Macro Quiz 2

Front 1

Purpose/ Location of HMP Shunt

Back 1

To generate important intermediates not produced in other pathways:
Pentose phosphates, necessary for the synthesis of the nucleic acids found in DNA and RNA
Reduced NADPH, used for important metabolic functions including:
the biosynthesis of fatty acids, cholesterol, and sterols
the maintenance of reducing substrates in red blood cells necessary to ensure the functional integrity of the cells (reduce glutathione/ GSH, in red blood cells)
and drug metabolism
Active in the LIVER, mammary glands, testes, adipose tissue

Front 2

Why is the HMP shunt a link with fat metabolism?

Back 2

Fatty acid synthesis
Makes NADPHs, used as a reducing agent (hydrogen doner) in multiple parts of fatty acid synthesis
Also used to make cholesterol and other sterols

Front 3

In Glycolysis how are substrate cycle enzymes regulated?

Back 3

Glucokinase (Liver)/ Hexokinase (muscle)
When ↑ glucose
Turned on by: insulin
Turned off by glucagon

PFK
Turned on by: AMP, insulin
Turned off by: ATP, Citrate, H+, glucagon

Pyruvate Kinase
Turned on by fructose, 1,6 biphosphate, insulin
Turned off by: ATP, alanine, glucagon, epinephrine (liver only)

Front 4

In Gluconeogenesis how are substrate cycel enzymes regulated?

Back 4

Glucose 6 – phosphatase
Turned on by: glucagon
Turned off by: insulin

Fructose 1,6 biphosphatase
Turned on by: glucagon
Turned off by AMP

Pyruvate carboxylase & PEPCK
Turned on by: glucagon
Turned off by: insulin

Front 5

Why might Fructose cause elevated lipid levels

Back 5

Fructose enters glycolysis after PFK, the key regulatory enzyme, encouraging the continued production of energy even when plenty is available.

Front 6

Glycogenolysis/glycogenesis: How are these regulated by hormones?

Back 6

Insulin (insulin receptors in muscle/liver)

Glucagon (glucagon receptors in liver only

Epinephrine (adrenergic receptors (B-type) in the musle)

Front 7

Glycogenolysis/glycogenesis: What are the two key enzymes?

Back 7

Glycogen synthase
Glycogen phosphorylase (breaking glycogen down)

Front 8

Describe the glucagon/epinephrine cascade

Back 8

Glucagon(liver)/Epinepherine(B-receptor in muscle and liver)

+ adenylate cylase, ATP, ↑ cAMP via G protein

+ protein kinase A
Cascade of P (Ca++ amplifies signal)

Important for muscle cells during contraction

Nerve impulse (depolarized membrane, Ca++ efflux from sarcoplasmic reticulum)

Front 9

Role of cAMP in glycogenolysis/glycogenesis

Back 9

Hormone-triggered cAMP cascade controls glycogen metabolism by reciprocally regulating glycogen synthesis and breakdown

Front 10

What is the end result? (P state of enzymes) during glycogenolysis/glycogenesis

Back 10

Glycogen phosphorylase is P and is active

Glycogen synthase is P and is not active

Front 11

What is the significance of calcium in muscle?

Back 11

Important for muscle cells during contraction

Front 12

Describe the insulin cascade

Back 12

Insulin binds to insulin receptor (2 a or 2 b subunits)

Insulin binding site on a subunits (conformational change)

B subunits have tyrosine kinase activity (phosphorylation = active)

Auto-P of tyrosine residues of B subunits

Activate various signal transduction systems = glucose gets in

Front 13

What is the end result (P state of enzymes)

Back 13

Tyrosine residue is phosphorylated

Insulin destroys cAMP = ↓ kinases (stops phosphorylating) = ↓ glycogenolysis

Front 14

In general – how do hormones influence the carbohydrate pathways?

