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Macro Nutrients - Carbohydrate


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1. Dietary CHO enter the body in what forms?

2. List the common CHO types consumed in USA.
1. disaccharides, polymers starch (amylose, amylopectin), and glycogen

2. Starch is predominant, refined table sugar (sucrose), lactose from milk products, corn syrup (partially hydrolyzed starch preparation), invert sugar (mixture of glucose and fructose produced by acid-hydrolysis of sucrose)


1. Describe the first step in CHO digestion (type of CHO, enzyme, and pH).

2. Is this enzyme an endo or exo?

3. Which bonds does it break?

4. List 3 functions of sa
1. Lingual/salivary amylase begins to break down polymeric sugar in the mouth. Lingual/salivary amylase works in the slightly acidic pH range of 6.8 in the mouth & esophagus only.

2. endoamylase

3. α-1-4 glycosidic bonds

4. lubrication, solvent for better taste receptor interaction, dilutes noxious tastes

5. 1-2 L


1. What type of digestion occurs in the stomach?
1. CHO digestion is continued by acid hydrolysis by the HCL. Salivary amylase is inactivaed by the 1-2 pH. Protein and fats are digested by the gastric proteases and lipases.


1. Name the main CHO enzyme in the SI.

2. Where is it secreted?

3. Is it endo or exo and which bonds does it break?

4. What does it require to function?

1. α-amylase (AKA pancreatic amylase)

2. pancreas

3. endoamylase breaks α-1-4 glycosidic bonds

4. CL ions

5. CCK-PZ (cholecystikinin-pancreozymin) stimulates the gallbladder to contract and pancreatic enzyme secretion. Vagus nerve stimulation also causes increased release of pancreatic amylase.

6. Secretin stimulated the release of bicarbonate and H2O from pancreas. This ↑ pH to the optimum 6.9 for pancreatic amylase action.

1. Explain how pancreatic amylase breaks down amylose.

2. Explain how pancreatic amylase breaks down amylopectin.

3. How are nondigestible polysaccharides involved in SI CHO digestion?

4. Name 4 intes
1. Amylose is UNBRANCHED, pancreatic amylase hydrolysis produces...... amylose → maltose α-1-4 + glucose

2. Amylopectin in BRANCHED, pancreatic amylase hydrolysis produces......
amylopectin → maltose α-1-6 + glucose + isomaltose α-1-6

Note: pancreatic amylase cannot hydrolyze the α-1-6 bonds linking the glucose at the branched points, isomaltose α-1-6 is produced as a result

3. Cellulose, hemicellulose, and pectin ma interfere with the amylase-starch interaction and ↓ digestion and absorption of CHO in the SI

Maltase (hydrolyze di- and maltotriosis)

1. Where does disaccharidase activity take place?

2. Name 5 disaccharidases, include additional info such as which bonds they breaks etc.

3. Describe how the resulting simple carbs are metabolized after SI digest
1. brush border (microvilii) of SI

a) lactase
b) maltase (hydrolyze di- and maltotriosis)
c) sucrase
d) isomaltase (AKA α-dextrinase, hydrolyzes α-1-6 bond of isomaltose)
e) trehalase (2 glucose units linked by α-1 α-1, trehalose is found in insects and mushrooms)

a) transported across intestinal lumen to the hepatic portal vein
b) delivered to the liver parechymal cells and other tissues for conversion to either fatty acids, AAs, glycogen, or metabolized via catabolic pathways

4. Glycolysis is the oxidation of glucose.

When oxygen is available, glucose is oxidized to form pyruvate (AKA Aerobic glycolysis).

When little oxygen is available, glucose is oxidized in most tissues to form lactate (AKA Anaerobic glycolysis)

Resistant Starch

1. Describe the 5 types of resistant starch.
RS = naturally occuring (can also be a result of food processing)

RS1 = physically inaccessible/undigestible by pancreatic amylase (ex. cellulose)

RS2 = native starch that can be made accessible/digestible by gelatinization

RS3 = retrograded starch formed from cooking and cooling (ex. potato chips & cereals)(not digestible & partly fermented by bacteria to form methane)

RS4 = chemically modified starch including starch esters and starch ethers (not digestible & partly fermented by bacteria to form methane)


1. Which digestive enzyme is lacking in a premature baby?

2. Explain the reason behind for dietary restriction advice given to parents of premies.

3. What happens to lactase as we age?
1. salivary amylase

2. Starch is not be given until the child is 6 months old. This will allow adequate time for salivary amylase to be fully functional. Mother's milk is purely lactose, which is digested in the SI. Starch requires salivary amylase for proper digestion.

3. Lactase is needed for digestion of breast milk and then declines either between 3-5 or 14-18 years in most people around the world.

Adult lactase deficiency occurs in approximately 5-20% of caucasian adults.

Hexose Transport System

1. What does this system transport?

2. What does it require and what are they called?

3. Where are they found (5)?
1. hexose molecules like glucose

2. Carrier proteins called Glucose Transporters (GLUT)are required to cross the enterocyte membrane.

GLUT1 - brain, placenta, RBC, intestine, fetal tissue
GLUT2 - intestine, pancreas, kidney, liver
GLUT3 - intestine, brain
GLUT4 - insulin-sensitive tissues such as heart, skeletal muscle, adipose tissue
GLUT5 - SI (jejunum), skeletal muscle, sperm
GLUT6 - not a functioning transporter

List the GLUT functions (5).
GLUT1 & 3 - basal glucose uptake

GLUT2 - bidirectional transport of glucose by the hepatocyte, movement of glucose in/out of absorptive epithelial cells into the circulation

GLUT4 - increases in response to insulin, makes adipose and skeletal muscle more receptive to isulin; liver, brain, and erythrocytes lack GLUT4

GLUT5 - can transport fructose

1. How are glucose and galactose absorbed into the enterocytes?

2. What is required for glucose or galactose to attach to the carrier?

3. What causes glucose-galactose malabsorption

4. Where do glucos
1. Active Transport via the SGLT1 carrier. It depends on a Na+/K+ ATPase pump.

2. Na+ must be preloaded on the pump.

3. Mutations of the SGLT1 gene

4. Glucose and galactose primarily leave the enterocyte via the GLUT 2 transporter to enter circulation

1. How is fructose absorbed into the enterocytes?

2. Is anything required for fructose to attach to the carrier?

3. Where does fructose go after entering through the SGLT1 carrier?

4. Does co-consumpt
1. facilitated diffusion supported by GLUT 5

2. no, Na+ is not required3.

