Nfs 243 Exam 2

Front 1

How do you determining L and D depends on what?

Back 1

The position of the hydroxyl group

HC=O #1 C
I
HC--OH #2 C<---- to the right = D
I
H2C--OH #3 C

Front 2

Sucrose is...

Back 2

a non-reducing sugar

Front 3

All mono-saccharides are...

Back 3

reducing sugars

Front 4

Carbonyl group vs. Aldehyde group vs. Ketose group

Back 4

I H R
C=O I I
I C=O C=O
I I
R R

Front 5

What type of sugars can react with alcohol? How?

Back 5

-Reducing sugars like glucose
*Carbonyl group can react with itself (which is an alcohol). Aldehyde reacts with # 5-OH group to form a hemiacetal

Front 6

What is a hemiacetal?

Back 6

It is formed from a sugar reacting with an alcohol on the #5 OH. This creates an asymmetric carbon which has an -OH branched off of the top and it can be either alpha (drawn on the same side of the D or L) or beta (drawn on the opposite side)

Front 7

What would be considered a reducing sugar?

Back 7

The carbonyl carbon (the 1st C) is not tied up in the linkage between the disaccharides

Front 8

what happens when glucose is put in a solution?

Back 8

-It reaches its equilibrium between alpha and beta (equilibrium must be met only if it is passed in the open chain form which is found in very small amounts)
-The solution would then contain 64% beta and 36% alpha

Front 9

What can glucose do in his open chain form?

Back 9

It can react with amines
*This causes an in vivo reaction (Mailard Reaction in your body)

Front 10

What is a function of reducing sugars?

Back 10

Reduce metal salts (change colors)

Front 11

Which is the only for of glucose that can react with hemoglobin?

Back 11

D-glucose (not alpha or beta)

Front 12

What can hemoglobin A1C be used for?

Back 12

-It can be tested for people with diabetes
-Measures glucose levels over a long period of time because it is glycosilated and bound to a sugar
*glucose binds irreversibly to hemoglobin and stays with it until hemoglobin turns over (about 3 months)

Front 13

Why is glucose a predominant fuel over galactose?

Back 13

-Although the structures are almost identical (C-4 OH is switched), glucose has the lowest % aldehyde
*This means less chances to react with sugars and have free aldehydes floating in the body
-Galactose in the open chain form can react with the amine groups of proteins and mess with their structure
-glucose is more stable
-galactose could become undigestible for plants

Front 14

Which enzymes help in the digestion of carbs?

Back 14

-Pancreatic amylase is secreted into the lumen and the stomach
-Enzymes are produced in the brush boarder cells of the small intestine (sucrase)
*These break down poly- and disaccharides into monosaccharides

Front 15

How do broken down carbs move thru the epithelial cells into the blood?

Back 15

From the apical side to the basolateral side of the membrane

Front 16

What helps the monosaccharides across the membrane towards the blood?

Back 16

Glucose sodium symport system

Front 17

How does the glucose sodium symport system work?

Back 17

-Na binds to the transporter protein to create a higher affinity for glucose
-Na is pumped out by an energy dependent system (Na/K ATPase)

Front 18

GLUT 2

Back 18

Transports glucose across the basolateral side of the intestinal cell into the blood
*Found in the Liver, pancreatic beta cell, and the kidneys

Front 19

GLUT 5

Back 19

-Brings fructose across the apical side of the intestinal cell membrane
(Then brought out of the cell by GLUT 5)

Front 20

Where is GLUT 1 found?

Back 20

-Erythrocyte (humans)
-Blood-brain barrier
-Placenta
-Fetal Tissue

Front 21

Where is GLUT 3 found?

Back 21

Brain neurons

Front 22

Where is GLUT 4 found?

Back 22

-Brown and white adipocytes
-Heart
-Skeletal muscles
*only GLUT transporter regulated by insulin

Front 23

Where is GLUT 7 found?

Back 23

The E.R. of hepatocytes

Front 24

How does fructose move best along the cell?

