Biochem Flashcards

1
Q

Recommended Dietary Allowance (RDA)

A

Amounts of nutrients that will provide satisfactory levels of nutrients for most people (2 STDs above average)
Categorized based on sex and age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Dietary Reference Intake (DRI)

A

New dietary guidelines
Goal is to prevent nutrient deficiency and reduce risk of chronic diseases
Includes revised RDA, plus EAR, AI, and UL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Estimated Average Requirement (EAR)

A

Nutrient intake that is estimated to meet the needs of 50% of the people in a designated group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Adequate Intake (AI)

A

Nutrient intake that appears to sustain good health in a group of people
For nutrients that haven’t received enough scientific study

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Tolerable Upper Level Intake (UL)

A

Highest level of a nutrient that will pose no risk of harmful effects for 98% of population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MyPlate

A
Simple nutritional messages
Half of plate fruits and veggies
Balance calories
Avoid oversized portions
Make half of grains whole
Drink water
Compare sodium
Switch to fat free/low fat milk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Malnutrition

A

Disorder of nutrition resulting from imbalance or insufficient diet OR defective assimilation or utilization of nutrients
Both overnutrition AND undernutrition can cause problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

calorie

A

Amount of energy needed to raise temp of 1 g H2O by 1 deg C (15 –> 16 deg C)
1 kcal = 1000 cal = 1 Cal = 4.18 kJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Respiratory quotient

A

Used to determine energy contribution from 1 type of nutrient in a mixed diet
RQ = vol CO2 produced or exhaled/vol O2 utilized or inhaled
RQ carb = 1, RQ protein = 0.8, RQ fat = 0.7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Daily energy expenditure

A

Amount of energy expended doing daily activities
To calculate:
1. Determine BMR and calculate daily (24 hr) energy requirement for BMR
2. Correct for 10% decrease in BMR during sleep (subtract 10%)
3. Determine energy requirements for daily activity (from table) for remaining hours (not sleeping)
4. Correct for thermogenesis (add 10% for mixed diet)
5. Add

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Direct Calorimetry

A

Determine amount of energy in food by combusting in calorimeter and determining amt of heat evolved in combustion (via thermometer)
Measures heat released from physical combustion of a food
Gives higher protein value b/c protein contains 16% N and is incompletely oxidized in the body (mostly excreted as urea, still contains unreleased energy)
Carbs = 4 kcal/g = 17 kJ/g
Protein = 4 kcal/g = 16 kJ/g
Fat = 9 kcal/g = 37 kJ/g
Alcohol = 7 kcal/g = 29 kJ/g

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Indirect Calorimetry

A

Estimates caloric yield in body by measuring O2 consumed, CO2 produced, and N eliminated
Gives lower protein value b/c protein is incompletely oxidized in body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Basal Metabolic Rate (BMR)

A

Energy expended to sustain basic life, involuntary life function (respiration, cardiac function, nerve function, etc.)
Depends on lean muscle mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Thermic effect of food OR dietary induced thermogenesis (DIT)

A

Extra heat produced when food is ingested b/c of work of digestion, absorption, and distribution of nutrients
Energy is lost from food and correction must be made when determining body needs
“Cost” of metabolizing food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Basal energy expenditure (BEE)

A

Calculated based on height, weight, age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Major energy expenditures in human body (3)

A

Basal metabolism
Physical activity
Thermic effect of food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pepsin

A

Secreted by chief cells in stomach in zymogen form
Digests proteins to polypeptides and AAs
Cleaves at N-terminus of hydrophobic (Phe, Tyr, Leu)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Trypsin

A

Produced in pancreas
Stimulated by cholecystokinin
Acts in duodenum
Activated from zymogen form by enteropeptidase
Hydrolyzes proteins
Activates chymotrypsin
Cleaves at C-terminus of basic (Arg, Lys)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Chymotrypsin

A

Produced in pancreas
Acts in duodenum
Activated from zymogen form by trypsin
Hydrolyzes proteins (primarily w/ aromatic ring)
Cleaves at C-terminus of hydrophobic (Phe, Tyr, Trp, Leu, Met)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Elastase

A

Produced in pancreas
Acts in duodenum
Breaks down elastin protein
Cleaves at C-terminus of small (Ala, Gly, Ser)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Carboxypeptidase

A

Produced in pancreas
Acts in duodenum
Activated from zymogen form by enteropeptidase
Cleaves proteins at C-terminus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Aminopeptidases

