Nutrition Exam 2

Front 1

food security

Back 1

the ability to meet one’s food needs

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food insecurity

Back 2

the inability to access enough food to lead active, healthy lives (1 in 8)

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Nutrition transition

Back 3

when a less developed or developing country starts to adopt eating habits of Western cultures

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Food Stamp Program

Back 4

1/11 people in US enrolled, ~$93/month

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WIC program

Back 5

Women, Infant's, and Children; for women who are pregnant, breastfeeding, postpartum; specific foods

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National School Lunch Program

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• All public schools receive govt money to provide school lunches to all children
• Those with a certain family income criteria receive lunch for reduced rate or free
• Have to meet federal guidelines for nutritional value

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Organic food

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foods that are produced using methods that do not involve modern synthetic inputs such as synthetic pesticides and chemical fertilizers, do not contain genetically modified organisms, and are not processed using irradiation, industrial solvents, or chemical food additives.

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Reasons to eat organic

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• 1) Reduce pesticide intake
• 2) Protect environment
• 3) Increase nutritional quality (??)

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Food irradiation

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The process of exposing food to ionizing radiation to destroy microorganisms, bacteria, viruses, or insects

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Food additives + types

Back 10

substances added to foods to produce a desired effect (longer shelf life, more appealing color, improved nutritional value)

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Polychlorinated Biphenyls (PCB’s)

Back 11

organic compounds that are long-lasting; health hazards within environment

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foodborne illness

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sickness caused by ingestion of food containing pathogenic microorganisms or toxins made by these parasites

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triglycerides

Back 13

glycerol backbone attached to fatty acids

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ester bond

Back 14

bonding between fatty acid and glycerol backbone

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esterification

Back 15

adding an ester bond (adding a fatty acid to a glyceride)

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deesterification

Back 16

removing an ester bond (removing a fatty acid from a glyceride)

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diglyceride

Back 17

glycerol + 2 fatty acids

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monoglyceride

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glycerol + 1 fatty acid

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functions of triglycerides

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1) provide energy in food + adipose tissue
2) storage (glycogen limited, fat storage unlimited)
3) insulation and protection (subcutaneous and visceral fat)
4) absorbing and transporting fat soluble nutrients

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phospholipid

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2 fatty acids + phosphorous +/or nitrogen

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function of phospholipids

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1) cell membrane
2) emulsification

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micelles

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tiny particle of fat that has a shell of a water-like (hydrophilic) compound; product of emulsification

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types of emulsifiers

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1) detergent
2) lecithin (in eggs)
3) bile (diet fat)

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cholesterol

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most common sterol; only found in animal products; precursor to fat-soluble vitamins and steroid hormones

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functions of cholesterol

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1) Creation of sex hormones
2) precursor to vitamin D
3) making bile
4) cell membranes
5) part of lipoproteins

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lipoprotein

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assembly of proteins and lipids water-bound to proteins

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function of fat in food

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1) gives you satiety (gastric inhibitory peptide -> food in stomach longer)
2) gives flavor to a meal
3) gives texture to a food
4) essential fatty acids

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very healthy fats

Back 28

extra virgin olive oil, olives, tree nuts

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health benefits of EVOO

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phytonutrients that decrease risk of all diseases esp. cancer; squalene - cancer-protective properties

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health benefits of tree nuts

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phytonutrients; improve blood fats; decrease risk of heart disease

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healthy? fats

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vegetable oils - EFAs

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unhealthy fats

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red meat products - related to cancer and heart disease, trans fatty acids / partially hydrogenated fats - related to cancer and heart disease, fried/commercial/baked - passive overconsumption

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fat replacements

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1. water (like in margarine)
2. gums (gives thickness)
3. protein
4. Olestra - sucrose polyester
5. carbohydrate/sugar (equal energy)

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lipase

Back 34

enzymes of fat digestion

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gastric lipase

Back 35

enzyme secreted by stomach to break down fats; removes short/medium-chain fatty acids from triglyceride so they go to portal system