Back 24

With glucose
(isolated fructose moves slower and pure fructose can mess with insulin response)

Front 25

What occurs in a GLUT 1 deficiency?

Back 25

-Not enough glucose is brought to the brain
*Provide with ketone bodies if caught early
-Very rare
-Severe symptoms (tremors, low cerebral spinal fluid, mental retardation)

Front 26

How does insulin transport glucose?

Back 26

-Insulin binds receptors which signal the cell to produce GLUT 4
-GLUT 4 gets translocated to the surface to facilitate glucose entering the cell
*When insulin decreases, GLUT4 stays in the cells as vesicles

Front 27

What is the hexosemonophosphate shunt?

Back 27

Glycolysis diverts metabolites to produce ribose sugars (for DNA and RNA synthesis) and NADPH (CP450 and lipid synthesis pathways)

Front 28

What can serve as a substrate for gluconeogenesis?

Back 28

Lactate

Front 29

What does insulin prefer?

Back 29

Glycolysis and glycogenesis

(glucagon favors gluconeogenesis and glycogenolysis)

Front 30

Which pathway is more favored for fructose in glycolysis? Why does is not happen

Back 30

Fructose to Fructose-1-P
*Does not really happen because it skips the rate limiting step (PFK-1) -creates a lot of pyruvate and other Krebs cycle substrates
-creates a build up of citrate leading to increased FA synthesis
**High fructose is lipogenic

Front 31

What is the rate limiting step in glycolysis?

Back 31

F-6-P to F-1,6-bisP
*When this is low the gluconeogensis occurs

Front 32

What are the 3 irreversible steps of glycolysis?

Back 32

- G to G-6-P
- F-6-P to F-1,6-bisP
- Pyruvate to PEP

Front 33

What can the reaction pyruvate to acetyl CoA be used for?

Back 33

-FA synthesis
-Krebs Cycle

Front 34

What can initiate the hexosemonophosphate shunt?

Back 34

G-6-P

Front 35

What do dehydrogenases do in the Krebs cycle?

Back 35

Catalyze the removal of H's from FAD and NAD
*Produces NADH (highly negative standard reduction potential = electron donator) and FADH2 to enter the ETC

Front 36

Glucokinase

Back 36

-In the Liver and has a high Km (reaction occurs slower and lasts longer)
-Grabs all of the glucose beyond what the muscle can use (liver clears glucose)
-Induced by insulin
*used for the reaction G to G-6-P

Front 37

Hexokinase

Back 37

-In the muscle and lower Km (higher affinity for glucose)
-Will not be able to take up a lot of glucose and cannot clear glucose
*used for the reaction G to G-6-P

Front 38

What can insulin stimulate in glycolysis?

Back 38

Irreversible steps (G to G-6-P)

Front 39

When is glucagon stimulated?

Back 39

During fasting

Front 40

What allosterically stimulates PFK-1?

Back 40

Fructose-2,6-bisP
*positively*

Front 41

What is PFK-2 involved with?

Back 41

F-6-P to F-2,6-bisP

Front 42

What indirectly regulates PFK-2 activity?

Back 42

insulin

Front 43

What does glucagon do with regards to gluconeogenesis?

Back 43

-Stimulates the 2nd messenger (ATP to cAMP)
-It then activates the protein kinase (a phosphorylating enzyme) protein kinase A which involves ADP to ATP
-The bifunctional enzyme is then phosphorylated

Front 44

What will be inhibited when glucagon stimulates the 2nd messenger?

Back 44

PFK-1

Front 45

What can high levels of fructose cause?

Back 45

-Fructose intolerance
-A decrease in the chances of carbonyl compounds binding to hemoglobin A1C (decreases the risk for heart disease)

Front 46

What has increased in consumption over the past 30 years?

Back 46

-Fat
-Refined Carbs
*sugar consumption has remained unchanged despite increase uses of HFCS

Front 47

Fructose intolerance

Back 47

-Deficient in Aldolase B
-Converts F-1-P to dihydroxy acetone phosphate
-Can cause hepatic failure and death

Front 48

What happens if pure fructose is consumed in the diet?

