Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
36 Cards in this Set
- Front
- Back
|
What are the functions of proteins? |
1. Muscle contraction (actin/myosin) 2. Structure (collagen) 3. Transportation (hemoglobin/ion channels) 4. Protection (antibodies) 5. Regulation (enzymes/hormones) |
|
|
Name the essential amino acids |
Leucine Isoleucine Valine Lysine Tryptophan Threonine Methionine Phenylalanine Histidine (semi-essential) Arginine (conditionally essential to infants) |
|
|
Protein digestion |
Begins in the stomach, where pepsin breaks down protein to smaller polypeptides; then in the duodenum trypsin, chymotrypsin, and carboxypeptidase break them down to peptides; and in the small intestine peptidases break them down to amino acids, dipeptides, and tripeptides |
|
|
Protein absorption |
In the lumen of the small intestine, amino acids, dipeptides, and tripeptides (which are broken down by brush border enzymes and peptidases) are taken into enterocytes where dipeptidase and tripeptidase break them down to amino acids; then they can exit the cell into the blood |
|
|
How does dietary protein affect insulin? |
Certain amino acids stimulate insulin secretion to help move amino acids into the cell -If a high protein, low CHO meal is eaten, both insulin and glucagon will be secreted to regulate blood sugar |
|
|
How areamino acids processed by the liver? (What is transamination and deamination?)
|
Transamination involves moving the amino group from the amino acid to a-ketoglutaric acid; converting the AA to an a-ketoacid and the a-ketoglutaric acid to glutamic acid; reversible r(x); via transaminase Deamination involves removing the amino group to form ammonia and a-ketoglutaric acid from glutaric acid; NAD is reduced to NADH Then ammonia + CO2 is converted to urea + H2O; via enzymes |
|
|
What arealpha keto acids? Give some examples
|
Amino acid without the amine group, instead has a double bond to Oxygen -Aspartate forms oxaloacetate -Glutamate forms a-ketoglutarate -Alanine forms pyruvate |
|
|
What arefates of alpha keto acids? |
1. Energy (Kreb's Cycle) 2. Gluconeogenesis 3. Ketones (via Acetyl-CoA) 4. Cholesterol synthesis 5. Fatty Acid synthesis (via Acetyl-CoA) |
|
|
Name thesubstrates for gluconeogenesis
|
Alanine Cysteine Glycine Serine Threonine Isoleucine Asparagine Aspartate Tyrosine Phenylalanine Valine Methionine Arginine Histidine Proline Glutamine Glutamate Tryptophan |
|
|
Differentiate between ketogenic and glucogenic amino acids. How are they potentially processed via metabolic pathways? |
Ketogenic: Gives rise to Acetyl-CoA; can form ketones Glucogenic: Gives rise to pyruvate; can form glucose |
|
|
What are dietary requirements based on?
|
Amount of a food needed to eat in order to achieve a certain physiological requirement amount of absorbable and utilizable nutrient; not all that is eaten is absorbed/used |
|
|
What is the process of a nutrient becoming bioavailable vs. bioefficient? |
Becoming bio-available involves the nutrient being liberated from the food matrix, converted into an absorbable chemical form, and entering GI cells; portion that is absorbed Becoming bio-efficient involves the nutrient being absorbed into GI cells, converted to the active form, and having a specific effect on the body |
|
|
What are bioavailability and bioefficacy governed by?
|
Internal factors: gender, age, nutrient status, life stage External factors: food matrix, chemical form
|
|
|
SLAMENGHI stands for (...)
Describe how each concept influences the bio-availability andbio-efficiency of nutrients |
Species: different physical and chemical properties Linkages: (molecular) various geometric isomers exist in food and human tissue (cis versus trans); esterification Amount: when certain compounds are consumed together they could inhibit absorption (competition for uptake site), metabolism, and transport (competition for incorporation) Matrix: food components trapped in structure of plants, decreasing bio-availability Effectors: other factors in diet can inhibit or improve bio-availability (changing solubility, binding to nutrient,supplements, competing for uptake, compete for carrier sites on transport proteins) Nutrient Status: Large amount of fat-soluble vitamins can be toxic; regulated by vitamin status (? - limited research) Genetics: individual variability; mutations/polymorphism- alter gene expression/ f(x) Host-related factors: GI, nutrient status/need, age, infection; enhanced renal conservation, absorption, utilization bone resorption Interactions: (between all) Data hard to come by |
|
|
What form of folic acid is most absorbable?
|
Folic acid = 100%; in supplements/fortifications as monoglutamate; most stable form Folic acid + food = 85% Food folate = 50%; as polyglutamate |
|
|
How is folate absorbed?
|
In jejunum: intestinal y-glutamyl hydrolase removes polyglutamyl chain from monoglutamate folate (folic acid) In enterocyte: monoglutamate folate reduced and methylated In colon: folate synthesized by colon bacteria is bioavailable also |
|
|
What increases bio-availability of folate in spinach? |
Chopping, mincing, or enzymatically liquefying |
|
|
Define DFE and explain why this unit is used when determining folate requirements |
Dietary folate equivalent Natural food folate + 1.7 X the synthetic folate -this is used because synthetic folate is more absorbable |
|
|
List the RDAs of folate foradults.