Back 14

Insulin:
1. + glycolysis (muscle)
2. + glycogenesis

Glucagon:
1. + glycogenolysis (liver)
2. + gluconeogenesis
3. – glycolysis

Epinepherine
1. + glycogenolysis (muscle)

Glucocorticoids/cortisol
Released under stress/starvation/exercise/diabetes
1. ↑ AA catabolism
2. + gluconeogenesis

Front 15

What is the fate of lactate during/after activity?

Back 15

During exercise
1. Consumed by the same tissue and never reaches the blood
2. At 60% V02 max or more spills into blood

After exercise
1. Goes to the heart and burned for ATP

2. Goes to the liver and is converted to glucose in Cori Cycle

Front 16

Main gist of the Cori Cycle

Back 16

Lactate goes to the liver and is converted to glucose through gluconeogenesis

Front 17

What is glycemic index (GI) and how is it measured?

Back 17

Blood glucose response of available carbohydrate in food relative to the effect of an equal amount of glucose (50 G)

Group of at least 10 subjects do two tests
1. Subjects are fasting
2. Test 1: 50 g card load of glucose
3. Test 2: 50 g carb load of test food
4. Blood is sampled (finger-prink or venous) at baseline and at 15-30 minute intervals for two hours
5. Typically 0min, 15 in, 30 min, 60 min, 90 min, and 2 hour intervals
6. A blood sugar response curve is constructed called area under the curve (AUC), AUC reflects the total rise in blood sugar levels after eating the test food
7. GI rating (%) = (AUC for the test food / AUC for glucose) x 100
8. Average of the GI rating from all ten subjects is published as the GI of that food

Front 18

Give a few examples of high, moderate, low GI foods

Back 18

i. High:
1. Gatorade
2. Jelly beans
3. Coco Puffs
4. White rice
5. Dates
ii. Moderate:
1. White bread
2. Sweet potato
3. Grapes
4. Raisins
iii. Low
1. Wheat bread
2. Carrots
3. Banana
4. Yams
5. Rye bread

Front 19

Describe factors that influence GI

Back 19

i. Gastric emptying
ii. Disruption digestion
iii. Amount of carb
iv. Ripeness of fruit
v. Nature of simple sugars (sucrose, fructose, lactose, glucose)
vi. Physical form of food: whole apple vs. apple juice
vii. Nature of starch: amylose, amylopectin, resistant starch

Front 20

What is glycemic load (GL)?

Back 20

i. The average GI of carbohydrate foods consumed and the total carbohydrate intake over a specific time period
ii. GL = GI x CHO g per serving
1. Ex. White bread
2. GI = 73
3. CHO per serving = 14
4. GL = 14 x .73 = 10

Front 21

What is meal/dietary GI and how it is estimated?

Back 21

i. Add up all the GL from each food
ii. Divide by total # CHOg
iii. Multiply by 100
iv. Ex: White Bread and cinnamon suger
v. White bread GL = .73 x 14g = 10
vi. 2 TB sugar = .68 x 10 = 7
vii. Total CHO = 24
viii. Total GL = 17
ix. (17/24)100 = 70
x. The GI for the meal is 70

Front 22

Describe some of the limitations of the GI

Back 22

i. Total AUC vs AUC with fasting level as baseline
ii. Is 2 hours sufficient for all foods/meals?
iii. Is it reproducible in individuals? Variability?
iv. Most Glycemic indices are from the average of 10 subjects
v. Assume Glycemic response = Insulin response when only 25% of variation in insulin response is explained by glucose response

Front 23

In brief, what is the relative glycemic impact? (RGI)

Back 23

i. The relative tendency of a given amount of food consumed in a single intake, such as serving, to induce a postprandial Glycemic response
ii. Determine amount of glucose reference required to give the same Glycemic response as a relevant amount of food (Equiglycemic) instead fo Equicarbohydrate

Front 24

Why might it be a better measure?