Back 48

-It is not rapidly absorbed
-Can end up in the G.I. tract and can ferment
*not reasonable because no one eats a pure fructose diet*

Front 49

Stable isotope of fructose

Back 49

Converted to a fatty acid but mostly converted to glycogen

Front 50

HFCS stimulates lipogenesis?

Back 50

-Fructose will not end up in the blood
-Can be catazlyzed by glucokinase but mostly by fructokinase
-Thought to provide a substrate for lipogenesis

Front 51

High pure fructose = High uric acid production?

Back 51

-The reaction converts F-1-P to DHAP and glyceraldehyde
-This reaction uses up ATP
(ATP-->ADP-->AMP-->Uric acid)
*uses up ATP because glyceraldehyde does not have the phosphate group needed to be used for energy*

Front 52

High Uric acid production = inhibition of nitric oxide-stimulated vascular endothelial function?

Back 52

-Inhibition of vascular relaxation = depressed insulin effect on glucose uptake
*insulin increases vasodilation and GLUT4
-Depressed glucose uptake = insulin insensitivity = metabolic syndrome

Front 53

What is an example of a transport protein?

Back 53

Albumin-->transports short chained fatty acids in their non esterified form into portal circulation

Front 54

What happens to an essential amino acid that is bound to glucose?

Back 54

-The amino acid can become unavailable (Mailard reaction)
-This only occurs with non-alpha amines (ex:lysine)
-The entire protein quality is reduced

Front 55

Histidine

Back 55

-Requirement is low
-Essential for infants with health problems
-No proven metabolic synthesis pathway

Front 56

What can Arginine be made from?

Back 56

-Glutamine
-Glutamate
-Proline

Front 57

Chemical score/AA score

Back 57

-Don't need animals
-Determines which is in the lowest amount relative to how much is required (limiting AA)
-Score = Limiting AA in food protein / content of same AA in reference protein

Front 58

Protein Efficiency Ratio

Back 58

-Rats in the study can be messy or eat their own feces (throw off protein count #'s)
-Use 21 day old weanling male rats
-Feed diet containing 10% "test" protein
-Feed control group 10% casein diet (correct control diet PER = 2.5)
-Feed animal for 28 days
-PER = gain in body wt (g) / protein consumed (g)
*growth assay*
-High PER = high quality protein

Front 59

Good quality protein has what effect on the daily value label?

Back 59

Daily value on label is low
*basis for labeling requirements

Front 60

Biological value

Back 60

-Rats are used
-100 is the best #
-BV = I - (F-Fo) - (U-Uo) / I - (F-Fo)
-BV = (N retained/ N absorbed)

Front 61

About what % of nitrogen is in protein?

Back 61

16%

Front 62

What is an equation that can be used to determine the amount of protein in a food?

Back 62

Amount of nitrogen X 6.25 (correction factor)

Front 63

Nitrogen eliminated in the feces can come from where?

Back 63

-Cells coming off of the intestinal lining
-Bacteria

Front 64

Net Protein Utilization

Back 64

-NPU = N retained / N consumed
-Accounts for the fact that some proteins aren't absorbed as well as others
-NPU = I - (F-Fo) - (U-Uo) / I
-Can use total carcass nitrogen
-NPU = (TCN on test prot.) - (TCN on prot.-free) / N consumed

Front 65

What is deamination?

Back 65

-Remove amine group
-Amine is sent through the urea cycle

Front 66

What is transamination?

Back 66

-Remove amine group
-Transfer the amine group to another product
*Critical for the body's use of non EAA by converting them from other non EAA or EAA
*The transfer of an amine group creates a carbon skeleton (alpha keto acid)

Front 67

How can a carbon skeleton be used once its amine group is removed?

Back 67

-In the Krebs cycle
-As a ketone body
-As glucose
-Converted to FA

Front 68

Alanine aminotransferase (ALT)

Back 68

-Catalyzes the transfer of an amine group from alanine to some alpha keto acid (alpha keto glutarate)
-Alanine then gets converted to glutamate
*Reaction is reversible

Front 69

What is pyridoxal phosphate's role with ALT?

