose

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17
Q

what is common amongst sucrose, maltose, and lactose?

A

they are all bonded to atleast one glucose molecule

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18
Q

what is another common name for sucrose?

A

table sugar

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19
Q

what is another common name for lactose?

A

milk sugar

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20
Q

in terms of enzymatic needs, what do disaccharides, oligosaccharides and polysaccharides have in common?

A

specific enzymes are needed for hydrolysis during digestion

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21
Q

True or False:

Carbohydrates are typically non-reactive

A

False

carbs are very reactive due to their reducing end

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22
Q

what types of sugars are classified as reducing sugars?

A

Sugars that comtain aldehyde groups (C1 carbonyl) and have an open chain form

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23
Q

How does glucose relate to reactivity?

A

more glucose molecules will increase the reactivity

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24
Q

How does carb reactivity relate to someone’s overtime mis-management of carb intake?

A

the reactivity of carbs on proteins may indicate someone’s overtime mis-management of carb intake

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25
Q

how does reactivity relate to recucing sugar structures?

A

reducing sugars are more reactive due to their reducing end being accesible

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26
Q

What is the relevance of glucose reactivity in diabetes mellitus?

A

The reactivity of glucose with hemoglobin is used to understand the status of diabetes

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27
Q

what is cellulose? how can it be digested in humans?

A

a glucose polymer connected by beta 1-4 linkages
- cannot be digested by mammalian enzymes but can be degraded by colonic bacteria

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28
Q

why are the carbohydrates in polymers (fiber) unavailable?

A

They are “unavailable” due to lack of expression of celluase

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29
Q

how do starch, cellulose and glycogen differ based on structure and function?

A

starch is made of amylose and amylopectin with α(1→4) bonds between glucose molecules
-helical structure makes it more accessible and it is digestible in humans

cellulose is dietary fiber with a linear structure with β(1→4) bonds between glucose. the structure is rigid and indigetsible for humans
-aids in digestion

Glycogen serves as energy storage in animals and humans with α(1→4) glycosidic bonds in the main chain and α(1→6) bonds at the branch points
-structurally similar to starch

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30
Q

what kind of linkages does amylose exhibit? what percentage of starch does it make up?

A

α(1→4)

20%

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31
Q

how does amylose and amylopectin differ in structure?

A

amylose- straight chain D-glucose

amylopectin- branched chain of D-glucose

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32
Q

other than α(1→4) linkages, what other linkages are present in amylopectin?

A

α(1→6)

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33
Q

how does solubility differ between amylose and amylopectin?

A

amylose is less soluble in water and amylopectin is more soluble in water

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34
Q

how do amylose and amylopectin differ in structure when hot water is added?

A

amylose does not form a gel while amylopectin does form a gel

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35
Q

what two groups are a Maillard reaction between?

A

rxn between a carbohydrate and an amine to form glycosides

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36
Q

what are the 2 major steps of carbohydrate digestion?

A

1) Intraluminal hydrolysis (amylases)
2) membrane digestion (brush border glycohydrolases)

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37
Q

what occurs during intraluminal hydrolysis?

A

1) initial digestion: salivary α-amylase and continues with pancreatic α-amylases (endosaccharides)
2) salivary α-amylase is deactivated by stomach acid
3) pancreatic juices in SI neutralize acid and α-amylase continues hydrolysis

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38
Q

what occurs in membrane digestion? what types of sugars are involved?

A

This occurs at the brush border of the small intestine, where enzymes break down disaccharides into monosaccharides for absorption

-Maltose, Maltotriose, trisaccharides, oligosaccharides, and α-limit dextrins (from starch breakdown)

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39
Q

how does digestion of monosaccharides differ from polysaccharides and disaccharides?

A

monosaccharides need no further digestion before absorption while polysaccharides and disaccharides must be hydrolyzed

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40
Q

what are dextrins?

A

carbs produced from the hydrolyses of starch and glycogen

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41
Q

where does most of starch digestion take place?

A

small intestine

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42
Q

what types of bonds does α-amylase cleave?

A

α-1,4 glycosidic bonds

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43
Q

where does breakdown of amylose and amylopectin occur? what enzyme catalyzes this? what molecule does this form?

A

in the mouth by α-amylase to form dextrins

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44
Q

how does digestion of dextrins continue in the stomach?

A

It doesn’t there is no further digestion of dextrins in the stomach

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45
Q

what causes enzamatic activity to stop in the stomach?

A

the acidity of gastric juice destroys activity of α-amylase

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46
Q

where is α-amylase released from and where does it go? what affect does this have on the body?

A

The pancrease releases α-amylase into the small intestine in order to:
1) break down amylose dextrins into maltose
2) break down amylopectin dextrins into maltose and limit dextrins

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47
Q

What occurs in the small intestine after Amylose is broken down to maltose?