3. fructose also leaves the enterocyte via the GLUT 2 transporter to enter circulation, some GLUT 5 transporters may complement GLUT 2 in the transporting of fructose only

4. speeds up

5. fructose and galactose are first converted to glucose and then the glucose can be converted to glycogen

1. Which hormones increase when blood glucose is falling?

2. How are metabolic defects detected?
1. glucagon and glucocorticoid steriod hormones (primarily cortisol)

2. Amniocentesis is used during preganacy to detect defects in the fetus, urinary and blood analysis may show inborn errors in some cases, a load test with the suspected metabolites may be helpful, tissue biopsies for microscopic examination work in some cases as well

1. Describe lactose intolerance.

2. What happens when the lactose is not digested?

3. How big of a problem is lactase deficiency (who does this affect)?
1. reduced production of the lactase enzyme (secreted by the brush border) means lactose cannot be broken down to glucose and galactose for absorption

2. lactose reaches the large intestine undigested, bacteria ferment the lactose which creates gas and diarrhea about 30 minutes to 2 hr after eating lactose foods

3. some children are born without lactase (rare), least common among people of northern European descent, 90% of Asian Americans, 75% of African Americans and Native Americans. Naturally humans decease production of lactase after 2 years, we have adapted to eating milk products into adulthood.

1. Describe the 3 testing methods used to diagnose lactose intolerance.

2. How is lactose intolerance treated?

3. Describe some tips to help a patient minimize the GI discomfort associated with lactose intoleranc
a) Breath Hydrogen Test (BHT) measures hydrogen at regular intervals in the breath after consuming a lactose containing beverage, fermented lactose produces hydrogen
b) Lactose Tolerance Test (LTT) after fasting a lactose beverage is consumed, blood is tested for glucose over a 2 hour period, if glucose rises it means lactose is being digested and the galactose + glucose is being absorbed
c) Stool Acidity Test is used for infants and young children, fermented lactose produces lactic acid and short chain fatty acid residues that can be detected in a stool sample

2. dietary control depending on individual tolerance

a) small amounts of lactose are better than large
b) better if eaten with other foods
c) heated lactose products are better than unheated
d) "Contains Active Culture" means lower in lactose
e) aged cheeses and processed American cheese have less lactose
f) lactase enzymes are very helpful (liquid to add to milk makes 90% lactose free, chewable lactase tablets for solid food)


1. List the monosaccharides.

2. What are pentose sugars?

3. Where are they found? Give examples.
1. glucose, fructose, galactose

2. Pentose is a 5-carbon sugar.

3. Seldom found in free state, in plants they are in polymetric forms called pentosans. Xylose and arabinose are pentosans found in plant fibers and vegetable gums. Also found as the sugar portion of nucleic acids and riboflavin (ribose & deoxyribose).

1. What are hexose sugars? Name 4.

2. How are they found in nature free or combined?

3. Give common names for glucose and fructose. List the common sources of fructose, galactose, and mannose.

4. Which
1. 6-carbon sugars; glucose, fructose, galactose, mannose

2. glucose and fructose are found free in nature, galactose and mannose are only in combined form

3. glucose (dextrose) & fructose (levulose)

fructose - ripening fruit and honey (sweeter than sucrose)

galactose - milk and in oligosaccharides of plant origin

mannose - in some plant polysaccharides, called mannans
aldoses: glucose, galactose, mannose
ketose: fructose

aldoses =

ketose =

1. What is a stereoisomer? Give an example.

2. What is an enantiomer?
Give an example.

3. What is an epimer? Give an example.
1. can occur in sugars with 3 or more carbons, are isomers that have the same atom connectivity but differ only in their orientation in space, example: galactose and mannose are stereoisomers of glucose (one OH group is in a different position on each)

Stereoisomers include geometrical isomers (cis-tran), diastereomers (AKA epimers - no mirror images - differ by one carbon attachment only), and enantiomers (D & L forms).

2. Enantiomers are stereoisomers that are mirror images of one another. The D forms all have an OH group to the right of the carbon farthest from the carbonyl (L form has OH to the left). The D form is physiologically significant. Example: D-glucose vs. L-glucose

3. Epimers are stereoisomers that are not mirror images and only differ by one carbon attachment, example: glucose vs. galactose have OH attached to opposite sides of the same carbon

Describe the following Monosaccharide Derivatives.

1. Uronic Acids

2. Amino Sugars

3. Deoxy Sugars
1. Uronic Acids are weak sugar acids w/ a terminal carboxyl group (COOH). Examples: D-Gluconic Acid, D-Glucuronic Acid (for drug detox), D-Galacturonic Acid, D-Mannuronic Acid

2. Amino Sugars have the C-2 hydroxyl replaced by an amino group. Examples: D-Glucosamine, D-Galactosamine, N-acetyl-D-Galactosamine (Amino sugars are often found acetylated)

3. Deoxy Sugars have the C-2 hydroxyl group replaced by a hydrogen. Exmples: 2-deoxy-D-ribose (found in DNA), L-fucose, L-rhamanose

1. Define disaccharides.

2. List the components, bonds, and whether they are reducing sugars for each of the five disaccharides.
1. covalent bond between the anomeric hydroxyls of two cyclic sugars

glucose + fructose
α(1,2) glycosidic bond
reducing sugar

glucose + galactose
β(1,4)glycosidic bond (only beta bond humans can digest)
reducing sugar

Glucose + Glucose
Maltose is mainly from starch
reducing sugar

not naturally occuring
from acid hydrolysis of starch (amylopectin)
α(1,6) glycosidic bond
reducing sugar

glucose + glucose
found in fungi, yeasts, insects
Nonreducing sugar (won't react with amino acids as part of browning reaction)

1. Define oligosaccharides.

2. Name 3 categories of oligosacharides.
1. Oligosaccharides contain 3-9 carbons and cannot be broken down by human enzymes. They can be digested by bacterial enzymes in the colon. Found in legumes (peas, beans, lentils).