A

Cleave proteins at N-terminus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Glutathione (GSH)

A

Tripeptide of gamma glutamate, cysteine, and glycine
Antioxidant (counteracts effects of ROS)
Mediates non-specific energy dependent transport of AAs in cells of intestine and kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

gamma-Glutamyltransferase (GGT)

A

Transfers gamma-glutamyl functional groups from GSH to AA outside cell –> causes transfer of AA across cell membrane
Resynthesis of GSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Glutamate

A

Oxidative deamination to form free NH4+ when energy is low (allosteric activation by ADP)
Synthesis from alpha-ketoglutarate and free NH4+ when energy level is high (allosteric activation by ATP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Urea cycle

A

NH4 + Aspartate + CO2 + 3ATP –> Fumarate + Urea + 2ADP + 2Pi + 1AMP + PPi
Takes place in liver
Energetically expensive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Essential Amino Acids

A

Body can’t make or can’t make in sufficient amounts, must be taken in from diet

Phenylalanine
Valine
Threonine
Tryptophan
Isoleucine
Methionine
Histidine
Arginine
Leucine
Lysine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Complete proteins

A

Maintain life and normal growth as sole protein source

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Partially complete proteins

A

Maintain life, but not growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Incomplete proteins

A

Cannot maintain life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Chemical store

A

EAA of a test protein are compared to egg protein (high quality standard) to determine which AA gives largest % deficiency
Essentially, the “limiting” AA
CS = mg EAA/g test protein/mg EAA per g egg protein x 100%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Biological value

A

Measures % of absorbed AA retained for protein synthesis during growth
BV = Dietary N - (Urinary N - Urinary No) - (Fecal N - Fecal No) / Dietary N - (Fecal N - Fecal No) x 100%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Digestibility

A

% of food nitrogen absorbed

D = food N eaten - (fecal N - fecal No)/ food eaten x 100%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Protein Digestibility Corrected Amino Acid Score (PDCAAS)

A

measures limiting AA, but compares it to human requirement of 2-5 yo instead of egg, measures supply of EAA to meet human needs, takes into account digestability

35
Q

Complementary Proteins

A

2 poor quality proteins that differ in limiting EAA will form higher quality, more adequate protein when mixed
Ex. beans (60% Met, 130% Lys) and wheat (95% Met and 40% Lys)

36
Q

Sparing effect

A

some nutrients can reduce/spare requirements of another by fulfilling one of the demands of the second nutrient (in whole or part)
Cystine or cysteine spares methionine (S)
Tyrosine spares phenylalanine
Carbs spare protein

37
Q

Available carbs

A

Can be digested and absorbed for use calorically or to make other metabolic products

38
Q

Unavailable carbs

A

Largely indigestible, provide bulk in diet, aid in elimination
Soluble- gums and muscilages as nonstructural plant components, pectins as parts of fruits, resistant starches
Insoluble- cellulose in place cell walls

39
Q

Dietary fiber

A

Comes from plant sources, remains after breakdown in digestive tract
Soluble- form gels, delay gastric emptying, slow transit through intestine, decrease nutrient absorption
Insoluble- speed up transit time, absorb water, create bulk in feces

40
Q

Crude fiber

A

remains after acid and alkaline digestion of food in lab

Less than dietary fiber

41
Q

Added fiber

A

isolated, nondigestible carbs that are added to foods and have beneficial physiological effects in humans

42
Q

Exchange groups

A

List of foods and serving levels that have approx. same composition of other members of group
Allows selecting exchanges w/o extensive calculations
Fruits, veggies, starch, milk, meat, fat

43
Q

Glycemic index

A

Ability of carb foods to raise blood glucose
Determined by comparing test food w/ glucose
Generally correlated to how highly processed carbs are

44
Q

Glycerides (triglycerides)

A
Store calories most efficiently
Can be converted to cholesterol, phospholipids, and other lipids when required for building material
Part of adipose tissue
Protects/pads skeleton and vital organs
Heat/cold insulation
45
Q

Phospholipids

A

Form interior and exterior of cell membrane

Precursors for prostaglandins, leukotrienes, thromboxanes

46
Q

Sterols (cholesterol)

A

Form interior and exterior of cell membrane

Precursors for bile acids, steroid hormones, vitamin D

47
Q

Essential fatty acids

A

w3 and w6 polyunsaturated fats

Absence from diet causes dermatitis, alopecia, thrombocytopenia, growth retardation