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CCK

Back 36

1. Goes into blood → gallbladder → release of bile, which has cholesterol and phospholipids (allow you to make mycelles)
2. Goes to pancreas → lipase → duodenum

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chlyomicron

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lipoprotein formed from a triglyceride once it has entered the absorptive cells; transport dietary lipids from the intestines to other locations in the body; mostly triglycerides

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postprandial fat

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chylomicron carrying fat in the blood after digestion

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lipoprotein lipase (LPL)

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located on blood vessels near tissues; takes TGs from chylomicron and converts to monoglyceride and glycerol so FAs can enter adipose and muscle tissue

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insulin and LPL

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- insulin near adipose LPL turns LPL ON
- insulin near muscle LPL turns LPL OFF

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types of lipoproteins

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1. chylomicron
2. very low density lipoprotein (VLDL)
3. low density lipoprotein (LDL)
4. high density lipoprotein (HDL)

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chylomicron composition

Back 42

primarily exogenous (diet-based) triglyceride, some cholesterol

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VLDL

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made by liver, primarily endogenous (self-made) TG and some cholesterol, enters blood from liver

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LDL

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primarily cholesterol; catabolized by liver into cholesterol, TG, and PL; can be oxidized when electrons are taken from fatty acids' double bonds; can go into scavenger pathways

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scavenger pathways

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places on arteries where oxidized LDL is taken up that it should not be going

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plaque

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injury (nicotine, high blood pressure) --> scab, blood doesn't flow properly --> build up along arterial wall

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atherosclerosis

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buildup of substances along arterial walls to form plaques; "arterial hardening"

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antioxidants

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substances that decrease oxidation by donating electrons so the body doesn't take them from fatty acids' double bonds

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high density lipoprotein

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some made in liver and some in intestinal cells; mostly protein; byproduct of VLDL-->LDL; decreases coronary heart disease

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theories of why HDL decreases coronary heart disease

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1. reverse cholesterol transport bringing cholesterol back to liver
2. HDL carries antioxidants to decrease LDL oxidation

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healthy HDL levels

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female >= 50
male >= 40

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formula for cholesterol

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TC = HDL + LDL + TG/6 (VLDL)

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effects of saturated fats on lipoproteins

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increases LDL
decreases HDL
VLDL doesn't change
net effect: increases cholesterol

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effects of MUFAs on lipoproteins

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decreases LDL
HDL increases or doesn't change
VLDL doesn't change
cholesterol decreases a little or doesn't change

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effects of PUFAs on lipoproteins

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**Decrease cholesterol but oxidize LDL
LDL decreases and oxidized
HDL decreases
VLDL doesn't change
cholesterol decreases

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effects of fatty acids on lipoproteins

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increases LDL
decreases HDL
VLDL doesn't change
TC~

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effect of low fat diet on lipoproteins

Back 57

increase triglycerides and decrease HDL
decreases LDL
decrease HDL
increases triglycerides
decrease cholesterol a little bit, but HDL down and TG up, so not good

Front 58

amino acid structure

Back 58

all amino acids have a central carbon, a hydrogen, a carboxyl group, an NH2 group, and an R group (acidic, basic, branched chain)

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transamination

Back 59

need a specific amino acid; transfer amine group from one amino acid to a carbon skeleton to make a new amino acid

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deamination

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removing nitrogen but not making an amino acid → becomes part of urea (liver) → kidneys → exits in urine; carbon structure can be used to make glucose or FAs

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protein quality

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- animal - high - contains all 9 essential amino acids
- plant - incomplete

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healthy proteins

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- beans, nuts (lower HD), whole grain, vegetables, soy - contain phytonutrients and fiber
- egg - nutrients
- nonfat dairy - calcium
- fatty fish - omega 3

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limiting amino acid

Back 63

the amino acid in the lowest quantity or not available, either in food or diet in general; related to body's need

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complementary proteins

Back 64

combine/eat 2 or more to create essential amino acids

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peptide bonds

Back 65

amino group + carboxyl (C=OOH)