Galactosylsucrose-oligosacchrides: raffinose (3Cs), stacyose (4Cs)

Malto-oligosacchrides: maltotriose (3Cs)

Fructo-oligosacchrides: nonreducing sugars

4 carbons: stachyose

1. Define polysacchrides.

2. What is the predominant monosaccharide in polysaccharides?

3. What term is used to decribe a polysaccharide composed of the same monosaccahride? Give examples.

4. 3. What t
1. Most of the CHO found in nature = high molecular weight polymers = polysaccharides. Contain greater than or equal to 10 Carbons.

2. D-glucose

3. Homopolysaccharides. Examples: Starch (amylose, amylopectin), Glycogen, Cellulose, Chitin, Pectin, Agar, Lignin, etc.

4. Heteropolysaccharides
Examples: Glucosaminoglycans, peptidoglycans

1. List 2 major types of digestible polysaccahrides.

2. Describe glycogens significance.

3. Name the glygogen linkages.

4. Describe the significance of starch.

5. Describe starch structure a
1. glycogen & starch

2. Glcogen is the only complex CHO of animal orgin, acts as the major storage form for energy, stored mostly in liver and muscle tissue

3.Homopolysccharide of glucose, α(1,4), HIGHLY branched at every 8-10 residues w/ α(1,6) linkages at branches

4. Starch is the major storage form of CHO in plants, it is the majot energy food provider for people

5. Starch has the same structure as same glycogen with less branching (amylose has no branching & amylopectin has same as glycogen just not every 8-10 residues).

1. Hydrolysis of amylose or amylopectin would result in more glucose being freed at once?

2. Digestion occurs more rapidly for amylose or amylopectin?

3. Amylose or amylopectin content will lower the glycemic ind
1. Amylopectin because it is branched and has more ends to work on at one time (greater surface area)

2. amylopectin

3. amylose

4. rice: long grain and brown (brown basmati is the best)
potatoes: harvested before the mature to ensure lower starch content

5. Yes-limited solubility (amylose is more soluble), food processing can lead to hydrogen bonding and less solubility in cold water and decreased digestibility by amylase

1. Which conformation of CHO is most physiologically significant?

2. Which side is the hydroxyl found on in this conformation?

3. Hayworth projects depict up and down of the OH group. What are "OH up" a
1. D-conformation

2. The right side

3. OH down = alpha
OH up = beta

1. Name 3 monosaccharides include food sources and molecular weight.
fruit, plant foods, honey, maple sugar, MW 180

fruit, plant foods, honey, maple sugar, MW 180

component of lactose, produced during digestion, MW 180

1. Name 3 disaccharides include food sources, bonds, and molecular weight.
cane sugar, beet sugar, fruits, maple sugar
α(1,2) glucose + fructose
MW 360

dairy products, milk sugar
β(1,4) Glucose + Galactose
MW 360

sprouted grain, produced during digestion of starches
α(1,4) Glucose + Glucose
MW 360

1. Name 4 Polysaccharides include food sources, bonds, and solubility.
starchy plants & starchy grains
α(1,4) no branches
water soluble

starchy plants and starchy grains, thickener
α(1,4) and α(1,6) branches
water soluble

GLYCOGEN (animal starch)
liver, muscle
α(1,4)and α(1,6) branches every 8-10 residues
water soluble

plant cell walls, wheat bran
β(1,4) no branching, All Glucose
Not Water Soluble

Type 1 Diabetes

1. Describe the 3 environmental factors thought to be related to Type 1 Diabetes.
exposure before 4 months can lead to an autoimmune response, bovine serum albumin antibodies are produced, these antibodies also bond to pancreas cells and cause damage

act in the early initiation of autoimmunity or add to the destruction already in progress
German Measles & Mumps viruses during pregancy have been suspected
Coxsackie B4 (bacteria) has also been suspected in initial bets cell damage

Type 1 Diabetes is more common in colder countries and is diagnosed more in the winter, cold weather alters metabolism and may increase load on beta cells

1. Fasting plasma glucose (FPG) requires fasting for how long?

2. What are the results ranges for normal, pre-diabetes, and provisional diagnosis for diabetes?

3. Diagnosis requirements?
1. fast at least 8 hours (preferably overnight)

2. normal = <100
prediabetes = >100 - <126
provisional diagnosis for diabetes = >126

3. FPG >126 on 2 or more tests on different days

1. How is the Oral glucose tolerance test measured?

2. What are the ranges for normal, pre-diabetes, and diabetes?

3. What is the diagnosis requirement?
1. Eat diet Hight in CHO for 3 days prior to test, Fasting plasma glucose is measured first, then 75 grams of glucose in a sweet liquid is taken, blood samples are taken up to 4 times to measure blood glucose over time

2. Glucose blood level after 2 hours
normal = <140
pre-diabetes = >140 - <199
diabetes >200

3. One result >200 is adequate for diagnosis.

1. What are the combination requirements for diabetes diagnosis?

2. Who should be screened for diabetes?
1. (polydipsia, polyuria, polyphagia) + casual plasma glucose >200

a) everyone age 45 or older, retest every 3 years
b) younger than 45 if pre-diabetes risk factors
BMI>25 (>=23 Asian Amer, >=26 Pacific Islander)
family history
high risk ethnic background (African Amer, Asian Amer, Native Amer, Hisp/Latino, Pacific Islander)
gestational diabetes
birthed baby >9 pounds
hypertension 140/90
abnormal lipid levels (<40 HDL for men & <50 for women, triglyceride >=250)
inactive lifestyle
Pre-diabetes FPG test results

Idiopathic Diabetes Mellitus

1. Describe Type 1 (IDDM)

2. Describe Type 2 (NIDDM)
1. onset usually in childhood (AKA juvenile onset diabetes), ketoacidosis without insulin therapy, autoimmunity destroys βcells in pancreas, patients are normal body weight, can be caused by virus or bacteria (coxsackie B4), also includes LADA (latent autoimmune diabetes of adulthood - slow onset, not obese, <40 years old)