Back 24

i. It manipulates the amount of food to give the same Glycemic response as 50g of glucose
ii. Easier to explain
iii. Gives a good visual (glucose tubes)
iv. Allows people to compare foods based on Glycemic response (impact)
v. Glycemic impact, defined as "the weight of glucose that would induce a glycemic response equivalent to that induced by a given amount of food" expresses relative glycemic potential in grams of glycemic glucose equivalents (GGEs) per specified amount of food.
vi. Therefore, GGE behaves as a food component, and (relative) glycemic impact (RGI) is the GGE intake responsible for a glycemic response.
vii. RGI differs from glycemic index (GI) because it refers to food and depends on food intake, whereas GI refers to carbohydrate and is a unitless index value unresponsive to food intake.
viii. Glycemic load (GL) is the theoretical cumulative exposure to glycemia over a period of time and is derived from GI as GI x carbohydrate intake. Contracted to a single intake of food, GL approximates RGI but cannot be accurately expressed in terms of glucose equivalents, because GI is measured by using equal carbohydrate intakes with usually unequal responses.
ix. RGI, on the other hand, is based on relative food and reference quantities required to give equal glycemic responses and so is accurately expressed as GGE.
x. The properties of GGE allow it to be used as a virtual food component in food labeling and in food-composition databases linked to nutrition management systems to represent the glycemic impact of foods alongside nutrient intakes. GGE can also indicate carbohydrate quality when used to compare foods in equal carbohydrate food groupings.

Front 25

How does DRI define Total Fiber and its components?

Back 25

i. (2002) Total fiber: the sum of dietary fiber and functional fiber
ii. Dietary fiber: consists of nondigestible carbohydrates and lignin that are intrinsic and intact in plants
iii. Functional fiber: consists of isolated (synthestic or natural) nondigestible carbohydrates that have beneficial physiological effects in humans

Front 26

How much fiber is currently being recommended for adults?

Back 26

i. Males: 38g/d
ii. Females: 25g
iii. Based on heart disease reduction or 14g/1,000 kcals

Front 27

What are the physical properties of non-viscous/non-fermentable(insoluble)?

Back 27

i. Highly resistant to digestion by bacteria
ii. ↑ fecal volume/bulk
iii. ↑ luminal diameter of colon
iv. ↓ intraluminal pressure
v. Reduces colonic transit time
vi. Most hemicelluloses, cellulose, lignins, functional fiber

Front 28

chemical composition of cellulose

Back 28

Important component of plant cell wall
Linear polymer of glucoses held together by B-1,4 bonds
Forms ribbon like structure
H-bonding between adjacent chains imparts a 3-D microfibril structure
Ex. Bran, root veggies, cabbage, apple skins, nuts

Front 29

chemical composition of hemicellulose

Back 29

Component of the plant cell wall
Heterogenous polysaccharide
Backbone: Linear polymer of xylose/glucose
Side-chains: xylose, arabinose, galactose, mannose + other sugards
Forms monolayer over cellulose microfibrils Ex. Bran, whole grains, nuts

Front 30

chemical composition Lignin

Back 30

A non-CHO
Polymer of phenols
Attaches to other noncellulose polysaccharides in the plant cell wall
Ex. Edible seeds, carrots, wheat

Front 31

What are the physical propertied of viscous/fermentable fibers (soluble)?

Back 31

Gel-forming
Enhanced satiety
Slows gastric emptying
Delay and interfere with absorption
Delays nutrient absorption
Lowers serum cholesterol
Fermentable by bacteris in loer GI: CO2, H2, methane, SCFAs

Front 32

What are some of the other fibers?

Back 32

i. Resistant starches
ii. Fructans

Front 33

What are Functional Fibers? Give a few examples

Back 33

a. Fibers added in food manufacturing
b. Cellulose, Pectin, lignin, gums, B-glucans, fructans, chitlin & chitosan, polydextrose & polyols, psyllium, resistant dextrins, resistant starches

Front 34

What are prebiotics, probiotics and synbiotics

Back 34

a. Prebiotics: nondigestible food ingredients that may beneficially affect the host by selectively stimulating the growth and or the activity of a limited number of bacteria in the colong. Thus to be effective, prebiotics must escape digestion in the upper gastrointestinal tract and be used by a limited number of the microorganisms comprising the colonic microflora
b. Probiotics: live microorganisms which when administered in adequate amounts confer a health benefit on the host. Resistant to gastric acid, pancreatic enzymes, etc.
c. Synbiotics: when prebiotic and probiotics are mixed together

Front 35

What gastrointestinal disorders are associated with fiber?