|
Adults >18 & women of childbearing age = 400 micrograms DFE Lactating women: 500 micrograms Pregnant women: 600 micrograms |
|
|
Whatare the two forms of iron? List food sources of each
|
Heme Iron: lean meat, seafood Non-heme Iron: nuts, beans, vegetables, fortified grains -absorbed by separate pathways; once inside mucosal cells, all iron enters a common pool |
|
|
Describe the movement of iron fromthe intestinal lumen through systemic circulation. What transport proteins areinvolved? What are its major destinations?
|
Absorption: Heme iron enters mucosal cell via heme transporter; non-heme iron is in Fe3+ (ferric) form and must be reduced to Fe2+ (ferrous) form via duodenal cytochrome B, it then can enter the cell via DMT1 Iron is bound to ferritin in mucosal cells of intestine (cells sloughed off every 2-5 days); Fe2+ (from both sources) exits cell via ferroportin1; then it is oxidized to Fe3+ by hephaestin and enters circulation; travels bound to plasma transferritin to liver for storage; to muscles, binding to myoglobin; to bone marrow to become RBCs (iron can be lost with blood loss) where it can circulate (bound to hemoglobin) to the liver/spleen where RBCs are broken down and iron is recycled |
|
|
Difference between bio-availability of heme and non-heme iron
|
Heme iron in meat hemoglobin and myoglobin can be absorbed intact without beingbroken down to elemental iron because of the porphyrin ring around it (protects it)
Non-heme iron in other foods (vegetables, grains) is often tightly bound to phytates (phytic acid) or other compounds that make is less available; it also must first be reducedto ferrous (Fe2+) iron from ferriciron (Fe3+) before it can be absorbed; absorption is also decreased by chelators or other agents (*absorption increased by HCl and vitamin C *) |
|
|
What is ferrous and ferric iron?What form is absorbable?
|
ferrous (Fe2+) -absorbable
ferric iron (Fe3+) - from non-heme food iron sources |
|
|
What role does vitamin C play iniron absorption? What about isoascorbic acid?
|
When consumed in the same meal forms chelate; helps prevent the formation of insoluble and unabsorbable iron compounds -Isoascorbic acid = steroisomer of ascorbic acid; potentenhancer of nonheme iron absorption |
|
|
How does protein influenceabsorption of non-heme iron?
|
Meat and animal protein enhances absorption; Protein from eggs, milk, dairy impair iron absorption (especially casein) |
|
|
How is folic acid transported in body? |
From enterocyte to the liver; half of body folic acid is in liver (!); it is secreted into bile and reabsorbed via entero-hepatic circulation then transported via systemic circulation to body tissues |
|
|
Why is hemoglobin and myoglobin iron more absorbable? |
It is bound in a protective porphyrin ring which shields it from interaction with other food components and keeps it soluble in the intestine (ring removed in mucosal cell)
|
|
|
Explain the bio-availability of supplemental iron |
Absorptionhighest for iron solublized in water or dilute acids; however, water and acids cause oxidative reactions unless encapsulated (!)
|
|
|
How does the liver regulate iron storage? |
Liver releases hepcidin, a peptide hormone, when stores are high,which signals brush border to make fewer receptors, therefore decreasing absorption/bio-availability
-Stored in liver as Hemosiderin- an insoluble iron-protein |
|
|
Explain iron absorption feedback loop of intestinal mucosal cells |
-Iron crosses enterocyte by active transport; the rate is regulated bymucosal cell iron stores; more is transported when stores are low
-When stores are high, more iron is storedas ferritin in the enterocyte than transported to plasma via transferritin ** mucosal cells sloughed off every 2-5 days and take the stored iron with (!) |
|
|
Explain iron transport and absorption into erythroid cells |
Transferrin binds ferriciron in plasma; enters maturing erythroid cells via specific receptor in whichthe iron is internalized and released into the cell
- transferrin and transferrinreceptor are recycled -increased erythropoiesis is associated with an increase in the numberof transferrin receptors -iron depletion and anemia are associated with increased concentrationof serum transferrin |
|
|
Explain how Iron is stored |
Iron binds to apoferritin and forms the complex, ferritin to be stored in intestinal mucosal cells and in macrophages in the liver, spleen,and bone.
When free iron levels are low: -Apoferritin synthesis is inhibited and the balance of iron binding shifts towardstransferrin When free iron is high: -More apoferritin is produced so that iron can be safely sequestered and thereby protectorgans from excess iron |
|
|
Explain how iron is excreted |
There is no direct way; small amounts are lost by sloughing of intestinal mucosal cells; very small amounts in bile, urine, sweat -Iron status is regulated bychanging intestinal absorption and storage of iron in response to the body’sneeds |
|
|
Explain iron deficiency |
Microcytic anemia:
Serum iron: < 40 g/dL Serum ferritin: < 10 g Hematocrit and hemoglobin = late stages
|
|
|
Explain iron toxicity |
Acute: over consumption of supplements; can be lethal in children bowel irrigation, chelation therapy
**Treatment: Chronic (Hemochromatosis)Results when excess iron is deposited in the heart, liver, pancreas –can lead to organ failure and death -Occurs due to inheritance or repeated blood transfusions **Treatment: Repeated blood withdrawals |
|
|
How do zinc and iron interact? |
Excesszinc (25 - 50 mg/day) decreases iron status
Iron mayinhibit both the uptake and transfer of zinc through intestinal cells |
