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Nutrition 301 > Carbohydrates > Flashcards

Carbohydrates Flashcards

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1
Q

4 characteristics of carbs

A
  • essential energy for brain/RBCs
  • sweet taste motivates behavior and food choice
  • can be stored as fat
  • fibre can impact intestinal microflora
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2
Q

Most carbs come from

A

plants

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3
Q

AMDR for carbs

A

45-65%

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4
Q

Monosaccharides - aldoses

A
  • 1 aldehyde
  • 1 C
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5
Q

Monosaccharides - ketoses

A
  • 1 ketone
  • 2 C
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6
Q

All hexose sugars have _ carbons, _ hydrogens, and _ oxygens

A

1:2:1

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7
Q

Glycosidic bond

A
  • condensation reaction between two monosaccharides
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8
Q

Alpha glycosidic bond

A

digestible
- facing down
ex. sucrose, maltose

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9
Q

Beta glycosidic bond

A

non-digestible
- facing up
ex. lactose

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10
Q

What end of a polysaccharides is reactive?

A

reducing end

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11
Q

What is a reducing sugar

A
  • sugars that contain an aldehyde group and have an open chain form
  • free anomeric -OH group
  • more accessible to enzymes
  • lactose and maltose
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12
Q

Advanced glycation end products

A
  • found in collagen-rich tissues like in blood samples
  • high blood glucose crosslinks important proteins
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13
Q

Cellulose

A
  • B-1,4 glycosidic bonds
  • unavailable carbohydrate or fiber due to lack of expression of cellulase
  • hydrogen bonds
  • insoluble fiber and non digestible
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14
Q

Starch

A
  • amylose (alpha 1-4) and amylopectin (alpha 1-4 and 1-6) from plant sources
  • source of fiber
  • potatoes, rice, pasta, carrots, root vegetables
  • insoluble fiber and digestible
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15
Q

Amylose and amylopectin % in starch

A
  • 20% amylose
  • 80% amylopectin
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16
Q

Is amylose or amylopectin less soluble in water

A

amylose

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17
Q

Does amylose or amylopectin form gel in water

A

amylopectin

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18
Q

Maillard reaction

A

between carbohydrate and amine groups to form glycosides

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19
Q

Two major steps of carbohydrate digestion

A
  1. intraluminal hydrolysis (amylases)
  2. membrane digestion (brush border glycohydrolases)
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20
Q

Digestion of amylose/amylopectin in the mouth

A
  • salivary a-amylases hydrolyzes alpha-1,4 bonds to form dextrins
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21
Q

Digestion of amylose/amylopectin in the stomach

A
  • acidity of gastric juice destroys enzymatic activity of salivary a-amylases
  • dextrins pass unchanged
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22
Q

Digestion of amylose/amylopectin in the small intestine

A
  • pancreatic a-amylases hydrolyzes alpha-1,4 bonds
  • amylose: dextrins broken to maltose
  • amylopectin: dextrins broken to maltose and a-limit dextrins
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23
Q

Digestion of amylose/amylopectin in the brush border of small intestine

A
  • amylose: maltose hydrolyzed by maltase to glucose
  • amylopectin maltose hydrolyzed by maltase to glucose and limit dextrins hydrolyzed by a-dextrinase to glucose (breaks a-1,6)
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24
Q

