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Spring 2014 > Metabolism - Exam #1 > Flashcards

Metabolism - Exam #1 Flashcards

1
Q

What are the dietary standards in the US based on?

A
  • Originally = RDAs for nutrient deficiencies;
  • Current= DRIs based on energy/nutrient intake
  • Organized by life-stage groups;
  • Meant for healthy people age 2 and above
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2
Q

What are the 6 groups of DRI’s?

A
  • Bone Health (Ca, P, Mg, Vit. D, Fluoride)
  • B vits. and Choline
  • Antioxidants (C, E, selenium, beta-carotene)
  • Energy and macronutrients (cals. and alcohol)
  • Electrolytes and water
  • Vits. A and K and trace minerals
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3
Q

What are the Estimated Average Requirements (EAR)?

A
  • General intake of the population
  • Would meet the needs of ~50% of the population;
  • Based on a CRITERIA of ADEQUACY or biological marker
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4
Q

What are the Recommended Dietary Allowances (RDAs)?

A
  • Specific recommended amounts per individual
  • Calculated from 2 standard deviations from the EAR
  • Meets the needs of ~97% of the population;
  • CANNOT specific an RDA without an EAR
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5
Q

What are Adequate Intakes (AI)?

A
  • Specific recommended amounts per individual;
  • OBSERVED to yield optimal health benefits
  • Used when NO RDA or EAR
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6
Q

What are UL’s?

A
  • Extremely high intake levels that cause toxicity
  • Intake BELOW UL in considered non-toxic
  • Might be based on concentrated intake of supplements only; toxic levels may not be attainable through foods
  • No adverse affects at high doses then considered safe at usual intakes
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7
Q

What is there is NO RDA/EAR or AI?

A

Compound NOT considered relevant or needed for health

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8
Q

What are Estimated Energy Requirements (EERs)?

A

-Calculated caloric intake to maintain a stable, healthy weight

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9
Q

What are the Acceptable Macronutrient Distribution Ranges (AMDRs)?

A
  • Ranges of % for each macronutrient as a part of total calorie intake; determines what amounts of macronutrients (CHO, fat, protein) should constitute the total energy intake;
  • Need to provide balance!
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10
Q

What are the ideal AMDRs for each macronutrient?

A
  • 10-35 % Protein
  • 20-35% Fat
  • 45-65% CHO
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11
Q

What are the Dietary Guidelines of Americans (DGA)?

A
  • Diet and lifestyle recommendations meant to promote optimal health and minimize the risk of chronic disease
  • Began 1980; Revised every 5 years → Most current is 2010
  • DGA began using MyPlate with the latest version in 2010
  • DGA = policy → MyPlate and School Lunch Program are tools to implement the policy
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12
Q

How have the DGA’s changed over the years?

A

1980 - consumer brochures;
2000 - both consumer and policy oriented
2005 - solely policy (plain language for education)
2010 - policy document (intended to design and carry out programs)

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13
Q

What is the USDA’s Nutrition Evidence Library (NEL)?

A
  • Created 2006, launched 2008 by USDAs CNPP
  • Evidence-based research reviews federal nutrition policy
  • All agencies must meet federal standards on qualiidance
  • Systematic research and review process
  • Specified Grading Criteria involving quality, quantity of studies/subjects, magnitude of impact, generalizability to the population
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14
Q

What are the QUALITATIVE descriptors of the NEL?

A

(best to worst)

  • Strong
  • Moderate
  • Limited
  • Expert
  • Opinion
  • Grade Not Assignable
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15
Q

What is the Data Quality Act of 2001?

A
  • Use of NEL ensure compliance
  • All agencies must meet federal standards on quality, objectivity, utility, an integrity of the information for it to be considered adequate for federal guidance
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16
Q

What are the NEW additions to the Dietary Guidelines?

A
  • Individuals at high risk of chronic disease;

- 2 overreaching concepts = calorie balance to maintain weight and focus on nutrient dense foods and beverages

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17
Q

What is included in the Executive Summary of the Dietary Guidelines?

A
  • Purpose, uses, concepts;
  • 2 overreaching concepts of calorie maintenance and nutrient dense foods;
  • 23 key recommendations;
  • Quantitative recommendations are listed as avg. daily/weekly intakes
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18
Q

What is Nutrient Density?

A
  • Provides vitamins, minerals, and other beneficial substances and relatively few calories WITHOUT….solid fats, added sugars/refined starches/sodium
  • Retains natural, beneficial components (fiber)
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19
Q

Nutrient dense foods

A

All veggies, fruits, whole grains, seafood, eggs, beans/peas, unsalted nuts and seeds, fat-free and low-fat dairy, lean meats and poultry
-when prepared WITHOUT added solid fats and sugars!