Back 35

i. Duodenal ulcers
ii. Constipation
iii. Diverticular disease
iv. Transit time/laxation
v. ↓ intraluminal pressure

Front 36

How does fiber lower risk of heart disease?

Back 36

i. Soluble fibers displace saturated fat and cholesterol in the diet
ii. Food sources rich in soluble fiber also good sources of tocotrienols/plant sterols
iii. Bind bile and increase bile excretion
iv. Bind bile and decrease micelle formation- interfere with bile/cholesterol absorption
v. SCFA production: proprionate inhibits cholesterol synthesis in liver
vi. Ratio of bile acids produced inhibits cholesterol/fat synthesis in the liver

Front 37

How does fiber attenuate blood glucose levels? Other links with diabetes.

Back 37

Slows digestion of CHOs

Front 38

What about the link with colon cancer? (possible mechanisms of action) (why is existing data weak?)

Back 38

i. Decreased exposure time to carcinogens
ii. Increase fecal bulk (dilute carcinogens)
iii. ↓ ratio of secondary bile which are carcinogenic
iv. Production of SCFAs induces cell apoptosis in human cancer cells
v. Epidemiological studies show some effect, but not all

Front 39

What are the benefits of whole grains?

Back 39

i. Antioxidants
ii. Antinutrients (tannins, saponins)
iii. Hormonally active components (phytosterols)
iv. Non-nutrient components
v. Unusual fatty acids
vi. Traditional nutrients

Front 40

Breanna’s study on HEI and preschoolers: What was the purpose of this study?

Back 40

i. To assess the diet quality of Greek preschoolers and the potential role of several sociodemographic factors leading to it

Front 41

Breanna’s study on HEI and preschoolers: In general, what 10 components make up the HEI?

Back 41

i. Grains
ii. Vegetables
iii. Fruits
iv. Milk
v. Meat
vi. Total Fat
vii. Saturated Fat
viii. Cholesterol
ix. Sodium
x. Variety

Front 42

Breanna’s study on HEI and preschoolers: Most of these preschoolers had poor diets (HEI scores <50), what diet components needed improvement?

Back 42

low veg
high sat fat
low PA

Front 43

Breanna’s study on HEI and preschoolers: What factors were associated with HEI scores (table 5)?

Back 43

i. Sex
ii. Age
iii. Place of living
iv. Maternal education status
v. Employment status

Front 44

Breanna’s study on HEI and preschoolers: Results

Back 44

e. Results: The majority of greek preschoolers had poor diets. Low HEI scores were associated with low levels of PA, low Veg intake, high sat fat intakes, lower maternal educational level and unemployment status

Front 45

Nicole’s study on Elderly Diet Index (EDI): What were the objectives of this study?

Back 45

i. To develop an index that assesses the degree of adherence to nutritional recommendations for older adults
ii. Investigate it’s association with risk factors related to cardiovascular disease

Front 46

Nicole’s study on Elderly Diet Index (EDI): In general, 10 components make up the EDI?

Back 46

i. Cereals
ii. Meat and meat products
iii. Vegetables
iv. Fruits
v. Legumes
vi. Fish and seafood
vii. Dairy products
viii. Bread
ix. Alcohol
x. Olive oil

Front 47

Nicole’s study on Elderly Diet Index (EDI): What CVD risk factors did the EDI correlated with?

Back 47

i. Obesity
ii. Hypertension
iii. Hypercholesterolemia
iv. Diabetes Mellitus

Front 48

Nicole’s study on Elderly Diet Index (EDI): In general, with every 1 unit change in EDI score what was the change in risk in CVD risk factors?

Back 48

i. For every 1 unit increase in the diet score was associated with almost 10% lower odds of being obese, HTN, or having at least one CVD risk factor

Front 49

Nicole’s study on Elderly Diet Index (EDI): In general, what are the strengths/limitations of scores?