Exoglucosidases

A
  • remove glucose units from the non-reducing ends
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25
Lactose and sucrose do not undergo:
luminal hydrolysis but are digested by brush border membrane hydrolysis
26
Fructose (source, bonds, brush border enzyme, monosaccharide product)
- fruit and honey - none - none - fructose
27
Glucose (source, bonds, brush border enzyme, monosaccharide product)
- fruit, honey, grapes - none - none - glucose
28
Amylopectin (source, bonds, brush border enzyme, monosaccharide product)
- potatoes, rice, corn, bread - alpha-1,4 and alpha-1,6 - maltase, glucoamylase, isomaltase - glucose
29
Amylose (source, bonds, brush border enzyme, monosaccharide product)
- potatoes, rice, corn, bread - alpha-1,4 - maltase, glucoamylase - glucose
30
Sucrose (source, bonds, brush border enzyme, monosaccharide product)
- table sugar and desserts - alpha-1,2 - sucrase - glucose and fructose
31
Trehalose (source, bonds, brush border enzyme, monosaccharide product)
- young mushrooms - alpha-1,1 - trehalase - glucose
32
Lactose (source, bonds, brush border enzyme, monosaccharide product)
- milk and milk products - beta-1,4 - lactase - glucose and galactose
33
Absorption of glucose and galactose
- transporter moves from lower to higher concentration - transporter requires sodium (Na+ dependent)
34
Absorption of fructose
- transporter moves from higher to lower concentration via facilitated diffusion
35
Absorption of glucose and fructose in a low sugar meal
- Glucose --> SGLT1 - Fructose --> GLUT5 - GLUT2 used as shuttle on basal side
36
Absorption of glucose and fructose in a sugar rich meal
- Glucose --> SGLT1 - Fructose --> GLUT5 - GLUT2 is upregulated to brush border to help bring in more sugar and on basal side
37
Malabsorption of lactose
- undigested lactose is fermented by bacteria in the large intestine
38
Rate limiting step for carbohydrate digestion
- transport across the epithelium
39
Dietary fibre definition
- plant-derived non-starch polysaccharides indigestible by human enzymes - polymers with 3 or more units - naturally occurring in food - physiological benefit to health
40
Humans lack the digestive enzyme that hydrolyzes what glycosidic bond
- Beta-1,4 linkages
41
Pectin
- soluble fibre - found in skin of ripe fruit
42
Gums
- highly soluble fibre - thicken foods
43
Lignin
- insoluble fiber - woody portion of plants
44
Total fibre =
Dietary fibre + Functional fibre - dietary: from plants - functional: not just from plants but animals too
45
Resistant starch
- not susceptible to enzymatic digestion due to food/physical factors, starch structure, fermentable by colonic microflora
46
Amylose retrogradation
- irreversible - strong stable retrograded starch
47
Amylopectin retrogradation
- reversible - with gentle heating
48
Examples of resistant starches
- unripe bananas - cooked and cooled rice and potatoes - beans and legumes
49
All indigestible fibers: _____ distention _____ bulk _____ satiety _____ daily kcals
- increase - increase - increase - decrease
50
Soluble fibers on gastric emptying
- delay gastric emptying - increase transit time - delay nutrient absorption - low GI
51
Soluble fiber structure
- attract water and form a gel that is highly viscous
52
Soluble fiber fermentation
- more fermentable
53
Soluble fiber examples
oatmeal, lentils, fruit, oat bran, nuts, flaxseeds, beans, peas, cucumbers, celery, carrots
54
Insoluble fibers on gastric emptying
- promote gastric emptying - decrease transit time - increase fecal bulk - prevents constipation
55
Insoluble fiber fermenation
- poorly fermentable
56
Insoluble fiber examples
- whole grains, corn bran, seeds, nuts, barley, couscous, brown rice, bulgur, zucchini, celery, broccoli, cabbage, tomatoes, dark leafy vegetables, grapes
57
Water binding capacity
- bind several times their weight in water - trap nutrients to slow digestion/absorption - mixing of GI contents with digestive enzymes decreases enzyme function as less contact with brush border - lowers nutrient diffusion rate into bloodstream - lowers GI - prevents obesity
58
Absorption/binding capacity