2. insulin production operates until final stage, rarely leads to ketoacidosis, manifests >40 years, high blood glucose & insulin resistance, insulin resistance OR insulin deficiency are primary causes (debatable), associated with obesity, abdominal fat, physical inactivity, lifestyle,

Secondary Diabetes Mellitus

1. Describe MODY

2. Describe possible pancreatic problems.

3. Describe endocrine involvment.

4. Explain drug-induced diabetes.

5. List the 3 remainin
1. Maturity onset type deiabetes of the young, genetic mutations of up to 12 different genes have been identified, <25 years, all have βcell impairment, some have insulin resistance

2. Cystic fibrosis and pancreatitis can destroy the pancreas, pancreatectomy also leads to diabetes

3. endocrie tumors can produce hormones that counter the effect of insulin (EPI, glucagon, growth hormone, cortisol)

4. treatment w/glucocorticoids and diuretics can interfere with insulin

5. mutations of insulin gene &/or receptor, gestational diabete, other genetic syndromes with diabetes or impaired glucose tolerance associated (lipoatrophic diabetes, Down syndrome, Wolfram syndrome, Kleinfelter syndrome, Turner syndrome, etc)

1. How does uncontrolled Type 1 diabetes lead to glucosuria, polyuria, polydipsia, and polyphagia?
1) low glucose in tissues (skeletal muscle, adipose, hepatic especially) due to low insulin (can't stimulate GLUT) stimulates gluconeogenesis even though blood glucose is high
2)hepatic phosphorylation by glucokinase is regulated by insulin, low insulin means low glucokinase & ↑glucose to blood
3) elevated blood glucose exceeds the kidneys capacity to reabsorb glucose it leaves in the urine (Glucosuria)
4) When glucose is lost in urine it takes water and electrolytes with it - osmotic diuretic (polyuria)
5) Water loss activates the thirst mechanism (polydipsia)
6) negative caloric balance results from glucosuria & tissue catabolism activates appetite and food intake increases (polyphagia)

1. What leads to hypoglycemia?

2. What is the progression of untreated hypoglycemia?

3. What are the symptoms?
1. inappropriate management, too much insulin, too much glucose lowering medication, extreme physical exercise, skipped meals, delayed meals, inadequate food intake, vomitting or severe diarrhea

2. untreated → unconsciousness → brain damage → death

3. hunger, headache, sweating, shakiness, nervousness, confusion, disorientation, slurred speech

1. List the 5 chronic complications of diabetes.

2. Glucose Homeostasis Hormones. Describe the action of each on glucose metabolism.
a) glucagon
b) insulin
c) ACTH & Growth Hormone
d) Glucocorticoids
1. cardiovascular disease (80% die from CVD), neuropathy, retinopathy (leading cause of blindness), nephropathy (leading cause of kidney failure), diabetic foot (amputation)

a) glucagon - triggered by low BG
b) insulin - triggered by high BG
c) ACTH & Growth Hormone - released by pituitary, inhibits hepatic uptake of BG
d) Glucocorticoids - inhibit glucose uptake
e) Cortisol - released by adrenal cortex (the major glucocorticoid), stimulate by ACTH
f) Epinepherine - activates glycogenolysis to ↑ glucose during stress

1. List the different types if insulin medications.
rapid acting (regular)
intermediate acting (NPH & Lent)
long acting (ultralente)

1. What is the glycemic index and how is it measured/documented?

2. Should an athlete eat high or low glycemic foods before an athletic event?

3. Describe some of the difficulties in determining the GI of a part
1. The GI measures how much the blood glucose rises after eating a particular food. It uses a standard of glucose or white bread as 100 and assigns a score to each food tested. The higher the number the faster the glucose is released into the blood.

2. Low glycemic foods are best because they provide a slow release of energy instead of a spike and then a letdown during the event.

3. The variety of the food, processing, particle size, ripeness, juiced, whole, type of starch, and the preparation all affect the GI.

4. No, because GI is a measure of quality of CHO not quantity.

5. No, GI is for high CHO foods only because it is measuring gluose release within the first 2-3 hours after consumption.

1. Rice with a high GI includes which types?

2. Rice with a lower/intermediate GI includes which types?

3. Which type of patotoes have the lower GI, sweet potatoes or white patotoes?

4. Is high fructo
1. Calrose, sweet, sticky rice, white, short-grain

2. Uncle Ben's converted rice, basmati, Doongara, brown, long-grain

3. Sweet potatoes (77) are much lower than white potatoes (121)

4. High fructose corn syrup is only ~50% fructose. The other 1/2 is glucose. The GI is similar to sucrose (table sugar).

1. How does bitter melon help diabetic patients?

2. Name the 2 active components and describe how they work?

3. What is the other commonly used name for bitter melon?

4. What is the botanical name for
1. The ripe fruit or extract of unripe fruit lowers blood glucose.

Charantin - hypoglycemic agent composed of mixed steriods (more powerful than prescription tolbutamide)
Momordica - contains an insulin-like polypeptide (polypeptide P)

3. Balsam Pear

4. Momordica charantia

1. What 2 active constituents in onion and garlic are known to be beneficial for diabetes?

2. What effect do they have on diabetic patients?
allyl propyl disulfide (APDS) &
diallyl disupfide oxide (allicin)
other flavanoids are assumed to play a role as well

2. lowering blood glucose

1. What effect does Asian Ginseng have on diabetes?
1. enhances the release of insulin, increases # of insulin receptors, a direct blood glucose lowering effect, and increases energy in patients with type 2 diabetes

1. Describe the current thinking about insulin resistance and why it occurs.

2. Explain how exercise can reduce blood glucose even when insulin resistance is a problem.
1. Insulin resistance involves a mechanism breakdown between insulin binding to receptor and the GLUT4 insulin responsive vesicle moving to the cell's surface. If GLUT4 doesn't move to the surface, glucose doesn't get transported into the cell.

2. Exercise activates 5'-AMP-activated kinase, which then moves the exercise-responsive GLUT4 vesicle to the cell's surface. Exercise stimulates nitric oxide release and bradykinin and appear to be connected in the activation of 5'-AMP-activated kinase

1. Why isn't there an RDA for fiber?

2. In 2001, the FNB - DRI Committee devised an AI recommendation for fiber. What did they recommend for M/W under and over 50 years old.