Back 69

-It's a coenzyme necessary for transaminase reactions
-pyridoxal phosphate gets converted to pyrodoxamine (takes the amine from alanine)
-pyrodoxamine transfers the amine group to alpha-ketoglutarate to form glutamate which in turn regenerates the pyridoxal

Front 70

Aspartate Amino Transferase (AST) reaction

Back 70

aspartate -----> oxaloacetate
AST

Front 71

Heart muscle have more of what transferase?

Back 71

AST
(an increase of ALT can show heart damage)

Front 72

What 2 tests can show liver damage?

Back 72

-increase of AST
-increase of ALT
*can be from lipitor*

Front 73

Glutathione

Back 73

-Gamma-glutamyl-cysteinyl-glycine (tripeptide)
-Cystein group deals with function (has disulfide bonds)

Front 74

Glutathione in leukotriene biosynthesis

Back 74

-Arachodonic acid enters the eicosanoid pathway from the cell membrane by phospholipase A-2
-Can enter the lipoxygenase pathway (inflammatory mediators)
*Activated by injury or inflammation of the cell

Front 75

GSH and it's effect on peroxides

Back 75

-Reduced form = GSH-peroxidase
-Selenium containing enzyme
-Breaks down peroxide
-GSH + H202 ------->2H20 + GSSG
GSH- peroxide
*GSSG = 2 glutathione's bound together

Front 76

Peroxides

Back 76

-Can be used to kill microorganisms (biproducts of metabolism)
-Found in lipid peroxidation
-Can be formed by free radicals

Front 77

Glutathione reductase

Back 77

-Riboflavin (Vit. B2) containing enzyme
-Converts GSSG back to GSH

Front 78

How does glutathione eliminate toxins?

Back 78

-Can bind to Leukotriene A4 (non-polar)
-This forms LTC4 which is more water soluble because a peptide is added to it by being bound to the sulfur part of glutathione
*LTC4 helps to eliminate toxins

Front 79

Carnitine

Back 79

-Carnitine acyl transferase 1 and 2 help fatty acyl CoA get across the mitochondrial inner membrane to generate energy
*It is structurally an amino acid

Front 80

Creatine

Back 80

-Can be a quick source of additional ATP(energy) when ATP is depleted from the muscle during strenuous exercise(exhaustion is reached)
-Should be constant in the muscle
-Can be a crude measurement used to determine muscle mass (more muscle = more creatine excreted in the urine)
*Structurally an amino acid

Front 81

The conversion of Creatine to phosphocreatine

Back 81

-Exothermic reaction (releases about -10,300 calories)
-Non-enzymatic (chemical breakdown)

Front 82

Phenylalaine and tyrosine metabolism

Back 82

-Uses a monoxygenase
*An oxygen added to it to form the hydroxyl group on the benzene ring of phenylalanine to create tyrosine
*The other oxygen used in the reaction used to form H2O

Front 83

Which micronutrients are used in phenylalaine and tyrosine metabolism?

Back 83

-Enzyme contains Fe and Copper
*Vit C (a H2O soluble reducing agent) is used to reduced the metals to the -ous form (2+)

Front 84

What can phenylalanine be metabolized to make?

Back 84

-Catacholamines (epinepherine and nor epinepherine)
-Acetyl CoA (for energy or FA synthesis)

Front 85

What does the adrenal cortex make?

Back 85

Steroid hormones

Front 86

What does the adrenal medulla make?

Back 86

Catacholamines

Front 87

PKU

Back 87

-Deficient in phenylalanine monoxoygenase (no conversion to tyrosine)
-Creates a build up of phenylalanine

Front 88

What can tyrosine amino transferase do?

Back 88

Can form glutatmate

Front 89

Tryptophan metabolism

Back 89

-Tryptophan serves as a substrate for seritonin (controls blood flow around the intestine)
-Seritonin can form melatonin (sleep regulation)
-Conversion occurs mostly in the intestinal tract

Front 90

What can tryptophan dioxygenase be used to generate?