A

maltose is broken down by maltase (brush border enzyme) to form glucose

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48
Q

what occurs in the small intestine to amylopectin after it has been broken down to maltose? what happens to the limit dextrins?

A

maltose is hydrolyzed by maltase (brush border enzyme) to form glucose

the limit dextrins are hydrolyzed by α-dextrinase to form glucose

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49
Q

after intraluminal hydrolysis, what type of sugars are left over?

A

oligosaccharides

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50
Q

after full brush border enzyme digestion, what type of sugars are left over?

A

monosaccharides

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51
Q

what structure needs α-1,6 bonds cleaved? what enzyme can do this and where is it done?

A

Amylopectin limit dextrins have α-1,6 bonds that are cleaved in the small intestine by the brush border enzyme α-dextrinase

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52
Q

what kinds of sugars are limit dextrins?

A

branched oligosaccharides containing α-1,6 bonds that must be hydrolyzed by α-dextrinase

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53
Q

If maltose and maltotriose are formed, what structure could have produced these sugars?

A

Maltose and maltotriose can be produced from the cleavage of amylose by α-amylase

they also form one of the final products from amylopectin hydrolysis, following the hydrolysis of limit dextrins

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54
Q

at what point in a childs life will salivary and pancreatic amylase levels increase?

A

after they are 1 year old

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55
Q

what end are sugars always cleaved from?

A

the reducing end

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56
Q

what percent of dietary carbohydrate is in starch (amylose, amylopectin) ?

A

60-70%

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57
Q

what percent of dietary carbohydrate is in lactose?

A

0 - 10%

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58
Q

what percent of dietary carbohydrate is in sucrose?

A

30%

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59
Q

what are the products of luminal hydrolysis of starch?

A

α-dextrins, maltose and maltotriose

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60
Q

what are the products of luminal hydrolysis of lactose and sucrose?

A

none

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61
Q

w

A
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62
Q

what are the products of brush border membrane hydrolysis of starch?

A

glucose

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63
Q

what are the products of brush border membrane hydrolysis of Lactose?

A

glucose and galactose

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64
Q

what are the products of brush border membrane hydrolysis of sucrose?

A

glucose and fructose

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65
Q

what are sources of amylopectin and amylose?

A

Starchy foods
-potatoes, rice, corn and bread

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66
Q

what kind of bonds are seen in lactose?

A

beta-1,4 bonds

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67
Q

how is fructose transported into enterocytes?

A

facilitated diffusion
- [high] to [low]

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68
Q

how is glucose transported into enterocytes?

A

active, Na+ dependent transport
[low] to [high]

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69
Q

how does galactose move into enterocytes?

A

through active transport

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70
Q

how are absorbed nutrients transported to the liver?

A

hepatic portal vein

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71
Q

what is SGLT1? where is it located and what molecules does it facilitate?

A

Na+ glucose linked transporter
- transports glucose or galactose with Na+ into the cells (in the small intestine and kidney)

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72
Q

what is GLUT5? where is it located and what molecules does it transport?

A

A facilitative transporter primarily responsible for fructose transport in the small intestine (also skeletal muscle and other tissues)

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73
Q

what is GLUT2? where is it loacted and what molecules does it transport?

A

A low affinity, high capacity transporter that can facilitate transport of glucose =, fructose and galactose without energy

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74
Q

what is the rate-limiting step in the final phase of the glycemic response?

A

the absorption of glucose by SGLT-1 and its transport into the bloodstream by GLUT 2

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75
Q

what physiological factors contribute to the side affects of lactsose intolerance?

A

1) fermentation of undigested lactose leads to increased gas production
- bloating
2) Undigested lactose can cause osmotic diarrhea
-lactose in the colon draws water into the intestinal lumen

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76
Q

what is the definition of dietary fiber?

A

Plant-derived, non-starch polysaccharides that are indigestible by human enzymes

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77
Q

why is there debate surrounding what classifies as fiber?

A

what about:
-starch resistant sources
-partially digestible oligosaccharides
-animal / industry sourced indigestible carbs

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78
Q

what bond can human enzymes not digest?

A

beta 1-4 glycosidic bonds

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79
Q

how does the structure of plants differ in regards to digetsable parts?

A

the cell wall- non-digestible carbs
cell lumen - digestible carbs

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80
Q

what part of a plant seed has majority of the fiber?