3. What is the difference between die
1. So far, not enough evidence to support a recommendation. Research is still trying to define and classify fiber to determine which types have specific effects.

2. Under 50: M = 38g W = 25g
Over 50: M = 30g W = 21g

3. Dietary fiber is FOUND NATURALLY naturally in plant foods. Function fiber is isolated or synthetic fiber ADDED to foods or taken as supplement.

4. Total fiber = dietary fiber consumed (found in foods naturally) + functional fiber (added or supplemented).

1. Describe the following forms of dietary fiber:
resistant starch
lignin - NOT a CHO, found in cell wall of woody plants & seeds

cellulose - glucose polymer, β(1,4) glycosidic, found in plant cell walls

beta-glucans - glucose polymers, β(1,4) & β(1,3), oats & barley

hemicelluloses - hexose & pentose sugars, found in plant cell walls

pectins - viscous polysaccharides, fruits & berries

gums - viscous polysaccharides, seeds

inulin & oligofructose - both are fructose chains, inulin terminates w/fructose, oligofructose terminated with fructose OR glucose, both found in onions & Jerusalem artichokes

resistant starch - naturally occuring, sequestered in plant cell walls, bananas & legumes

1. Describe the following forms of functional fiber:
chitin & chitosan
polydextrose & polyols
resistant dextrins
psyllium - viscous mucilage, isolated from husks of psyllium seeds

chitin - NOT digestible CHO, exoskeletons of crustaceans, long polymer of acetylated glucosamine units, β(1,4) glycosidic

chitosan - deacteylated chitin, nondigestible glucosamine polymer

fructooligosaccharides - short synthetic fructose chains termating w/glucose, food additive

polydextrose & polyols - synthetic polysaccharides, buling agents & sugar substitutes

resistant dextrins - resistant maltodextrins, NOT digestible, polysaccharides, heat treated, food additives

1. Descibe the classification of Viscous vs. Nonviscous fiber.

2. Describe the classification of Fermenting vs. Nonfermenting Fiber.

3. Pectin and wheat bran result in which SCFAs after fermentation?

1. Some fibers form viscous solutions/gels in water
VISCOUS EFFECTS: slowed emptying of stomach, reduced mixing of GI contents w/enzymes, decreased nutrient diffusion/absorption in SI (delayed glucose absorption → ↓bood glucose), increases transit time (slow down), and lower cholesterol.
VISCOUS EXAMPLES: pectins, beta-glucans, some gums (guar gum), and mucilages (psyllium).

2. Some fibers are fermented by colon bacteria to produce short-chain fatty acids (acetate, propionate, butyrate), lactate, and gases. SCFAs especially butyrate are their preferred energy source.
FERMENTABLE EXAMPLES: pectins, beta-glucans, guar gum, inulin, oligofructose. Food sources include: oat bran, wheat bran barley, fruits, vegetables

3. oat bran → propionate
wheat bran → butyrate

4. psyllium, gums, oat gum, pectin

5. oat bran, soybean fiber

6. corn, wheat, rice bran

1. Describe 4 Physiological Effects of fiber.
a) Blood Lipid Profiles are improved (total serum & LDL decrease) by consuming viscous dietary fibers (legumes & oats partcularly). 10g/day increase in viscous fiber is very effective

b) Viscous fiber in a meal leads to smaller but more sustained increase in blood glucose and significantly lower insulin levels, preventative for type 2 diabetes and CVD

c) Constipation can be aleviated by softening and bulking the stool while also speeding the transit time. Fiber most effective: wheat bran, fruits, vegetables, psyllium, celulose. MUST DRINK ADEQUATE FLUID w/fiber.

d) Diverticulosis risk is decreased by consuming nonviscous/insoluble dietary fiber, cellulose.

1. List 5 medical conditions that can be improved by incorporating fiber into the treatment plan.
1. Cardiovascular disease, Type II Diabetes, Colorectal Cancer, Breat Cancer (helps to excrete estrogen), & Weight Control

1. Describe the classification of Soluble vs. Insoluble fiber.
1. Refers to solubility in water, was thought to be true division for fiber's physiological effects such as viscous properties and fermentability were assigned to soluble fiber, not this simple.
SOLUBLE EXAMPLES: beta-glucans, gums, mucilages (psyllium), pectins, some hemicelluloses.
SOLUBLE EFFECTS: dissolve in hot water, delay gastric emptying, slow down transit time, decrease nutrient absorption
INSOLUBLE EFFECTS: does not dissolve in hot water, speeds up transit time, increase fecal bulk

1. Describe the classification of Adsorption or binding capacity of fiber.
1. Viscous and/or soluble fibers tend to bind/absorb enzymes and nutrients in GI tract depending on pH, particle size, food processing, and fermentability.
↓ absorption of lipids - may bind to FA, cholesterol, or bile acid, once bound cannot form miscelles to be absorbed,

↑ fecal bile secretion - bile bound to fiber cannot form miscelles with lipid for absorption

↓ serum cholesterol - 1)excretion of bile acids ↓ bile recycling, cholesterol must be used to create more bile acids 2) shifts bile acids from cholic acid to chenodeoxycholic acid, chenodeoxycholic acid inhibits HMG-CoA reductase & ↓cholesterol synthesis

altered mineral balance - viscous fibers (hemicelulose, pectin, gums) contain uronic acid, which form cationic bridges with minerals making them unavailable for absorption, speed of fermentation is the determinant (slow ferm = more mineral binding)

1. Describe 4 effects of SCFAs generation from fiber fermentation.
a)↑ sodium & H20 absorption because they follow the SCFAs when absorbed

b) mucosal cell proliferation due to adequate energy source

c) energy benefits for more than just enterocytes, Buyrate - used by enterocytes
Acetic Acid - liver, skeletal, and cardiac muscle Propionic Acid - liver

d) acidification of luminal environment - ↑SCFAs → ↓pH in colon's lumen, bile becomes less soluble, calcium is better able to find to bile and FAs (may be protective against colon cancer)