- bind to fatty acids, cholesterol and bile acids - prevent micelle formation, lipid absorption and enterohepatic circulation - decreases serum cholesterol concentrations
59
SCFAs - Lactate
- lowers pH
60
SCFAs - Propionate
- energy source - metabolized in liver - decreases HMGCoA reductase (cholesterol formation)
61
SCFAs - Acetate
- energy source - metabolized in liver
62
SCFAs - Butyrate
- important energy source for colonocytes
63
SCFA production has net effect of
- increase water and sodium absorption in colon - increase mucosal cell proliferation - provision of energy - acidification of luminal environment
64
Fecal bulk ____ as fermentability ____
increases decreases
65
Detoxification
- increase fecal bulk - dilutes effect of toxins and heavy metals - decrease time with intestinal walls
66
Prebiotics
- resistant to digestion/absorption - stimulates growth of select bacteria in gut flora
67
5 mechanisms of fiber with lowering cholesterol
- delayed gastric emptying - interference with digestive enzymes - interference with micelle formation - interference with mixing of intestinal contents - inhibition of cholesterol biosynthesis
68
How fast does digestion/absorption occur?
30-90 min
69
From the portal vein the liver:
- removes 1/3 glucose and most fructose/galactose on first pass - remaining glucose circulated to provide energy to cells and stimulates insulin release
70
Sources of glucose
- diet - glycogen stores - endogenous synthesis from gluconeogenic precursors
71
When the body has excess glucose:
- shifts to anabolic pathways - synthesis of other carbohydrates and sugar residues in other compounds
72
Blood glucose is tightly regulated by:
- the liver - balance between oxidation, biosynthesis and storage
73
What cell types are very dependent on glucose and why
- RBCs, nerves, intestinal mucosa, brain - don't have mitochondria so no complete oxidation - has to consume more glucose per ATP
74
Mean plasma glucose level
90 mmol/L
75
What occurs at at 80 mmol/L plasma glucose level
decreased insulin secretion
76
What occurs at a 70 mmol/L plasma glucose level
- increased glucagon and epinephrine secretion
77
What occurs at a 50 mmol/L plasma glucose level
- symptoms - decreased cognition, aberrant behavior, seizure, coma
78
What occurs at a 18 mmol/L plasma glucose level
- brain death
79
Glycolysis vs Complete oxidation
- glycolysis: produces some ATP, occur in all cells, anaerobic - complete oxidation: lots of ATP, can't occur in RBCs, aerobic
80
Glucose metabolism in muscle cells
- selfish - uses glucose but does not give it back - produces lactate - glycolysis/complete oxidation or store as glycogen for use
81
Glucose metabolism in cardiac cells
- completely oxidize glucose - more mitochondria uses FAs as primary fuel source
82
Glucose metabolism in liver/hepatocytes
- completely oxidize glucose - store it as or produce it from glycogen - uses carbons from glucose for AA/FA synthesis - synthesize it from lactate, pyruvate, alanine - can produce R5P via pentose pathway - gives away glucose and takes in lactate
83
Glucose metabolism in RBCs
- no mitochondria = no oxidation - glucose metabolized to lactate and released into circulation - pyruvate can only come from glucose - obligate glucose user
84
Glucose metabolism in brain
- complete oxidation of glucose - very dependent on blood concentrations - little/no storage of glycogen - can also oxidize ketones - pyruvate can only come from glucose - obligate glucose user
85
Glucose metabolism in pancreas beta cells
- complete oxidation of glucose - lots of mitochondria - most efficient - tightly regulated as a glucose sensor - releases insulin
86
Glucose metabolism in adipocytes
- synthesis of glycerol OR complete oxidation - metabolize excess glucose to acetyl-CoA then store as fat
87
Adipose, muscle, brain, cardiac cells respond to blood glucose changes but...
do not contribute to blood glucose homeostasis by releasing glucose into the blood
88
How many ATP required to start glycolysis
- 2 ATP
89
Fructose in glycolysis
- liver, fructose --> GAP (fructokinase) - it cannot be converted back to fructose - muscle, fructose --> F6P (jexokinase)
90
3 irreversible steps in glycolysis
1. hexokinase 2. phosphofructokinase (PFK) 3. pyruvate kinase