A

the bran

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81
Q

what type of fiber is cellulose? give examples of food sources

A

Predominantly insoluble fiber being a major structural component of cell walls

-whole wheat flour, bran, root veg, broccoli, apple, cabbage

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82
Q

what type of fiber is hemicellulose? give examples of food sources

A

predominantly insoluble fiber
-bran, cereals and whole grains

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83
Q

what type of fiber is pectin? give examples of food sources

A

predominantly soluble fiber found in the skin of ripe fruits (made to make jellies/jams)
-apples, citrus fruits, strawberries, raspberries

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84
Q

what type of fiber is beta glucan? give examples of food sources

A

non starch polysaccharide
-mushrooms, barley oats

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85
Q

what type of fiber are gums? give examples of food sources

A

Highly soluble and viscous non-starch polysaccharodes
-oatmeal, dried beans and legumes

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86
Q

Give examples of fruits high in insoluble fiber vs soluble fiber

A

soluble: orange
insoluble: apples and bananas

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86
Q

what type of fiber is lignin? give examples of food sources

A

an insoluble non-polysaccharide dietary fiber found within woody portion of plants
-berries and wheat

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86
Q

are vegetables more likely to have more soluble or insoluble fiber? give examples of vegetables high in fiber

A

insoluble
-broccoli, carrots and corn, potato (higher in soluble fiber)

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87
Q

give examples of high fiber grains. Note which ones are high in soluble vs insoluble fiber?

A

All bran cereal- insoluble
Oat bran- both types
rolled oats- insoluble
whole wheat bread- insoluble

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88
Q

are legumes more likely to have more soluble or insoluble fiber? give examples of legumes high in fiber

A

Insoluble fiber

kidney beans, pinto beans, lentils,
green peas

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89
Q

what is total fiber composed of?

A

dietary fiber and functional fiber

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90
Q

what is the difference between dietary fibers and functional fibers? give examples of each

A

functional fibers are isolated and added to products to provide targeted health benefits like improving digestion or lowering cholesterol while dietary fibers are typically found naturally in plants

dietary- cellulose, hemicellulose, pectin, lignin, gums
functional- chitin, resistant starches, cellulose, pectin, lignin,

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91
Q

what is a resitant starch? what percent of it reaches the colon?

A

carbohydrate that resists digestion in the small intestine and reaches the colon intact
-acts like dietary fiber

5-20% reaches the colon intact

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92
Q

what factors make resistant starches inable to be digested by humans enzymes?

A

structure, colonic microflora and physical food factors

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93
Q

how are resistant starches able to be formed?

A

through cooling of starchy foods following high heat processes that may result in irreverible retrodegradation (amylose)

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94
Q

how does fermentability differ in soluble vs insoluble fiber?

A

soluble fiber- fermentable
insoluble fiber- poorly fermented

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95
Q

how does soluble fiber affect the body? what causes this to happen?

A

delays gastric emptying
-increases transit time
-decreases nutrient absorption

due to the gel like structure that is formed once interacted with water, it creates a highly viscous form which slows digestion

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96
Q

what are food sources of soluble fiber?

A

oatmeal, lentils, apples, oranges, pears, strawberries, nuts, flaxseeds, beans, dried peas, blueberries, cucumbers, celery and carrots

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97
Q

how does insoluble fiber affect the body? what causes this to happen?

A

they decrease transit time and increase fecal bulk (gut healthy)
-since they are insoluble they pass through the GIT in tact, speeding up the passage of food / waste (laxative effect)

98
Q

what are sources of insoluble fiber?

A

whole wheat,grains and bran, seeds, nuts, barley, couscous, broccoli, onions, tomatoes, carrots, dark leafy vegetables, root vegetable skins

99
Q

how does the viscosity of soluble fibers impact its function / effects on the body?

A

-traps nutrients (decreased nutrient diffusion rate into bloodstream)
-increases satiety (slowed gastric emptying)
-decreases mixing of GI contents with digetsive enzymes (physical barrier decreases contact with brush border enzymes)
-decreases glycemic response

100
Q

how does fiber binding ability impact responses in the body? what does fiber bind with?

A

fiber binds with FA, cholesterol and bile acids which prevents micelle formation, lipid absorption and enterohepatic circulation

this will:
-increase bile acid excretion
-decrease cholesterol levels
-decrease fat absorption
-alter mineral absorption

101
Q

how does dietary fiber interfere with mineral absorption?

A

ionized groups on polysaccharides are usually (-) charged which causes them to bind with (+) minerals

-Ca2+, Mg2+, Na+, K+

102
Q

give examples of which fibers are most fermentible?

A

fructans, pectin, gums, psyllium, polydextrose and starch (soluble fibers)

103
Q

give examples of fibers that are not likely to ferment

A

cellulose and hemicelluloses

104
Q

what indirect effects does fiber metabolization by bacteria have?

A

lactate - decreases pH
SCFA’s - important energy sources

105
Q

what effect does the production of SCFA through fiber metabolism have on the body?

A

-increasing water/Na+ absorption in colon
-increases mucosal cell proliferation
-energy source (if fat is large part of diet)
-acidification of lumen environment (increases bile excretion)
-changes in enzyme activity

106
Q

if fermentability decreases, what happens to fecal bulk?