Back 49

Strengths:
Easily used for evaluating diet quality in elderly
Can be used for prevention of CVD daily
Easily understood and goal oriented to patients
Wide-range scoring system instead of binary (better accuracy)

Limitations
Components contribute equally to the calculation of the total score- not all food groups impact health the same
Done in a cross sectional design- may not be valid

Front 50

Jenny’s study on diet sugar, GI and adiposity/insulin in Latino Youth: What was the aim of this study?

Back 50

a. To determine which aspects of dietary CHO (sugar), fiber, Glycemic index or Glycemic load are associated with adiposity and insulin dynamics in overweight Latino children

Front 51

Jenny’s study on diet sugar, GI and adiposity/insulin in Latino Youth: Who were the subjects?

Back 51

a. 8-13 yrs
b. BMI > 85 precentile for age and sex
c. Latino ancestry
d. Hx of type 2 diates in > 1 relative

Front 52

Jenny’s study on diet sugar, GI and adiposity/insulin in Latino Youth: What do figures 1 and 2 show?

Back 52

a. Subject characteristics
i. Sex, age, tanner stage, BMI, BMI z scores, total fat in kg, total lean tissue mass in kg, fasting glucose, 2-h glucose, insulin sensitivity, acute insulin response, disposition index
b. Dietary variables
i. Energy
ii. Fat
iii. CHO
iv. Protein
v. Total sugars
vi. Added sugars
vii. Dietary Fiber
viii. Glycemic index
ix. Glycemic load

Front 53

Jenny’s study on diet sugar, GI and adiposity/insulin in Latino Youth: What % of total variation in fat mass and insulin sensitivity was associated with dietary sugar?

Back 53

a. 2.4% variance in total body fat mass
b. 5.6% variance in SI

Front 54

Jenny’s study on diet sugar, GI and adiposity/insulin in Latino Youth: How do the authors explain the results – why was only sugar associated?

Back 54

a. With adjustments total dietary sugar was the only dietary variable significantly correlated with adiposity variables and insulin dynamics
b. Total sugar was positively correlated with BMI
c. Total sugar was positively correlated with total fat mass
d. Total sugar was inversely correlated with insulin sensitivity and disposition index

Front 55

Leslie’s study on diet and HbA1C: What was the objective of this study?

Back 55

a. Determine whether diet composition was associated with subsequent glycated hemoglobin concentrations during intensive therapy for type 1 diabetes

Front 56

Leslie’s study on diet and HbA1C: Who were the subjects?

Back 56

a. Male and female
b. 13-39yrs
c. From DCCT study

Front 57

Leslie’s study on diet and HbA1C: What dietary factors were associated with higher HBA1C values (table 2)?

Back 57

a. Total fat
b. Saturated fat
c. Monounsaturated fat
d. Insulin dose

Front 58

Leslie’s study on diet and HbA1C: What are the main findings from Table 2?

Back 58

a. Saturated, monounsaturated, total fat and total insulin dose were directly associated with HbA1c
b. CHO inversely associated with HbA1c

Front 59

Leslie’s study on diet and HbA1C: What did the authors conclude?

Back 59

Diets higher in fat and saturated fats and lower in CHO were associated with worse glycemic control

Front 60

Marsha’s study on whole grains, refined grains and cereal fiber and risk factors of disease: What was the objective of the study?

Back 60

Examine associations between whole grains, refined grains and cereal fiber and selected disease risk factors

Front 61

Marsha’s study on whole grains, refined grains and cereal fiber and risk factors of disease: Who were the subjects?

Back 61

a. 1958: White men
b. 1978: women and minorities
c. 27-88 years

Front 62

Marsha’s study on whole grains, refined grains and cereal fiber and risk factors of disease: What were the main findings from tables 3/4?

Back 62

a. As WG & CG intake increased:
i. BMI, weight, waist circumference decreased
ii. Total and LDL cholesterol decreased
iii. Postprandial glucose decreased
iv. HDL decreased with increased whole grains

Front 63

Marsha’s study on whole grains, refined grains and cereal fiber and risk factors of disease: What does figure 1 show?