Back 90

-Acetyl CoA
-NAD+
-NADP+
*Can be used for energy or FA synthesis

Front 91

Methionine and Cysteine Metabolism

Back 91

-Meth. converted to homoC
(Rarely, some people are deficient in the enzyme that converts homoC back to Meth.)

Front 92

Homocysteine

Back 92

-Intermediate of the conversion of methionine to cysteine
-Possibly a risk factor for heart disease
-Excess can lead to death of atherosclerosis (toxic to blood vessels)

Front 93

What are micronutrients involved in Methionine metabolism?

Back 93

-Vitamin B12 (homoC to meth.)
-Folate
-Vitamin B6

Front 94

What can the metabolism of cysteine do?

Back 94

-Create taurine to make bile acids
*Cysteine can also make glutamate

Front 95

Where is insulin excreted from?

Back 95

The beta cells of the pancreas from a rise in plasma amino acids

Front 96

What does insulin stimulate?

Back 96

-The entry of AA into the cells
-Protein synthesis
*Anabolic hormone

Front 97

What does glucagon increase the uptake of?

Back 97

-AA in the liver (provides carbon skeletons for gluconeogensis)
*Secreted from the alpha cells of the pancreas
*Catabolic hormone

Front 98

what does the EPA deal with?

Back 98

Pesticide control

Front 99

What does the FTC deal with?

Back 99

Advertising

Front 100

Difference between a food and a drug

Back 100

-Food = Cholesterol lowering (not a disease)
-Drug = Prevents heart disease

Front 101

When can a food have prevention against disease claims?

Back 101

Congress allows heart disease prevention claims on foods high in oat fiber under strict guidelines

Front 102

What does a drug have to proven in order to be placed on the market?

Back 102

-Safety
-Efficacy

Front 103

Label

Back 103

Refers to what is on the product

Front 104

Labeling

Back 104

What is on the product and anything associated with the producr

Front 105

What prevents a food additive from being allowed on the market?

Back 105

If it is found to cause cancer in humans or animals (Delaney Cause)

Front 106

What is not considered a food additive?

Back 106

-Pesticide
-Color additive
-New animal drug
*F.A.'s should be GRAS

Front 107

What is the federal register?

Back 107

A daily publication of the executive branch which states enforced laws

Front 108

What does not have to be considered GRAS?

Back 108

Dietary Supplements

Front 109

FDA inspections

Back 109

-Refusing entry to an inspection violates the law
-Don't need a warrant (4th amendment)

Front 110

Crepe Label

Back 110

-Stated that dietary supplements must contain a label stating that vitamins and minerals can be supplied by the diet
-FDA never got it finalized in 1973

Front 111

FDA and its minimum and maximum of nutrients (1973)

Back 111

-Dietary supplements should have more than 50% of a nutrient and less than 150% or considered a drug

Front 112

What happened in 1976 to the FDA?

Back 112

-They had to stop trying to consider dietary supplements as drugs
-The vitamin and mineral amendment which got congress involved

Front 113

Implicit claim vs. Explicit claim

Back 113

High fiber vs. Contains high fiber and low fat which decreases the risk of heart disease

Front 114

What happened in 1985?

Back 114

-Kelloggs did not wait to change the regulation
-Made explicit claims to violate the law (promoted themselves as a drug) to make the FDA take action
-Got the National Research Counsel involved to endorse their ad

Front 115

Who has the "Burden of Proof"?

Back 115

FDA
*Determines safety for dietary supplements after they are placed on the market

Front 116

NLEA of 1990

Back 116

-Congress included authority for the FDA to decide which explicit health claims were allowed on foods
-FDA gets to determine the wording on the label and which foods qualify
*Did not allow dietary supplements to make explicit claims*

Front 117

What are 2 health claim exceptions allowed on pills?