91
Why don't other tissues such as brain or skeletal muscle produce glucose
- lack conversion step from G6P to glucose - don't have the G6Pase enzyme
92
Substrates for gluconeogenesis
- uses lactate (Cori cycle), alanine (muscle proteion catabolism and glycerol (lipolysis)
93
Lactate as substrate new ____ ATP
more
94
Important regulatory step in gluconeogenesis
- PEPCK - levels are very low until neonatal period - need dietary sources of glucose
95
How do glycolysis and gluconeogenesis work together?
- occur at the same time just one side is amplified depending on allosteric/covalent modifications or changes in enzyme concentration at key steps
96
4 irreversible steps in gluconeogenesis
- pyruvate carboxylase - PEPCK - fructose bisphosphatase - glucose-6-phosphatase
97
Hexokinase regulation
- activated by F1P and insulin - inhibited by F6P
98
PFK regulation
- activated by AMP, Pi, F26P, insulin - inhibited by ATP, citrate, H+
99
Pyruvate kinase regulation
- activated by F16P, protein dephosphorylation, insulin - inhibited by ATP, alanine, protein phosphorylation,
100
Pyruvate carboxylase regulation
- activated by acetyl-CoA
101
PEPCK regulation
- inhibited by insulin
102
F16BP regulation
- inhibited by AMP, insulin, F26P
103
Glucose-6-phosphatase regulation
- inhibited by insulin
104
Why store glucose as glycogen in polymeric rather than in free form?
- must maximize storage in smallest possible volume, while still 'readily' available
105
How much space in the liver can be glycogen storage
10%
106
Glycogen and water holding capacity
- uses much less space and holds less water than the same amount of free glucose - minimizing osmotic pressure differential in the cell
107
2 forms of glycogen synthase
- A/GYS1 gene: more active, unphosphorylated, expressed everywhere (muscle, brain, kidney, adipose), rapid response in fed state - B/GY2 gene: less active, phosphorylated, expressed only in liver, replenish glucose pools in fasted state
108
B form of glycogen synthase has less...
- less affinity for UDP-glucose - less sensitive to allosteric activation by G6P
109
What stimulates both forms of glycogen synthase
- insulin
110
Glycogenolysis is stimulated by
- low blood glucose levels - glucagon - epinephrine
111
Fed state =
- increased glycogenesis - insulin promote storage of glucose - prefers to use G6P from gluconeogenesis - lactate is preferentially pushed to glycogen
112
glycogen --> G1P --> G6P --> (liver and muscle)
- liver: G6P --> blood glucose or ATP - muscle: G6P --> ATP (no G6Pase)
112
Fasting state =
- increased glycogenolysis - liver is depleted of glycogen within 24h of fasting - needed to supply plasma glucose
113
Glycogen phosphorylase regulation
- in the liver if glucose is needed, glucagon and epinephrine induce cAMP response which activates glycogen phosphorylase - in muscle, phosphorylation control depends on ratio of phosphorylase A (more active, not sensitive to ATP) and phosphorylase B (less active) - efflux of calcium from muscle contraction also activates phosphorylase kinase that generates phosphorylase A
114
Pyruvate to lactate reaction
- produces NAD+ and 2 ATP - lactate dehydrogenase - reduced oxygen states - rate of glycolysis is way faster than oxidative phosphorylation but it depletes NAD+ quickly so this replenishes it
115
Cori/Alanine Cycle
- pyruvate to lactate and alanine in muscle - blood transfers lactate and alanine to liver - liver recycles lactate and alanine
116
Pyruvate transformed into CADA depends on
- availability of oxygen - metabolic state of the cell - limited by expression of enzyme - requires PDH to transport across mitochondria (requires many cofactors) - tightly controlled via production inhibition (acetyl CoA, NADH, ATP) and covalent modification (phosphorylation)
117
Citric acid cycle points of inhibition
- pyruvate dehydrogenase activity - ATP availability - excess NADH inhibits - Ca2+ stimulates
118
Cells requiring greater respiration (CAC) have more _____ and _____
- mitochondria - cristae
119
What is a cristae
- closed internal compartment to generate concentration gradient for movement of protons - greater surface area = greater respiration