A

it increases

107
Q

what are prebiotics?

A

non-digestible fibers that feed and stimulate the growth of beneficial bacteria in the gut

108
Q

how does delayed gastric emptying decrease cholesterol?

A

Soluble fiber binds to bile acids (made from cholesterol and needed for fat digestion)- The binding promotes their excretion in feces causing the liver to use cholesterol to produce more bile acids

109
Q

how does fibers interference with digestive enzymes lower cholesterol?

A

Viscous fibers may sequester lipids, proteins and carbs from digestive enzymes which will impact absorption

110
Q

How does fiber decrease cholesterol biosynthases directly?

A

Fermentation of fiber by bacteria in the colon produces propionate which inhibits the rate limiting enzyme responsible for making choloesterol (HMG-CoA)

111
Q

is the water binding capacity of insoluble fibers zero?

A

no, insoluble fibers do have some water-holding capacity but soluble fibers bind up to seven times their weight in water

112
Q

what is the RDA for fiber intake of men age 19-50? what about after 50years?

A

38g/day
lowers to 30g / day

113
Q

what is the RDA for fiber for women age 19-50?
how does this change after 50, during pregnancy, and lactation?

A

25g/day

-21g/day
28g/day
29g/day

114
Q

what molecule is the primary energy gateway for the continuation of glucose in certain pathways?

A

G6P

115
Q

what organ is the primary storage location for glycogen?

A

liver

116
Q

when skeletal muscle stores glycogen, how does this differ from the liver storing glycogen?

A

glycogen stores in the muscle is only used as an energy source for the muscle (greedy cells)

117
Q

in addition to energy needs, why is glucose essential? give examples

A

it is a precursor for synthesis of other carbs, sugar residues and compounds?
-ribose, glycoproteins, glycolipids, protoglycans

118
Q

True or False: all cells are able to use glucose as an energy source

A

True

-however, some are more dependent (RBC’s, nerves, brain)

119
Q

what is the average plasma glucose level?

A

5mmol (~90 mg/dl)

120
Q

what is the upper limit for plasma glucose?

A

6mmol (110mg / dl)

121
Q

at what glucose plasma level is insulin secretion decreased? when is glucagon secreted? when do symptoms occur?when does neuronal death occur?

A

1) ~4.5mmol (~80 mg/dl)
2) ~4mmol (~70mg/dl)
3) ~3mmol (~50mg/dl)
4) ~1mmol (~15mg/dl)

122
Q

True or false: mitochondria density varies between cells

A

TRUE

123
Q

How does glucose metabolsim vary in the skeletal muscle, cardiac and liver?

A

Skeletal: can completely oxidize, only glycolysis or store glucose
Cardiac: complete oxidation of glucose
Liver: can do everything
-store,produce and distrubute glucose
-make glucose from lactate,pyruvate,alanine
-can use glucose to make FA
-can make ribose-6-phosphate

124
Q

does glucose exit the muscle?

A

no, lactate does

125
Q

why doesn’t the brain store glycogen?

A

large amounts of glycogen use large amounts of water
-Storing glycogen would be inefficient and insufficient to meet the brain’s constant high energy demands

126
Q

what cells are obligate glucose users?

A

RBC’s and the brain

127
Q

How does glucose metabolism differ in the pancreas vs adipocytes?

A

Pancreas (beta cells): very efficient complete oxidation due to high [mitochondria]
-tightly regulated as a glucose sensor

adipocytes: fat synthesis or complete oxidation
-metabolizes glucose to Acetyl coA and stores fat

128
Q

how does adipose, muscle, brain and cardiac cells contrubute to blood glucose homeostasis?

A

They don’t contribute to homeostasis because they dont release glucose from their cells
-they respond to changes in blood glucose

129
Q

what types of sugar kinase enzymes are found in the liver?

A

glucokinase and fructokinase

130
Q

when is the kidney important for glucose synthesis? what is its role?

A

during starvation or times when carbohydrate levels are low
-it signals the body to increase gluconeogenesis to help maintain blood glucose levels

131
Q

why don’t all tissues make glucose? what are examples of these tissues?

A

they lack the enzyme which converts G6P to glucose
-brain and skeletal muscle

132
Q

what 2 AA cannot be used in gluconeogenesis?

A

Leucine and lysine

133
Q

what substrates are used for gluconeogenesis? which one yields the most ATP?

A

lactate (most ATP), AA, and glycerol

134
Q

what is PEPCK? when are levels of this expected to be low?

A

an allosteric enzym that converts oxaloacetate into PEP, allowing other sources (AA, glycerol and lactate) to be used as substrates for gluconeogenesis

-low levels until neonatal period (constant energy supply needed for babies)

135
Q

based on the structure of glycogen, how would this explain its function / storage?