1. Effective constipation treatment should have what effect on the stool?

2. Which types of fiber are the best for this purpose?
1. bulking effect

2. Wheat bran (best! absorbs 3 times it weight in water), rice bran

1. Give examples of viscous fiber.

2. Give examples of fermentable fiber.

3. Give examples of soluble fiber.

4. Give examples of insoluble fiber.
1. VISCOUS: beta-glucans, pectins, guar gum, psyllium

2. FERMENTABLE: beta-glucans, inulins, oligofructose, guar gum,

3. SOLUBLE: beta-glucans, gum, pectin

4. INSOLUBLE: wheat bran, rice bran, cellulose

1. Describe the 7 mechanisms involved in fiber reducing serum cholesterol.
1) ↓bile recycling

2) increased propionate (SCFA) from pectin due to fermentation in colon causes bile acid pool to shift from cholic acid to chenodeoxycholic acid (inhibits HMG-CoA for cholesterol synthesis)

3)delayed gastric emptying (affects lipid absorption and lipoprotein formation)

4) interference with digestive enzymes (impairs absorption of lipids)

5) inteference with micelle formation (impairs absorption of lipids)

6) interferes with mixing of intestinal contents (decreases ability of enzymes to hydrolyze lipids)

7) inhibition of cholesterol synthesis

1. What is the primary form of stored glucose?

2. Where is glycogen stored?

3. What is the major site of glycogen consumption?

4. Can skeletal muscle provide glycogen for the rest of the body?
1. glycogen

2. liver and skeletal muscle (more by total mass, but less per unit)

3. brain (75%)

4. no, it lacks the glucose-6-phosphatase enzyme

5. buffer

1. List the steps including enzymes of glycogen synthesis.

2. At which linkage does glycogen synthase add glycogen to the chain?
Glucose → {ATP}→Glucose-6-Phosphate (G6P)

G6P → {phospoglucomutase}→ Glucose-1-Phosphate (G1P)

G1P + UTP → {UDP-glucose pyrophosphorylase} → UDP-glucose + PPi

Glucose + UDP-glucose → {glycogen synthase} → glycogen (n+1) + UDP

2. α(1,4) [glucan enzyme addsdoes to the branches at the α(1,6) linkages]

1. List the steps including enzymes of glycogenolysis.

2. What pathway occurs in skeletal muscle if they don't have G6Pase to release glycogen stores?
glucose + Pi → glucose + G1P

this step is repeated until the 4th glucose from a branch point is reached, all removed glucose is free glucose

3 more glucose units are removed from the same location by the "debranching enzyme" {4-α-D-glucanotransferase / amylo-α(1,6) glucosidase} and attaches them to the end of a new α(1,4) linkage

the "debranching enzyme" then removes the very last glucose from the branch by hydrolyzing the (1,6) linkage, this one is released as free glucose

G1P (from the 1st step)→ {phosphoglucomutase} → G6P

G6P → {glucose-6-phosphatase} → glucose

2. Glycolytic pathway

1. How is glycogen synthase regulated?

2. Give examples of the kinases able to phosphorylate GS.

3. What is a major inactivator of glycogen synthase?

4. What enzyme serves the same purpose as glycogen
1. Phosphorylation inactivates glycogen synthase. Many different kinases are able to phosphorylate GS.

1) phosphorylase kinase (phosphorylated by protein kinase A)
2) calmodulin-dependent protein kinase (regulated by calcium binding to calmodulin)
3)protein kinase C (activated by diacylglycerol)

3. glucagon receptor (hepatocyte) binding and/or Epinepherine receptor (muscle) binding → activates adenyl cyclase → ↑cAMP → ↑protein kinase → phosphorylates GS to inactive form

4. glycogen phosporylase

5. phospoprotein phosphatase removes the phosphate and activates glycogen phosphorylase in skeletal muscle

6. insulin

1. Describe Von Gierkes Disease.
1. deficiency of G6Pase leads to excess glycogen in non skeletal muscle (mostly liver/kidneys/intestinal cells)
1/3 of all glycogen storage diseases (most common)
SYMPTOMS: growth retardation, lipolysis (↓blood glucose), ketoacidosis
TREATMENT: small meals w/glucose administration, avoid high protein diets(gluconeogenesis)

1. Describe Type II Glycogen Storage Disease (Pompe's Disease).
1. defect in α(1-4, 1-6) glucosidase [acid maltase]

present in lysomes to digest glycogen, lysosomes enlarge and disrupt function of cell, primarilt affects skeletal muscle cells

3 Forms exist
1) Infantile - most common, death after first few months, damage to muscle fibers, enlargement of heart, accumulation of glycogen in liver

2) Childhood Form - progresses slower than infantile, fatal by 20yrs, mental retardation and loss of muscle tone

3) Adult Form - much milder, usually not fatal, muscle weakness

1. Describe Type III Glycogen Storage Disease (Cori's/Forbes Disease).
1. lack of the debranching enzyme results in abnormal glycogen structure and an inability to break glycogen down to free glucose

Symptoms: hepatomegaly, low blood sugar, glycogen accumulation in theheart, liver, & other cells, normal mental development, not fatal

Corn starch at night to prevent hypoglycemia

1. Describe Type V Glycogen Storage Disease (McArdle's Disease).
1. deficiency of skeletal muscle glycogen phosphorylase, skeletal muscles accumuate glycogen and can't use it for energy, rely on FA, AA, and blood glucose for energy, unable to be active, muscle weakness, pain, and cramping

1. Describe Type VI Glycogen Storage Disease (Her's Disease).
1. deficiency of the Liver phosphorylase enzyme leads to excessive glycogen storage in liver (enlarges liver), reduces growth and hypoglycemia

1. Glucosamine comes from what sources?

2. Why is glucosamine an important supplement for joint health?
1. In the body, glucosamine is synthesized by the conversion of fructose-6 phosphate to glucosamine-6 phosphate by the enzyme, fructose-6 phosphate amide transferase, in the hexosamine biosynthetic pathway.

Glucosamine also comes from the exoskeletons of crustaceans and mushrooms. They contain contain chitin and glucosamine is a major component of chitin. The β(1,4) undigestible linkage is processed commercially to make glucosamine supplements.

2. Glucosamine sulfate is normally synthesized by chondrocytes and serves as the precursor to the production of N-acetyl-galactosamine sulfate, an essential component of chondroitin sulfate (GAG).