Back 117

-Folic acid (neural tube defects)
-Ca (osteoporosis)

Front 118

How did the DSHEA of 1994 changed the NLEA for dietary supplements?

Back 118

-Created a new category of food substances (dietary supplements)
-Created a new "safety standard" (significant or unreasonable risk of illness or injury)
-Defined what can be a dietary supplement
-Can use 3rd party materials to inform consumers about health benefits
-Use of nutritional support statement (bodily function not disease)
-Must include "has not been evaluated by the FDA"

Front 119

What happens if the advertisment is misleading?

Back 119

The FTC can get involved

Front 120

Acetalaldehyde

Back 120

-Toxic
-Mutagenic (interacts with amine groups by effecting the normal structure and function of DNA) and carcinogenic

Front 121

Disulfiram

Back 121

-Blocks aldehyde dehydrogenase
-Decreases the sickness from alcohol (no conversion to acetate)

Front 122

What type of tests are used to determine if something is mutagenic?

Back 122

In vitro tests (easy and takes 48 hrs)
*Carcinogenic = doses to animals and have to wait a lifespan (time consuming and expensive)

Front 123

CP450

Back 123

-Inducible enzyme
-Heme protein
-Uses oxidation reactions (binds to a substrate [R-H] to create a hydroxyl group [R-OH]
-Reduces Fe to -rrous state (+2)

Front 124

What induces CP450?

Back 124

Alcohol
*It changes the metabolism processes of the liver

Front 125

Where do most oxidation reactions occur?

Back 125

Smooth E.R. (microsomal fraction)
*can be non-microsomal (alcohol DH)

Front 126

Hydrolysis rxn

Back 126

-Split with water
*structural modification

Front 127

Reduction rxn

Back 127

-Azoreductase can split azo bond (R-N=N-R) to form 2 separate amines
-Common in colon because lots of bacteria
*structural modification

Front 128

Conjugation rxn

Back 128

-Addition of a side chain to a molecule
(Ex:methylation-->does not necessarily make the compound water soluble)
*phase 2 structural modification

Front 129

What is the 1st metabolic reaction a toxic is exposed to?

Back 129

CP450
*found in the lungs, liver ER (highest), skin, and intestinal lining

Front 130

What do PCB's induce?

Back 130

CP450

Front 131

What is a proximate carcinogen?

Back 131

A cancer causing substance (can be activated by gut flora)
*found in the environment as a pre/pro carcinogen (stable)

Front 132

What can the cell do when it is affected by a carcinogen?

Back 132

-Try to repair the DNA
-Die
-Mutate

Front 133

Metabolism of toxins

Back 133

-Host defense=immune response and encapsulation
-Elimination of the chemical in an "unchanged form" = Expire air, vomit, urine, sweat, feces
-Structural modification = metabolize the toxin by altering the structure to make it less toxic and easily excreted

Front 134

What is impermeable to many toxins?

Back 134

The skin

Front 135

What can be used for joint pain?

Back 135

DMSO on the skin
*Can easily carry material in the body and can taste within minutes of putting on the skin

Front 136

What are cruciferous vegetables high in?

Back 136

-Glucosinolate
-Isothiocyanate

Front 137

Sulforaphane

Back 137

-A glucosinolate / metabolic enzyme
-Potent inducer of phase 2 metabolism
-Suppresses CP450
-Induction of apoptotic pathways
-Suppresses cell cycle progression (cell division)
-Inhibition of angiogenesis
-Anti-inflammatory activity

Front 138

Formation of Indole-3-Carbinol

Back 138

-Glucosinolate
-Glucobrassicin is affected by myrosinase (when Indole-3-Carbinol is eaten or broken up, this is released)
-Myrosinase cleaves off the S-glucose and sulfate group
-A cyanide group is left over, Isothiocyanate (Indole-3-Methylcyanate)
-The isothiocyanate is unstable so it loses the cyanide to form the Indole-3-Carbinol

Front 139

What does Indole-3-Carbinol induce?

Back 139

CP450 which increases production of estrogens because of an increase of hydroxylases