A

its greater branching decreases its density and prevents tight packing of the molecule
-stored with water
-more space is needed for the storage (affects the capacity of storage)

136
Q

why not store glucose rather than glycogen?

A

glycogen allows maximization of storage while still making the molecule readily availible
-uses less space and holds less water in the same amount of free glucose

137
Q

what percentage of the liver weight does glycogen storage take up? what about skeletal muscle?

A

10%
-1%

138
Q

what are the 2 forms of glycogen synthase? how do they differ?

A

GYS1: more active (unphosphorylated), expressed in muscle, kidney, brain and adipose
-used in rapid response to glucose in fed state (quick storage)

GY2: less active (phoshorylated), only expressed in the liver to ensure large pools availible for [glucose]

139
Q

how does insulin affect each type of glycogen synthase?

A

it stimulates both of them in the liver and muscle

140
Q

what glycogen synthase has lower affinity for UDP-glucose?

A

GY2 gene
-also less sensitive to allosteric activation by G6P

141
Q

what is glycogenolysis? what stimulates it?

A

the use of glycogen
-low blood glucose levels

142
Q

when is glycogenesis increased?

A

in the fed state
-promotion of glycogen storage

143
Q

when is glycogenesis increased?

A

in the fasting state
-supplies blood glucose

144
Q

how does the purpose of glycogen breakdown differ from the muscle to the liver?

A
145
Q

what molecules promote glycogen synthases through glucagon receptors?

A

Glucagon, epinephrine, glucocorticoids induce cAMP response to activate glycogen phosphorylase

146
Q

how is the rate of glycogen breakdown regulated in skeletal muscle? what can you expect from each of these enzymes?

A

dependent on the ratio of phosphorylase A (phoshorylated) to phosphorylase B (dephosphorylated)

A: not sensitive to ATP, more active, increases glycogen breakdown
B: less active, doesn’t breakdown glycogen

(and Ca+/cAMP resonses-other slides)

147
Q

what effect does Ca+ have on glycogen breakdown?

A

increased [Ca+] from muscle contraction will activate phosphorylase kinase, generating phosphorylase A
- stimulates breakdown of glycogen

148
Q

Overview of glycogen regulation:

explain:
1) what enzymes catalyze the rxn between Glycogen and G1P
2) The enzymes that regulate the enzymes that catazlyze the rxn converting glycogen to G1P
3) what insulin regulates
4) what glucagon / epinephrine regulate

A

https://youtu.be/LJYTFtiTVXA?si=d023lctHiyEsh3lU

149
Q

How does the conversion of pyruvate to lactate aid in continuation of step 6 in glycolysis?

A

it produces NAD+ in order to be used in step 6 to make NADH

150
Q

where is lactate from anaerobic glycolysis recycled? what about alanine?

A

the liver
-can be used for gluconeogenesis

151
Q

when lactate builds up, what should be done to increase recycling rate?

A

keep blood pressure up by moving around
-increases perfusion

152
Q

what is so important about the transfer of pyruvate from the cytosol to the mitochondria?

A

it is the rate limiting commited step

153
Q

what carrier transports pyruvate into the mitochondria?

A

monocarboxylate carrier

154
Q

what enzyme converts pyruvate into Acetyl coA?

A

pyruvate dehydrogenase complex (PDH)

155
Q

explain the regulation of PDH complex

A

PDH kinase phosphorylates (inactivates complex)
Activated by:
High ATP
High NADH
High acetyl-CoA

PDH phosphatase dephosphorylates (activates complex)
Activated by:
Ca²⁺
Insulin

Allosteric inhibitors:
Acetyl-coA
NADH

Allosteric activators:
Pyruvate
ADP

156
Q

what percentage of volume do mitochondria take up in cardiac myocytes?

A

~50%

157
Q

how is the [gradient] created by the structure of the mitochondria?

A

compartmentation of the mitochondria allows for contorl of the [gradient] and regulation of the ETC
-move protons to drive ATPase

158
Q

what shuttle is responsible for transport of electrons from NADH into the inner mitochondria?

A

malate-aspartate shuttle

159
Q

why is Ca+ so tightly regulated?

A

because it is always propogating a signal as a second messanger or sending signals
-always bound to something

160
Q

explain how the translocase of ADP/ATP contributes to the [gradient]

A
161
Q

what are important inhibitors for the ATP/ADP translocase?

A

CATR (carboxyatraxtyloside) and BA (bongkrekic acid)

162
Q

why is the pentose pathway important

A

1) linked to glycolysis during excess energy and uses G6P as the gatekeeper
- during upregulating anabolic conditions
2) responsible for reducing glucose into other 5C sugars
- used to make other macro molecules

163
Q

how many ATP are used and produced in the pentose phosphate pathway?

A

NONE

164
Q

what are the 2 primary products of the pentose phosphate pathway?