120
Fate of G6P - cell's need for
- energy (ATP/ADP ration) - biosynthesis (NADP+/NADPH)
121
Overview of pentose phosphate pathway
glucose --> 5C sugars --> 6C and 3C sugars
122
Where does pentose phosphate pathway occur
- RBC, adipocytes, liver, mammary gland - in the cytosol, not in mitochondria
123
Purpose of pentose phosphate pathway
- generates NADPH then used to form fatty acids, sterols, and cholesterol - anabolic reactions - generates ribose-5-P for nucleotides and nucleic acids
124
Going into the pentose pathway depends on need for:
- NADPH - ribose 5-phosphate - ATP
125
pentose pathway shunt can reconnect with
glycolysis from ribose 5-phosphate
126
Is ATP consumed or produced in the PPP
no
127
What is more abundant in the body: NAD+/NADH NADP+/NADPH
- NAD+ - breaking down glucose - NADPH - building up other things
128
Fates of postprandial glucose
- muscle --> ATP + CO2 and glycogen - liver --> glycogen - brain --> ATP + CO2 - adipose tissue --> triacylglycerol
129
Hepatic portal vein with absorbed monosaccharides first enter the
liver - 1st pass metabolism of monosaccharides and insulin - removes glucose and most fructose and galactose - insulin stimulates use of sugars for energy and glycogen synthesis
130
Glucose travels to skeletal muscle
- insulin promotes translocation of GLUT4 to increase glucose uptake - glucose taken up for energy and glycogen synthesis
131
Glucose travels to adipose tissue
- insulin promotes translocation of GLUT4 - glucose taken up for energy and fatty acids, glycerol, TG synthesis - excess glucose stored as TG
132
Glucose travels to cardiac muscle
- insulin promotes translocation of GLUT4 - glucose taken up for energy and glycogen synthesis
133
Glucose travels to other tissues
- glucose taken up by GLUT 1 and GLUT 3 based on energy needs of cell
134
High uptake of glucose by the liver is due to high amounts of
GLUT2 and glucokinase which are not inhibited by G6P
135
Does insulin increase glucose uptake into hepatocytes
- nope - liver is generally considered insulin independend
136
Which cells are dependent on insulin for glucose transport
- adipose and muscle
137
Glucose transport from GIT to portal blood involves
- Na2+ by SGLT1 and facilitated diffusion by GLUT2
138
Glucose transport from portal blood into cells involves
- GLUT1-4 family of membrane transport proteins
139
Rate of glucose uptake depends on
- # of transporters - rate of transport, phosphorylation, utilization of glucose
140
GLUT 1 (monosaccharide substrates, sites, affinity, capacity, functions)
- glucose, galactose, mannose - CNS, BBB, RBCs - high - low - basal glucose transport
141
GLUT 2 (monosaccharide substrates, sites, affinity, capacity, functions)
- glucose, galactose, mannose, fructose - liver, pancreas, SI, kidney - low - high - glucose dependent - absorption/reabsorption
142
GLUT 3 (monosaccharide substrates, sites, affinity, capacity, functions)
- glucose, galactose, mannose - high in brain, placenta, muscle, spermatozoa - high - low - basal glucose transport
143
GLUT 4 (monosaccharide substrates, sites, affinity, capacity, functions)
- glucose - skeletal/cardiac muscle, adipose tissue - - high - insulin dependent - role in glucose homeostasis
144
GLUT 5 (monosaccharide substrates, sites, affinity, capacity, functions)
- fructose - SI, kidney, brain, muscle, adipose, spermatozoa - med - - weakest isoform of GLUT
145
Insulin
- synthesized and released by beta cells in pancreas - gut hormones, innervation and activity regulation secretion - promotes uptake of glucose into muscle/adipose cells - promotes conversion of glucose to glycogen in liver/muscle cells - promotes protein synthesis in muscle cells - promotes fat synthesis in adipose tissue - increase glucose uptake by GLUT 4 protein via targeted exocytosis
146
Glucagon
- released by alpha cells in pancreas - inhibited by insulin - promotes breakdown of glycogen to glucose in liver - promotes breakdown of fats to fatty acids in adipose - promotes use of noncarb sources to make glucose in liver
147
How is insulin secretion triggered