48
Q

Interconversion of FAs

A
Linoleic acid (18:2 ω6) can be desaturated and elongated to arachidonic acid (20:4 ω6)
Linolenic acid (18:3 ω3) can be substited for linoleic acid (not converted)
Oleic acid (18:1 ω9) will be elongated to 20:3 ω9 FA (no function) in absence of linoleic and linolenic acid
Arachidonic acid corrects most EFA deficiencies
49
Q

Trans fatty acid

A

Double bond is trans (happens during saturation process) –> no bend, like a saturated FA
Higher MP
Increased LDL/HDL ratio
Interferes w/ desaturase that catalyzes production of arachidonic acid

50
Q

Body Mass Index

A

body weight (kg)/height^2 (m)
High BMI correlated w/ increased risk of hypertension, dyslipidemia, sleep apnea, female infertility, CVD, osteoarthritis, adult-onset diabetes
Healthy <25

51
Q

Satiety

A

Ventromedial hypothalamus controls eating, responds to bedta agonists

52
Q

Propanolol

A

Beta agonist that induces eating

53
Q

Isoproterenol

A

Inhibits feeding

54
Q

Set point theory

A

Internal mechanism regulates amount of body fat that one carries
Body eats to regain whatever amount the body is “set” for or will stop to lose weight until this genetically programmed level is achieved
- Exercise lowers set point
- Regaining lost weight heightens set point

55
Q

Leptin

A

Released by adipocytes whose level indicates level of fat in body
Stimulates hypothalamus to release neuropeptides to regulate food intake and metabolic activity
Inhibited by sleep deprivation
Weight gain causes increase in leptin, which decreases food intake and increases energy expenditure

56
Q

Ghrelin

A

Short term
Secreted by parietal cells in stomach fundus
Acts on hypothalamus
Causes release of GH and increase of food intake
Stimulated by fasting, hypoglycemia, sleep deprivation
Inhibited by food intake, hyperglycemia, obesity, bariatric surgery

57
Q

Peptide YY

A
Short term
Secreted by ileum and colon
Acts on hypothalamus
Suppresses appetite, lowers food intake
Slows down passage of nutrients through gut
Opposes ghrelin
58
Q

Orexin (A and B)

A

Produced in lateral hypothalamus
Acts on hypothalamus
Stimulates appetite an causes commencement of eating
Dysfunction causes sleep disorder narcolepsy

59
Q

Effect of fructose on metabolism

A

Fructose is normally absorbed slow, but paired with glucose (in sucrose) it is absorbed quickly
Once in the blood, very efficiently taken into liver (glycemic index is low b/c it doesn’t stay in blood)
Doesn’t go through same pathway as glucose, but produces pyruvate and enters TCA cycle
Citrate has nothing to inhibit w/o glycolysis (loses feedback inhibition)
Citrate makes more and more FA instead of glycogen
Also promotes transcription factors that enhance all these pathways
Lipid droplets accumulate in liver

60
Q

Toxic minerals

A
Copper
Fluoride
Molybdenum
Selenium
Arsenic
61
Q

Selenium

A

tRNA associated w/ serine is enzymatically converted to selenocysteine, mRNA signals it to insert at neighboring UGA codon
Function: antioxidant, regulates thyroid function, contributes to immune response

62
Q
Vitamin A
(Active form, biological function, deficiency diseases, toxicity, sources)
A

Fat soluble
Active form: alcohol (retinol), acid (retinoic acid), aldehyde (retinal)
Biological function: vision (rhodopsin), differentiation of epithelial cells (normal mucosal secretion), growth/reproduction (spermatogenesis)
Deficiency: skin lesions, night blindness, infection, Xeropthalmia
Toxicity: Polar bear syndrome- rash, hair loss, hemorrhage, birth defect, fracture, liver failure, death
Sources: animal foods

63
Q

Pro-vitamin A

Active form, biological function, sources

A

Fat soluble
Active form: B-carotene (2 molecules of A)
Biological function: antioxidant
Sources: plants