A

1) ribose-5-phosphate
- precursor used to produce DNA and RNA
2) NADPH
-donates electrons

165
Q

how does NADPH differ from NADH?

A

NADPH has a stronger reducing power and helps maintain antioxidants in the body
- important in anabolic rxns

NADH is primarily involved in catabolic rxns and helps to provide electrons in the ETC

166
Q

what are the 2 stages of the pentose phosphate pathway?

A

Oxidative phase
-production of NADPH
-irreversible

Non-oxidative phase
-reversible pathways and allows interconversion of sugars to increase Ribose-5-phosphate production

167
Q

what feature of the pentose phosphate pathway allows for increased production of ribose-5-phosphate?

A

interconversion between sugars with different number in carbons

168
Q

how is glucose a substrate and a regulator for metabolic pathways?

A

1) signal molecule (glucose homeostasis)
2) regulation molecule
(secretion, transcription enzymatic activity)

169
Q

what is an oral glucose test used for? what is the average measure?

A

measurement of how body stores sugar over time
~120mg/dL is considered normal

170
Q

what percent of the muscle takes up postprandial glucose?

A

40-60%

171
Q

what organ recieves the first pass of glucose and insulin from the hepatic portal vein?

A

the liver

172
Q

Why does the liver have a high uptake of glucose?

A

The liver has a high uptake of glucose due to the presence of high amounts of GLUT2 and glucokinase, which is not inhibited by G6P

173
Q

What happens to the remaining 2/3 of glucose after the liver takes up its portion?

A

About 2/3 of glucose travels into peripheral circulation for cellular use, stimulating insulin release.

174
Q

Which tissues are dependent on insulin for glucose transport?

A

Adipose tissue and muscle are dependent on insulin for glucose transport.

175
Q

What factors determine the rate of glucose uptake?

A

the number of transporters, the rate of transport, phosphorylation, and the utilization of glucose (rate/fate of G6P).

176
Q

How is glucose transported from the gastrointestinal tract (GIT) into the portal blood?

A

Glucose is transported from the GIT into the portal blood via active symport with Na+ by SGLT1 and facilitated diffusion by GLUT2.

177
Q

What is the affinity and capacity of GLUT1 for glucose, and where is it primarily located?

A

GLUT1 has high affinity and low capacity for glucose. It is primarily located in most tissues in low amounts

178
Q

What is the affinity and capacity of GLUT2, and how does it function in glucose transport? where is it expressed?

A

GLUT2 has low affinity but high capacity for glucose. It functions as a glucose “sensor” and is insulin independent
- liver, pancreas and SI

179
Q

What are the affinity and capacity characteristics of GLUT3, and where is it found?

A

GLUT3 has high affinity and low capacity for glucose, ensuring basal glucose transport. It is found in neurons, placenta, skeletal muscle, and spermatozoa.

180
Q

How does the affinity and capacity of GLUT4 relate to its regulation, and where is it expressed?

A

GLUT4 has high capacity for glucose and is insulin-dependent, allowing for rapid glucose uptake during increased insulin levels. It is expressed in skeletal muscle, cardiac muscle, and adipose tissue.

181
Q

what metabolic effects does insulin promote?

A

anabolic
-synthesis of glycogen, proteins, fat and energy

182
Q

what kind of metabolic process does glucagon promote?

A

catabolic
-breakdown of glycogen, fat, and proteins to make energy

183
Q

what transporter is increased in response to insulin spike? what does the transport of glucose depend on?

A

GLUT 4
-rate of transport depends on [GLUT 4]

184
Q

explain the mechanism for insulin release

A

In the pancrease:
1) Glucose enters the cell through GLUT 2, propertionaly to the amount of glucose digested
2) Glucose then goes through glycolysis, being catalyzed by glucokinase
3) ATP produced from glycolysis will inhibt K+ eflux from the cell
4) the decreased K+ outside of the cell will depolarize Ca+ channels
5) depolarization of Ca+ channels willopen them, causing Ca+ to move inside the cell
6) increased Ca+ in the cell will stimulate the release of insulin into the bloodstream

185
Q

what other ways can insulin be stimulated other than glucose?

A

amino acids, parasympathetic activity, and incretins (GLP1)

186
Q

why doesnt fructose stimulate insulin release?

A

there are not enough GLUT 5 transporters to allow for high levels of fructose to stimulate insulin in the pancreas

187
Q

why has fructose consumption increased and what are the affcets of this?

A

increase fructose consumption due to high intake of processed foods
-associated with T2D and insulin resistance

188
Q

explain using metabolic reasoning why frucotse in excess is an issue

A

it is only metabolised in the liver so excessive fructose intake overwhelms the liver’s capacity for processing and contributes to a variety of metabolic diseases

189
Q

How does the GLUT2/glucokinase system function in beta cells of the pancreas?