Chondroitin sulfate forms the ground substance (glycosaminoglycans, proteoglycans or mucopolysaccharides) of joint cartilage. Thus, any reduction in glucosamine sulfate synthesis results in a decline in joint cartilage (articular cartilage) ground substance production, with subsequent joint space narrowing and arthritic degeneration.

As we age, it appears that the fructose-6 phosphate amide transferase enzyme concentrations decline or become less active, resulting in reduction of glucosamine synthesis seen with aging.

1. Why is glucosamine sulfate the preferred supplement?

2. Does adding chondroitin sulfate to the supplement improve its functionality?
1. Glucosamine sulfate delivers sulfur to the joint cartilage. Sulfur is required to stabilize the connective tissue matrix of cartilage, tendons, and ligaments. This form of glucosamine offers a double benefit in the management of osteoarthritis cases by providing glucosamine and sulfur.

2. Glucosamine is a small and simple molecule that is readily absorbed from the GI tract. 90-98% of glucosamine sulfate is absorbed intact from the GI tract when less than 13 % of chondroitin sulfate is absorbed. Glucosamie sulfate stimulates the production of chondroitin sulfate, so taking it alone is adequate especially since the condroitin is not absorbed very well.

1. Which joints are most affected by decreased glucosamine synthesis in the body?

2. What are the symptoms of decreased glucosamine synthesis?

3. Which is better for osteoarthritis, glucosamine sulfate or non-ste
1. The articular cartilage (joint catilage) of knees, hips, hands

2. morning joint stiffness is the first symptom, cartilage destruction, hardening and formation of bone spurs in the joint, pain deformity, limited joint motion

3. NSAIDs address immediate symptoms, but inhibit cartilage repair by inhibiting glucosaminoaglycan (GAG) sythesis, and accelerate cartilage destruction.

4. 500mg/3times/day (for avg weight)

Note: obese 20mg/kg/BW/day, if taking diuretics may need higher dose

1. Describe the relationship between glucoronate, glucosamine, glycosaminoglycans (GAGs), Proteoglycans, and Glycoproteins.
1. glucose → UDP-glucoronate

UDP-glucoronate & glucosamine → GAGs

GAGs → glycoproteins & proteoglycans

1. What is glucoronate and what is it used for in the body?

2. What is the glucoronate synthesis pathway called?

3. Describe the steps in glucoronate synthesis.
1. glucoronate is a highly polar molecule and is used to form cojugates and increase the solubility of bilirubin, steroid hormone, GAGS, proteoglycans, xenobiotics, and drugs

2. Uronic Acid Pathway

G6P → {phosphoglucomutase} → G1P

G1P + UTP → {UDP-glucose pyrophosphorylase} → UDP-glucose + PPi

UDP-glucose + H2O + 2NAD+ → {UDP-glucose dehydrogenase} → UDP-glucoronate + 2NADH + 2H+

UDP-glucoronate → glucoronate

1. How is glucoronate related to jaundice in premature infants?
1. When erythrocytes (RBCs) dies they are degraded. Porphyrin is left over once the iron is removed from heme. Porphyrin is degraded and yields the non-polar/insoluble product bilirubin. Bilirubin must be conjugated with glucoronate to form bilirubin diglucoronide, a soluble form able to be secreted into the bile. When bilirubin exceeds the amount of available glucoronate, jaundice occurs.

1. What are glycosaminoglycans (GAGs)?

2. What are they made of?
1. most abundant heterpolysaccharides in the body, unbranched, highly negatively charged, found either on surface of cells or in extracellular matrix, bristle portion of proteoglycans

N-acetylgalactosamine (GalNAc)
N-acetylglucosamine (GlcNAc)



1. What makes GAGs functionally perfect for connective tissue?

1. high viscocity, low compressibility, lubricating fluid for the joints, also rigidity provides structural integrity for cell, not totally solid and allows passage for cell migration

1. Describe the locations and possible clinical significance of the 6 physiologically significant GAGs.
hyaluronate - no sulfur, can't attach to proteoglycans, large polymers displace H2O, excellent lubricant and shock absorption, synovial fluid, vitreous humor, ECM of loose connective tissue

chondroitin sulfate - cartilage, bones, heart valves (most abundant GAG)

heparan sulfate - basement membranes, component of cell surface

heparin - component cell granules in mast cells that line vessels, contain more sulfate that heparan, role in preventing clotting/coagulation of the blood

dermatan sulfate - skin, blood vessels, heart valves

keratan sulfate - cornea, bone, cartilage aggregated with chondroitin sulfate

1. How are GAGs related to the MPS diseases?
1. Lysosomes inside cells are designed to degrade cellular debris, 14 known defects called "lysosomal storage diseases" involve problems with the degradation of GAGs in the lysosomes. They are referred to as Mucopolysaccharidoses (MPS), which is another terms used for glycosaminoglycans (GAGs), all are autosomal recessive disorders except Hunter's syndrome

1. Describe MPS I H (Hurler's) include the enzyme, affected GAGs, and symptoms.

dermatan sulfate
heparan sulfate

corneal clouding
early mortality
mental retardation
heart disease
dystosis multiplex

1. Describe MPS II (Hunter's) include the enzyme, affected GAGs, and symptoms.

dermatan sulfate
heparan sulfate
Note: GAGs are the same as MPS I H (Hurler's)

NO corneal clouding
early mortality (<15 yrs severe, <60 yrs mild)
mental retardation
facial & physical deformities
X-linked MPS (not autosomal recessive)
dystosis multiplex

1. Describe MPS III A (Sanfilippo A) include the enzyme, affected GAGs, and symptoms.
Heparan N-sulfatase

heparan sulfate

NO corneal clouding
NO organomegaly
NO early mortality
profound mental deterioration
skin, brain, lungs, heart, skeletal muscle greatly affected

1. Describe MPS IV A (Morquio A) include the enzyme, affected GAGs, and symptoms.

keratan sulfate

NO corneal clouding
NO organomegaly
NO early mortality
odontoid hypoplasia (cervical instability at attachment to skull)
aortic valve disease
distinctive skeletal abnormalities

1. What are glycoproteins?

2. What is the main difference between glycoproteins and proteoglycans?

3. What type of linkagea are present? Which one is found most often in mammals?

4. N-linked glycoprote
1. proteins covalently linked to CHO (sugars include glucose, galactose, mannose, fructose, GalNAc, GlcNAc, NANA)

2. glycoproteins do not include complex modification to the CHO attachement

3. O-glycosidic or N-glycosidic, N-glycosidic in mammals via asparagine

4. 3 mannose residues & 2 GlcNAc

1. Describe the 3 clinically significant functions of glycoproteins.

2. Why are cell-surface glycoproteins important in cases of rape and in HIV?
communication between cells
maintaining cell structure
self-recognition by the immune system

2. ABO blood group antigens often have glycoproteins (CHO + PRO) associated to the blood type and are secreted into the serum. Some people do not secrete the ABO glycoproteins. This has forensic significance and has been used to identify rapists.