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dipeptide

Back 66

two peptide bonds

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tripeptide

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3 peptide bonds (50-100 amino aicds)

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# of aas in protein

Back 68

50-2000 aas

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primary structure

Back 69

amino acid sequence of a protein; dictated by chromosomal DNA --> RNA --> amino aicds

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secondary structure

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local sub-structures, determined by sequence; alpha helix or beta strand

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tertiary structure

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3D structure, determines protein function

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denaturation

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irreversible process rendered by heat, agitation, acid, etc. that causes the protein’s normal function to cease through alteration of protein configuration

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sources of protein

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1) diet
2) tissue recycling via aa pool
3) cells of GI tract sloughing off

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nitrogen balance

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nitrogen consumption and loss measured
intake = output
positive nitrogen balance: intake > loss, usually during periods of growth
negative nitrogen balance: intake < loss; breakdown

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ideal body weight of protein

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0.8 g/kg

males ~ 56 g/day
females ~ 44 g/day

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pepsin

Back 76

- released by stomach
- converts polypeptide chain --> shorter chains + dipeptide
- stored in inactive form called pepsinogen
- release controlled by hormone gastrin

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CCK and proteins

Back 77

CCK --> pancrease --> protein enzymes

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peptidase

Back 78

protein enzymes released by pancreas, convert proteins to amino acids

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amino acid absorption

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absorption --> portal system --> liver --> amino acid pool ; excess can be converted to glucose (gluconeogenesis) or fatty acids

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functions of proteins

Back 80

1. necessary vital body component
2. maintaining fluid balance
3. acid-base balance / maintaining pH
4. hormones, enzymes, and NTs
5. immunity
6. transporting nutrients
7. gluconeogenesis
8. providing energy

Front 81

edema

Back 81

fluid around tissue that is created if blood protein is too low and fluid is not drawn back into capillaries

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role of insulin and growth hormone in protein metabolism

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-insulin - gets aas into muscle
-GH - used to grow tissue

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albumin and globulins

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proteins that draw fluid back into capillaries

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anergy

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lack of immune response, happens when you are malnourished

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gluconeogenesis

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survival mechanism; if liver glycogen is depleted gluconeognesis happens *at the expense of protein synthesis

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protein energy malnutrition (PEM)

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happens when energy needs are not met; most prevalent in growing children; marasmus or kwashiorkor

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marasmus

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starvation - inadequate protein consumption with insufficient caloric intake

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kwashiorkor

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inadequate protein consumption with sufficient caloric intake; failure to grow, apathy/listlessness, swollen belly

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effects of high-protein, low-carb diets

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1) red meat --> heart disease and cancer
2) red meat causes oxidation
3) EAAs cause insulin secretion
4) increases ketones, incomplete lipid catabolism --> increased LDL oxidation, increased calcium loss
5) kidney issues --> increased urine output --> increased water need

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functions of metabolism

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1. release energy from food
2. synthesize products
3. waste products and excretion

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vitamins and minerals in metabolism

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vitamins - coenzymes
minerals - cofactors

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anabolism example

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glycolysis

Front 93

catabolism examples

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carbohydrates --> glucose
lipid --> TG and FA
protein --> amino acids

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photosynthesis

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CO2 from air and H2O and energy from sun → glucose (plant)

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ATP

Back 95

O-P-P-P , high-energy phosphate bond that when broken by enzymes provides energy

Front 96

oxidation

Back 96

loss of an electron/hydrogen (oxidized)

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reduction

Back 97

gain of an electron/hydrogen (reduced)

Front 98

metabolism and oxidation-reduction reactions

Back 98

anabolic pathways - reduction
catabolic pathways - oxidation

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dehydrogenase

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enzymes that release hydrogen

Front 100

B vitamins

Back 100

niacin and riboflavin

Front 101

niacin

Back 101

coenzyme form of niacin is NAD – can accept hydrogen and becomes NADH (reduced form)