A

In beta cells, the GLUT2/glucokinase system senses blood glucose levels. Glucose metabolism through glycolysis produces ATP, leading to insulin secretion when glucose levels are high.

190
Q

At what glucose concentration does glucagon secretion increase to maintain glucose levels?

A

Glucagon secretion increases when blood glucose levels drop below about 4 mmol/L (70 mg/dL), helping to raise blood glucose by promoting glycogen breakdown

191
Q

What happens to GLUT4 translocation in insulin resistance?

A

GLUT4 translocation to the cell membrane is reduced, meaning that glucose uptake into cells is diminished even when insulin is present.

192
Q

What are the consequences of insulin resistance on blood glucose and insulin levels?

A

Insulin resistance leads to hyperglycemia (elevated blood glucose) and hyperinsulinemia (elevated insulin levels), as the body tries to compensate for the decreased effectiveness of insulin

193
Q

What effect do catecholamines (e.g., adrenaline/epinephrine) have on glucose regulation?

A

stimulate production of glucose (increased glycogenolysis and gluconeogenesis)

194
Q

How do glucocorticoids (e.g., cortisol) influence glucose levels?

A

increase blood glucose
* -increase hepatic glucose output

195
Q

What role does Tri-iodothyronine (T3) play in glucose metabolism?

A

regulates metabolism by regulating hormones and actions
(increases BMR using anabolic / catabolic activity)

196
Q

What is the glucose-sparing effect and why is it important during starvation?

A

the body’s shift away from using glucose as a primary fuel in muscle and adipose tissue, instead using lipids (fats). This conserves glucose for tissues that rely on it, such as the brain and red blood cells

197
Q

what is the GI based on?

A

blood glucose response curve of a 50g test portion
-typically white bread or glucose

198
Q

what differentiates low GI vs high HI foods?

A

low GI foods are digested slowly
high GI foods are digested rapidly

199
Q

why does fructose have a low GI?

A

because GI is a measure based on glucose

200
Q

why are high GI foods considered bad?

A

the high glucose spike means that more stress is put on the body in order to bring the system back to homeostasis

201
Q

How does the physical interaction of starch with fat or protein influence the glycemic index?

A

The physical interaction with fat or protein slows down starch digestion, leading to a lower glycemic index.

202
Q

How does reduced ripeness in fruit influence the glycemic index?

A

Less ripe fruits have a lower glycemic index because they contain more resistant starch and less simple sugar, which takes longer to digest

203
Q

What is the key difference between Glycemic Index (GI) and Glycemic Load (GL)?

A

Glycemic Index (GI) measures the effect of 50 grams of carbohydrates on blood sugar levels without considering serving size, while Glycemic Load (GL) takes into account both the GI and the quantity of carbohydrates in a typical serving.

204
Q

What is the formula to calculate Glycemic Load (GL)?

A

GL=(GI/100)×(gramsofcarbsper
serving)

205
Q

What is considered a high GL? what abt GI?

A

> 20 is high GL
70 is high GI

206
Q

What is considered a low GL? what abt GI?

A

< 10 is a high GL
<55 is a high GI

207
Q

what enzymes are needed to break down ethanol?

A

none, it is small, volatile and lipid / water soluble

208
Q

how quick does methanol enter the bloodstream?

A

within 5 minutes

diffuses into the body based on [ethanol]

209
Q

what is ethanol metabolized into?

A

Acetyl-coA

210
Q

what percent of kcals can make up the diet in alcoholics? why is this a concern?

A

~50%

this displaces other nutrients (micro and macros)

211
Q

where does alcohol absorption / metabolism begin? where does majority of absorption take place?

A

there is some ADH in the stomach so absorption and minimal metabolism can begin there (~20%)

majority of absorption will take place in the intestine

212
Q

why does food affect alcohol metabolism?

A

it acts as a physical barrier as well as promotes dilution of the alcohol

213
Q

how does the rate of alcohol metabolism differ from absorption?

A

metabolism is slower (0.5 oz / hour of pure alcohol)

214
Q

what is the first organ to metabolize a large amount of alcohol? what is this called?

A

the liver
-1st pass metabolism

215
Q

in what scenario would the microflora in our gut produce a large enough amount of alcohol to produce intoxication effects?

A

1) people taking a large amount of antibiotics
2) people on a high carb diet

216
Q

what is the major pathway for alcohol metabolism? where does this occur?

A

ADH pathway in the cytosol of liver cells

217
Q

what does the metabolization of alcohol produce in the liver using the ADH pathway?

A

1) acetaldehyde
2) NADH
3) H+

218
Q

what is the toxic component of alcohol breakdown?

A

acetaldehyde

219
Q

what are the by-products of alcohol metabolism? what is their effect on metabolism in the body?