64
Q
Vitamin D
(Active form, biological function, deficiency diseases, toxicity, sources)
A

Fat soluble
Active form: 1,25-dihydroxyvitamin D3
Biological function: maintain homeostasis of plasma Ca2+ concentration
- active form stimulated by PTH
- production stimulated by low serum phosphate
- opens “valves” from intestine, kidney, and bones to deposit Ca2+ in blood
- calcitonin closes valves when levels get high enough and Ca2+ is deposited in bones
Deficiency: Ricketts (children)- poor calcification of bones, bow-legged; osteomalacia (adults)- demineralization of skeleton
Toxicity- anorexia, excessive thirst, vomiting, weight loss, hypercalcemia, Ca2+ deposition in soft tissues, atherosclerosis, cardiomyopathy
Sources: fish oils, egg yolks, butter, milk, (NOT IN PLANTS), steroid prohormone formed in skin

65
Q
Vitamin K
(Active form, biological function, deficiency diseases, toxicity, sources)
A

Fat soluble
Active form: K1 (phylloquinone), K2 (menaquinone), K3 (menadione)
Biological function: gamma-carboxylation of glutamic acid (helps Ca2+ bind better), 4 blood clotting factors and osteocalcin for bone metabolism
Deficiency: newborns are deficient b/c gut is sterile, bleeding (K3 causes RBC lysis)
Toxicity: none
Sources: green leafy veggies, intestinal bacteria, very little in breast milk, very little in liver

66
Q
Vitamin E 
(Active form, biological function, deficiency diseases, toxicity, sources)
A

Fat soluble
Active form: alpha-tocopherol (b/c of alpha-T binding protein)
Biological function: antioxidant, prevents oxidation of PUFA in membrane
Deficiency: reproductive failure, hemolytic anemia, muscular dystrophy, nerve damage
Toxicity: high doses interfere w/ vit K metabolism
Sources: vegetable oil, wheat germ, nuts, green leafy veggies

67
Q

Vitamin C

A

Water soluble
Active form: ascorbic acid
Biological function: antioxidant (regenerate vit E, fight bacterial infection), hydroxylation (w/ Cu or Fe) for collagen biosynthesis, degradation of cholesterol, synthesis of biogenic amines
Deficiency: Scurvy (swollen legs, loose teeth, bleeding gums, poor wound healing)
Toxicity: none
Sources: citrus fruits, potatoes
Other: deficiency caused by poor nutrition, smoking, oral contraceptives, wound healing

68
Q

Thiamin (B1)

Active form, biological function, deficiency diseases, toxicity, sources

A

Water soluble
Active form: thiamin pyrophosphate (TPP)
Biological function: energy releasing, co-enzyme for pyruvate decarboxylase (TCA cycle), alpha-ketoglutarate (TCA cycle), transketolase (pentose-phosphate shunt)
Deficiency: Beri beri (mental confusion, anorexia, muscle weakness, peripheral paralysis, edema, muscle-wasting, tachycardia, enlarged heart), Sudden Unexplained Nocturnal Death
Toxicity: none
Sources: whole grains, enriched flour, meat

69
Q

Riboflavin (B2)

Active form, biological function, deficiency diseases, toxicity, sources

A

Water soluble
Active form: flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD)
Biological function: energy-releasing, coenzyme for ETC (oxphos), succinic dehydrogenase (TCA cycle), FA oxidation, AA oxidases, monoamine oxidase, xanthine oxidase, glutathione reductase
Deficiency: glossitis (tongue), dermatitis, lesions of mouth, skin, scrotum, cheilosis (cracked lips), sebhorreic dermatitis (lesions of nasal-labial folds, eyelids, ears, vulva, anus, free border of prepuce)
Toxicity: none
Sources: milk, grain, meat, poultry, fish

70
Q

Niacin (B3)

Active form, biological function, deficiency diseases, toxicity, sources

A

Water soluble
Active form: NAD+, NADPH
Biological function: energy releasing, coenzyme in glycolysis, TCA cycle, FA synthesis and oxidation
Deficiency: Pellagra (3Ds), mental changes (fatigue, insomnia, apathy, hallucination, confusion, loss of memory)
Toxicity: none
Sources: meat, poultry, fish, grain, can be produced from tryptophan

71
Q

Biotin

Active form, biological function, deficiency diseases, toxicity, sources

A

Water soluble
Active form: biotin
Biological function: energy releasing, carboxylation rxns- acetyl CoA carboxylase (FA synthesis), pyruvate carboxylase (oxaloacetate formation), propionyl CoA carboxylase (FA and AA metabolism), B-methylcrotonyl CoA carboxylase (Leu degradation)
Deficiency: rarely, but can occur w/ large amounts of raw eggs (GASTON), pregnant women, infants, alcoholics, elderly, long-term antibiotics usage –> dry skin, dermatitis
Toxicity: none
Sources: liver, milk, egg yolk, synthesized by intestinal bacteria