Back 63

a. Participants who ate more WGs and CG: older women, lower weight/BMI, had a positive association with vitamin use and did not smoke
b. Participants who ate more refined grains were younger and inversely associated with being female, positively associated with PA and being a college graduate

Front 64

Marsha’s study on whole grains, refined grains and cereal fiber and risk factors of disease: What can we say about whole grains/cereal fiber?

Back 64

a. Weight, BMI, waist circumference inversely associated
b. Total and LDL cholesterol inversely associated
c. 2-H glucose inversely associated

Front 65

Priya’s study of Prebiotics: What was the purpose of this study?

Back 65

a. To investigate the effect on an infant milk formula with 6g/L scGOS and lcFOS on the development of the fecal sIgA response and on the composition of the intestinal microbiota in 215 healthy infants during the first 26 weeks of life

Front 66

Priya’s study of Prebiotics: What prebiotic was used?

Back 66

Short chain galacto-oligosaccharides and long chain fructo-oligosaccharides

Front 67

Priya’s study of Prebiotics: How long was study?

Back 67

a. 6 month intervention period

Front 68

Priya’s study of Prebiotics: What were the main findings and their meaning?

Back 68

a. An infant milk formula with 6g prebiotic in a ratio of 9:1 resulted in higher concentrations of fecal sIgA, suggesting a positive effect on mucosal immunity
b. Prebiotic formula fed infants had a lower % of E.coli and Clostridium than the control group
c. In the whole group, prebiotic formula fed infants had higher % of bifidobacteria than the control group

Front 69

Letisia’s study on Diet and type 2 diabetes: What was the purpose of this study?

Back 69

Test the effect of low GI diet on glycemic control and CVD risk factors in men and postmenopausal women with type 2 diabetes

Front 70

Letisia’s study on Diet and type 2 diabetes: What were the 2 diet groups?

Back 70

a. Low GI diet
i. Quinoa, flaxseed, pumpernickel bread, oatmeals, oat bran, lentils, beans, 5 veg/ 3 temperate fruit (apples, pears, peaches)
b. High-Cereal fiber diet
i. Whole wheat, brown rice, 5 veg/3 tropical fruit

Front 71

Letisia’s study on Diet and type 2 diabetes: Make note of the distribution of kcals, fiber, and dietary GI in the low GI group.

Back 71

a. Carbs = 42% Kcals
b. Total Kcals: 1706
c. Fiber: 18.7g
d. GI: 69.6

Front 72

Letisia’s study on Diet and type 2 diabetes: How long was the study?

Back 72

24 wks

Front 73

Letisia’s study on Diet and type 2 diabetes: What were the major findings?

Back 73

a. Low GI diet = moderate decrease in HbA1c
b. Moderate decrease in BW
c. Moderate increase in HDL-C compared with a modest drop in HDL-C for high CF group

Front 74

Courtney’s study on the CCD study: What was the purpose of this study?

Back 74

a. Compare the effects of alternating the glycemic index or amount of CHO in subjects with T2DM
b. Effects on HbA1c, plasma glucose, lipids, CRP

Front 75

Courtney’s study on the CCD study: What were the 3 diet groups studied?

Back 75

a. High GI: ↑CHO & ↑GI
b. Low GI: ↑CHO & ↓GI
c. Low-CHO: ↓CHO & ↑MUFA

Front 76

Courtney’s study on the CCD study: Make note of the distribution of kcals, fiber, and dietary GI in the low GI group.

Back 76

a. Low GI: CHO 20-25% of kcals
b. GI: 55.1

Front 77

Courtney’s study on the CCD study:How long was this study?

Back 77

a. 1 yr

Front 78

Courtney’s study on the CCD study: What were the major findings?

Back 78

a. Lower CRP in Low GI group
b. No change in HbA1c
c. Lower OGTT in Low GI group
d. Initial decline, then steady rise in FPG that exceeded baseline