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riboflavin

Back 102

coenzyme form of riboflavin is FAD – can accept two hydrogens and become FADH2 (reduced form)

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mitochondria

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major site of energy production in a cell; aerobic metabolism

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types of carb metabolism

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o Aerobic (with oxygen) – produces more ATP
o Anaerobic (without oxygen)

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glycolysis (first step)

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catabolism of glucose --> 2 3-C pyruvates; NAD converted to NADH; produces a few ATP and NADH

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citric acid cycle / tricarboxylic acid cycle (TCA)

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pyruvate --> releases CO2 --> 2-C acetate + COA --> acetyl COA

2-C acetate added to 4-C compound called oxaloacetate --> 6-C citrate

creates FADH2, CO2

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electron transport chain

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major site for ATP production; takes place in mitochondria and requires O2

creates H2O, traps energy as ATP, turns NADH and FAD2 to NAD and FAD so they can return to citric acid cycle

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aerobic metabolism

Back 108

- glycolysis: 6-C glucose --> 3-C pyruvate
- citric acid cycle: 3-C pyruvate --> NADH and FADH2
- electron transport chain: NADH and FDH2 --> H2O and free NAD and FAD

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anaerobic metabolism

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catabolize glucose but create lactic acid from buildup of NADH

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lipolysis

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catabolism of triglycerides in adipose; turns triglyceride into monoglyceride and 2 fatty acids

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hormone sensitive lipase (HSL)

Back 111

allows adipose to release FAs

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free fatty acids

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fatty acids released from cell by HSL

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beta oxidation

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fatty acids --> clip off the end at the beta carbon (2nd carbon) → 2-carbon compound acetate

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catabolism of fatty acids

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FFAs attach to carnitine --> taken up by mitochondria --> beta oxidation breaks down to 2-C acetate and NADH and FADH2 --> acetates go to TCA cycle, NADH and FADH2 go to ETC

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low blood glucose: ketogenesis

Back 115

low blood glucose → low blood insulin → HSL turned on → increase in FFAs in blood → liver → beta oxidation (lots of 2C acetate) → lots of ATP synthesis

2C acetates join to form 4C ketone

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ketogenesis

Back 116

the process of synthesizing ketones from 2C acetates due to low blood glucose

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diabetic ketoacedosis

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in a Type I diabetic (no insulin), lots of ketones being made → pulls minerals out in urine → blood imbalance --> ketoacedosis

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amino acid catabolism

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- in the liver, NH2 is deaminated, R is removed, left with 2C acetate
- 2C acetate enters citric acid cycle
- either gluconeogenesis or ketogenesis

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gluconeogenesis

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- gluconeogenic aas enter citric acid cycle and bypass acetate --> 4C oxaloacetate loses a carbon as CO2 --> becomes 3C carbon compound --> 2 of these join together as glucose (requires ATP)

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ketogenesis

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makes acetate; deaminated portion (NH2) of ketogenic aas used to make ammonia --> urea --> urine

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metabolism during fasting

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1. glycogen stores in liver --> broken down to maintain blood glucose (runs out while fasting)
2. fatty acids --> beta oxidation --> ketones
3. gluconeogenesis

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effects of fasting

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1) increase in blood urea (ketogenesis; catabolizing body protein)
2) increase in minerals in the urine

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metabolism during feasting

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1) extra fat --> adipose
2) extra protein --> aa pools --> fatty acids --> fat
3) extra carb --> glycogen --> fat

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lipogenesis definition

Back 124

- synthesis of a fat from extra carbohydrate and protein
- happens mostly in liver
- requires ATP

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lipogenesis process

Back 125

carb and protein reduced to 2C acetate --> insulin stimulates an enzyme to combine or ELONGATE them to create FAs --> when 3 FAs are produced this way they are joined to a glycerol --> TG --> liver packages them into VLDL

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lipogenesis effects on cholesterol

Back 126

- increases VLDL (not catabolizing to LDL)
- decreases LDL
- decreases HDL