72
Q
Pantothenic acid 
(Active form, biological function, deficiency diseases, toxicity, sources)
A

Water soluble
Active form: CoASH
Biological function: energy releasing, part of CoA, involved in acylation rxns
Deficiency: unlikely, but neuromotor disorders
Toxicity: none
Sources: whole grains, liver, kidney, egg yolk

73
Q
Folic acid
(Active form, biological function, deficiency diseases, toxicity, sources)
A

Water soluble
Active form: tetrahydrofolic acid (THF)
Biological function: hematopoetic, 1C metabolism in AA, purine, and thymine metabolism
Deficiency: fetus development- spina bifida
Toxicity: none
Sources: liver, dark green leafy veggies, wheat germ, whole grains
Other: deficiency can occur from B12 deficiency, pregnancy, alcoholics, drugs

74
Q

B12

Active form, biological function, deficiency diseases, toxicity, sources

A

Water soluble
Active form: cobalamin
Biological function: hematopoetic, methionine synthetase, methylmalonyl CoA mutase
Deficiency: megaloblastic anemia, pernicious anemia, nerve damage
Toxicity: none
Sources: liver, meat, eggs, sea food, made by intestinal bacteria, NOT IN PLANTS
Other: deficiency can result from antibiotics

75
Q

Pyridoxine (B6)

Active form, biological function, deficiency diseases, toxicity, sources

A

Water soluble
Active form: pyridoxal phosphate
Biological function: multiple effect, coenzyme (transamination, decarbosylation)
Deficiency: dermatitis, cheilosis, glossitis, anemia, neurological changes
Toxicity: nerve damage to arms and legs
Sources: grains, meat, fish, fruits, veggies
Other: deficiency from oral contraceptives, drugs, protein intake

76
Q

Pyruvate

key junction: can produce…

A
Lactate
Oxaloacetate
Alanine
G6P
Acetyl CoA
77
Q

Acetyl CoA

key junction: can produce…

A

Fatty Acids
CO2
Cholesterol
Ketone bodies

78
Q

Glucose-6-Phosphate

key junction: can produce…

A

Glycogen
Pyruvate
Ribose-5-phosphate

79
Q

Acute stress response

A

Catecholamines (epinephrine)

  • ** Muscle: increase glycolysis (but no TCA cycle), increase glycogenolysis, decrease glycogen synthesis, increase lipolysis
  • Liver: decrease glycolysis, increase glycogenolysis, decrease glycogen synthesis, increase gluconeogenesis, decrease FA synthesis
  • Adipose: increase lipolysis
80
Q

Long-term stress response

A

Glucocorticoids (cortisol)

  • Muscle: increase protein degradation to produce AAs
  • ** Liver: gluconeogenesis (w/ AAs and glycerol), increase glycogen sythesis
  • Adipose: increase lipolysis
81
Q

Fed state

What happens to carbs? proteins? fats?

A

Carbs: insulin stimulates uptake of glucose by muscle and fat, promotes glycogen storage in liver and fat
Proteins: insulin stimulates AA uptake and protein synthesis in liver and muscle
Fats: insulin stimulates storage of fats as triglycerols by stimulating synthesis of VLDL in liver (carried to fat tissues)

82
Q

Fasting state

A
  1. Glycogenolysis (liver): stimulated by glucagon –> increases [cAMP] –> stimulates PKA –> activates phosphorylase kinase (inhibits glycogen synthase) –> converts glycogen phosphorylase b to a –> degrades glycogen to G1P –> G6P –> glucose
    12-30 hours
  2. Gluconeogenesis: requires lactate (anaerobic resp in muscle and RBC), glycerol (lipolysis in adipose tissue, activated by glucagon), AAs (muscle breakdown)
  3. FFA converted to acetyl CoA via B-ox –> converted to ketone bodies that can be used later in brain
83
Q

Starvation

A

Triacylglycerols become primary fuel

  1. Ketone bodies used in brain as fuel after 3-5 days
  2. Gluconeogenesis by liver slows so AAs and proteins are spared
  3. Blood glucose maintained around 65 mg/dL for 50-60 days, while adipose stores are depleted and muscle is used
  4. Death from cardiomyopathy/muscle weakness, NOT hypoglycemia