HIV attaches a chemokine receptor and uses the glycoprotein as a portal to gain entry into immune cells

1. In hepatocytes glucose can be used for what 5 things?

2. Skeletal muscle and heart muscle use glucose for what 2 things?

3. Adipose tissue uses glucose for what 3 things?

4. The brain uses glucose f
1. complete oxidation for energy, stored as glycogen, biosythesis of FAs and AAs, used to produce NADPH, and ribose-5-phosphate via the HMPS(PPP)

2. oxidixed for energy, stored as glycogen (muscle glycogen doesn't supply other tissues with glucose)

a) partially degraded by glycolysis to provide glycerol for triacylglycerol synthesis
b) can be metabolized to acetyle CoA for FA synthesis/storage
c) when energy is needed, FAs are given to blood for energy supply

4. total oxidation via glycolysis and Krebs Cycle

What are the energy releasing steps of glycolysis, including enzymes.
1. glyceraldehyde-3-phosphate + NAD+ → {glyceraldehyde-3-phosphate dehydrogenase} → 1,3-bisphosphoglycerate

1,3-bisphosphoglycerate + ADP → {phosphoglycerate kinase} → 3-phosphoglycerate + ATP

Phosphoenolpyruvate (PEP) + ADP → {pyruvate kinase} → pyruvate + ATP

1. What is the significance of glucokinase vs. hexokinase in the first step of glycolysis?
glucokinase is found only in hepatocytes, hexokinase is in all other cells

they both phosphorylate glucose to trap it inside the cells

glucokinase only phosphorylates/traps glucose when BG is very high, this allows other tissues dependent on glucose to use the dwindling supply, this also allows the liver to release glucose during gluconeogenesis and not trigger the glucokinases to trap it before it is released

1. What happens to pyruvate when oxygen is available?

2. What happens to pyruvate when oxygen is not available?

3. What is the most important allosteric regulator of glycolysis?
Pyruvate is metabolized through the KREBs cycle

pyruvate + CoA + NAD+ → acetyl-CoA + NADH + H+ + CO2

Pyruvate is metabolized
to lactate

Pyruvate + NADH + H+ → {lactate dehydrogenase} → lactate + NAD+

3. fructose-2,6-bisphosphate (F-2,6-BP) is not an intermediate of glycolsis, but it stimulates phosphokinase-1 and inhibits fructose 1,6-bisphosphatase

1. Describe the steps including enzymes of alcohol breakdown.

2. What causes a hangover?
ethanol + NAD+ → {alcohol dehydrogenase (ADH)} → acteylaldehyde + NADH + H+

→ {acetaldehyde dehydrogenase (AcDH)} → acetate

2. ethanol metabolism products (acetylaldehyde & acetate) are toxic

1. Describe the 5 energy releasing steps of the KREBs cycle including enzymes.
isocitrate + NAD+ → {isocitrate dehydrogenase (IDH)} → α-ketoglutarate + NADH + CO2

α-ketoglutarate + CoASH + NAD+ → {α-ketoglutarate dehydrogenase} → succinyl-CoA + NAPH + CO2

succinyl-CoA + GDP + Pi → {succinate thiokinase} → succinate + CoASH + GTP

succinate + FAD → {succinate dehydrogenase} → fumarate + FADH2

L-Malate + NAD+ → {malate dehydrogenase} → oxaloacetate + NADH

1. How many of the following are produced in the KREBs cycle?

2. What is the HMPS/PPP pathway?

3. What does the PPP produce?

4. Which cell types use the PPP?
ATP = 0
NADH = 3
FADH = 1
GTP = 1

2. The pentose phosphate pathway is an alternate oxidation pathway for glucose

3. NADPH to supply FA synthesis, 5-carbon sugars for nucleotides, CO2

4. liver, adipose tissue, adrenal cortex, testis, lactating mammary gland, erythrocytes (for reduction of glutathione)

1. What are the two stages of the PPP called? What is produced during the 1st stage, but not the 2nd?

2. What substrate is 1st in the PPP?

3. What is the end result of the PPP?

4. What 2 types of enzy
1. oxidative stage & non-oxidative stage, NADPH is produced in the 1st stage

2. glucose-6-phosphate

3. glyceraldehyde-3-phosphate & (2) fructose-6-phosphates [transformed dietary sugars into substrates for glycolysis]

transketolases - requires thiamine pyrophosphate (TPP)

1. Gluconeogenesis is essentially the reverse of which metabolic pathway?

2. What is the energy usage difference between these 2 pathways?

3. Which substrate is primarily used in gluconeogenesis? What other subst
1. glycolysis

2. 6 ATP are used in gluconeogeneis, 2 ATP are used in glycolysis

3. primarily lactate via the Cori cycle, pyruvate via the glucose-alanine cycle, and amino acids (except leucine & lysine) from muscle tissue catabolism, glycerol, propionate

1. Describe the Cori cycle.
glucose → 2 pyruvate + 2 ATP → 2 lactate

2 lactate → 2 pyruvate + 6 ATP → glucose

1. How many total ATPs are used during the aerobic total oxidation of glucose?

2. How many total ATPs are produced during the aerobic total oxidation of glucose?

3. How many total ATPs are used during the anaero
1. (glucose to OAA) 2 ATPs

2. (glucose to OAA) 40 ATPs



1. How many ATPs are the following worth?
FADH2 = 2 ATPs

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