- glucose enters B-cells by GLUT2 --> phosphorylated by glucokinase --> retained in cel - glycolysis and complete oxidation occur - increased ATP to ADP ratio --> depolarization --> Ca2+ channels open --> fusion of insulin vesicles --> release of insulin - ATP production in mitochondria drives insulin secretion coupling glucose metabolism
148
Does fructose stimulate insulin release?
- fructose requires GLUT 5 for uptake which is not present in the pancreas so no
149
What is the glucose sensor in the pancreas
- combined action of GLUT2 transport and rate of glucokinase
150
Insulin resistance
- same amount of insulin but less GLUT 4 translocation - action of insulin via receptor is diminished
151
What happens in insulin resistance
- higher glucose levels will force pancreas to secrete more insulin - hyperglycemia and hyperinsulinemia - type 2 diabetes - beta cell fatigue
152
What are catecholamines
- secreted by adrenal medulla (adrenaline/epinephrine) stimulates glycogenolysis and gluconeogenesis - increase in blood glucose concentration
153
What are glucocorticoids
- steroid hormones secreted by adrenal cortex (cortisol) - increase hepatic glucose output and expression of gluconeogenic genes - increase in blood glucose concentration
154
What are tri-iodothyronine (T3)
- modulate and amplify other hormones and actions - increases gene expression for enzymes to regulate metabolism - both anabolic and catabolic - increase BMR
155
How is glycemic load different from glycemic index
- GI does not account for serving size (50g only) - GL takes into account both GI and amount of food in each serving
156
Alcohol enters blood in _ min.
5
157
How many kacl/g in alcohol
7 empty calories
158
Alcohol RQ
0.66
159
Alcohol is structurally similar to ____ but metabolized more like ___
- carbohydrates - lipids
160
Alcohol is metabolized to _____
acetyl CoA
161
Alcohol requires no ____
digestion - it diffuses easily
162
Alcohol digestion rate depends on
- food intake - dilutes it - alcohol concentration - lean tissue mass/body fluid volume - sex - medications - genetics
163
Alcohol is metabolized primarily by the
- 80% liver - 20% stomach
164
Clearance of alcohol is ____ than absorption
slower
165
3 pathways of alcohol detoxification
- ADH (small amounts) - MEOS (large amounts) - catalase
166
ADH alcohol pathway
- ADH metabolizes ethanol to acetaldehyde generating NADH - ALDH metabolized acetaldehyde to acetic acid generating more NADH - acetic acid + coenzyme form acetyl-CoA and enter mitochondria and CAC
167
Build of acetic acid/acetyl-CoA
- increased lactate - increased blood glucose - increased fatty acid synthesis
168
3 negatives ADH pathway
- acetaldehyde adducts formations (binds proteins) - increases ROS formation (lipid oxidation, cancer) - increases NADH/NAD+ ratio
169
Other isoforms of ADH and ALDH metabolize
- oxidize retinol (vit A) to active forms retinoic acid for vision, growth, differentiation - competition effect with acute alcohol intake creating deficiencies
170
MEOS pathway
- occurs in the ER microsomes - uses NADPH and H+ to breakdown alcohol to acetaldehyde using E source via ADH pathway - displaces energy and nutrients from diet
171
Importance of the cytochrome P450 pathway during acute alcohol intoxication
- alcohol inhibits metabolism of barbiturates because it takes precedence - barbiturates remain at high levels and depresses CNS
172
Upregulation of MEOS
- during frequent intoxication - responsible for alcohol tolerance - faster metabolism when alcohol is not present - slower metabolism when alcohol is present - functional vit A deficiency
173
Effects on alcohol consumption connecting to glucose metabolism
- increases mitochondria ratio of acetyl-CoA/CoA and NADH/NAD+ - lactic acidosis (PDH complex inhibited and pyruvate needs NAD+ to convert) - acute hyperglycemia and hypoglycemia (glycolysis is inhibited then gluconeogenesis is inhibited)
174
Effects on alcohol consumption connecting to fat metabolism
- weight gain, fatty liver, hyperlipidemia, ketoacidosis - increased FA and TAG synthesis --> decreased CAC --> increases acetyl CoA and NADH diverts away from FA oxidation towards FA synthesis - increased ketone body formation

Nutrition 301 (7 decks)

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