A

Acetaldehyde: reactive, toxic compound (causes cell damage)

Acetyl-coA: promotes lipogenesis and may lead to fatty liver

NADH: excess NADH causes imbalance between NAD+/NADH which may inhibit gluconeogenesis and promote the conversion of pyruvate to lactate

220
Q

how will natural alcohol intake affect ADH production?

A

it will upregulate ADH to better deal with alcohol

221
Q

what is the inducible pathway of alcohol metabolism? what impact does this have on other drugs ?

A

Large intake of alcohol will induce the CY2E1 metabolism

by switching to this pathway and using CY2E1 (cytochrome P450) as an enzyme, this limits the availability for this enzyme to break down other drugs which is a major enzyme used for detoxification

222
Q

what are the negative effects of the CY2E1 pathway?

A

1) Acetaldehyde adducts formation (binding of acetaldehyde to proteins which alters their function)
2) Increases in ROS formation
3) Increases NADH:NAD+ ratio

223
Q

True or False: genes can affect the rate of metabolism of alcohol and acetaldehyde

A

True

This is an important factor as the rate of metabolism determines detoxification which determines toxicity of the alcohol to each person

224
Q

True or False: ADH and ALDH only metabolize alcohol

A

FALSE

there are multiple isoforms some of which are needed to oxidize retinol (vit A)
-reason why vision may be impaired when ingesting high amounts of alcohol

225
Q

what pathway is used when small amounts of alcohol are ingested?

A

ADH pathway

226
Q

what pathway is used when large amounts of alcohol are ingested?

A

MEOS pathway

227
Q

what is the effect of NADH on the CAC?

A

inhibits it through product inhibition

228
Q

where does the MEOS pathway occur?

A

in the endoplasmic reticulum (ER) microsomes

229
Q

what coenzyme does the MEOS pathway use to breakdown alcohol?

A

NAPDH and H+

230
Q

what are barbiturates? how does alcohol affect them?

A

Barbiturates are drugs that act as CNS depressants (used to treat anxiety, insomnia and seizures)

alcohol inhibits the metabolism of this drug due to cytochrome P450 (CYP2E1) prioritizing the metabolism of alcohol over the metabolism of the barbiturates
-causes sustained depressed of CNS and risks of respiratory failure

231
Q

what is alcohol affect on the CNS?

A

CNS suppresant

232
Q

what path is responsible for alcohol tolerance?

A

MEOS

233
Q

what is the legal limit of blood alcohol concentration?

A

0.08%

234
Q

at what [BAC] are control of reflexes lost?

A

0.11% -15%

235
Q

at what [BAC] is consciousness lost?

A

> 0.40%

236
Q

at what [BAC] do you feel relaxation and relief?

A

below 0.05%

237
Q

what do toxic effects of alcohol MOSTLY depend on?

A

the dose size

238
Q

True or False: regular, moderate alcohol consumption can be good for you

A

True

-controversial topic but there is a J shaped curve between the relationship between CVD risk and alcohol intake

239
Q

what are 6 examples of adverse effects of high chronic alcohol consumption? what are majority of the effects a cause of?

A

1) malnutrition (displacement of nutrients)
2) Fetal alcohol spectrum disorder (disturbance of Vit A metabolism and toxicity from acetaldehyde during pregnancy)
3) Fatty liver, liver disease
4) CVD, hypertension, stroke
5) pancreatic inflammation (decreases in blood glucose regulation)
6) Cancer- mouth, liver, breast

major causes due to acetaldehyde toxicity

240
Q

provide an examples of 1 water-soluble vitamin, fat soluble vitamin and mineral that is impacted by high alcohol intake. how do they impact the body?

A

Water soluble:
Thiamin- impaired absorption results in memory loss

Fat-soluble:
Vit A deficiency will reduce conversion of retinol to retinal which will impair vision

Mineral:
Zinc deficiencies from decreased absorption results in impaired wound healing

241
Q

why is hyper and hypoglycemia common with increased alcohol consumption?

A

Hyperglycemia due to inhibition of glycolysis and reduction in full oxidation

Hypoglycemia due to inhibition of gluconeogenesis

242
Q

why is lactic acidosis a concern when alcohol consumption is high?

A

when NADH levels are elevated due to alcohol metabolism, the enzyme lactate dehydrogenase favors the conversion of pyruvate to lactate and pyruvate dehydrogenase is inhibited

243
Q

what 2 classifications encompass fatty liver disease?

A

1) alcohol-related fatty liver disease

2) Non-alcoholic fatty liver disease
excessive cal intake, somewhat reversible through weight loss
- simple steatosis

244
Q

what type of fatty liver disease is irreversible? which one is reversible?

A

simple steatosis is reversible
-associated with non-alcoholic fatty liver

hepatic steatosis is irreversible
-associated with both types of fatty liver

NUTR 301 - nutritional BIOCH and Metabolism (5 decks)

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