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20
Q

What are the Key recommendations of the DGA?

A
  • Balancing Calories to Manage Weight
  • Foods/Components to Reduce
  • Foods/Components to Increase
  • Building Healthy Eating Patterns
  • Recommendations of Specific Populations
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21
Q

Foods and Food Components to REDUCE

A
  • Reduce Sodium;
  • Less than 10% kcals from sat. fats
  • Less than 300mg cholesterol
  • Trans fats as low as possible;
  • Reduce intake of SOFAs;
  • Limit REFINED grains;
  • Alcohol in moderation
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22
Q

Foods and Nutrients to INCREASE

A
  • Variety of fruits and veggies
  • Half grains WHOLE;
  • Fat-free and low-fat dairy;
  • Variety of PRO (seafood, lean, poultry, eggs, beans/peas, nuts);
  • Oils replace solid fats;
  • More potassium, fiber, calcium, Vit. D
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23
Q

What are the groups with specific recommendations?

A
  • Over 50 (fortified Vit. B12);
  • Women capable of becoming pregnant;
  • Women pregnant/breastfeeding
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24
Q

What are the recommendations for women capable of becoming pregnant?

A
  • Food high in HEME IRON;
  • Iron enhancers (Vit. C);
  • 400 micrograms of synthetic folic acid (fortified food and sups) in addition to folate from the diet
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25
Q

What are the recommendations for women who ARE pregnant/breastfeeding?

A
  • 8-12 ounces of seafood/wk;
  • iron supplementation;
  • LIMIT albacore tuna to 6oz/wk;
  • DONT consume tilefish, shark, swordfish, and king mackerel
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26
Q

What are the recommendations for Sodium limitation?

A
  • Less than 2300mg/day;
  • Less than 1500mg/day for 51+, African Americans, those with high BP, DM, or kidney disease (about half the population)
  • Meant to lower BP!
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27
Q

Why the change to MyPlate?

A

-Released June 2, 2011
-Easier to understand
-Food groups =
Grains
Veggies
Fruits
Dairy
Proteins

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28
Q

What is shown on Food Labels?

A

-Serving size and servings per container
-Calories and calories from fat
-Carbs
-Sugars
-Protein → No daily value
For the purpose of limiting → Fats, Cholesterol, Sodium
-Vitamins to increase → Vit. A and C
-Minerals to increase → Calcium and iron
-Ingredients

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29
Q

What are the Daily Reference Values?

A
  • Macronutrients
  • Total fat, saturated fat, cholesterol, total carbohydrates, dietary fiber, protein, potassium, and sodium → Didn’t have a basis of an RDA
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30
Q

What are the Reference Daily Values?

A

-Daily intake level of a nutrient that is considered to be sufficient to meet the requirements of 97–98% of healthy individuals → Based on the 1968 RDAs and have not been changed

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31
Q

What are the 3 Health Claims allows to be stated on food labels?

A
  • Significant scientific agreement – food and dietary supplements
  • Authoritative statement from recognized scientific body
  • Qualified health claims – emerging, but not yet well-established
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32
Q

What are the Exchange Lists?

A
  • Food group system to plan diets and meet certain dietary needs → Variety of diets, not just diabetics
  • Created by the ADA for the American DM Association
  • May exchange foods within the SAME group as long as the equivalent servings are known
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33
Q

What are Carbs?

A
  • Main energy source;
  • Over 50% energy consumed from CHOs;
  • Simple sugars and complex carbs;
  • Half dietary CHO are polysaccharides (starch/dextrin) from cereal grains and veggies;
  • Other half are simple sugars (mono’s and di’s)
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34
Q

What are the forms complex carbs?

A

Oligo = 2-10;
Poly = more than 10 (cereal grains, veggies: Glycogen, starch, cellulose);
*Dextrins are produced from starch and found in foods or in digestion products)

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35
Q

How is weight maintenance achieved?

A

Calories consumed = Calories burned

  • POSITIVE energy balance – CONSUMING more than is burned
  • NEGATIVE energy balance – BURNING more than is consumed
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36
Q

What is High Fructose Corn Syrup?

A
  • AKA – Isoglucose, Maize syrup, or Glucose-fructose syrup;
  • Enzymatic conversion of glucose to fructose then mixed with corn syrup (pure glucose) to a set sweetness;
  • Combines the mono’s of glucose and fructose in the lab → Same components that natural make sucrose with weak glycosidic bond
  • Common sugar substitute in the US for table sugar (sucrose)
  • AMA states HFCS contributing more to weight gain and other medical conditions not likely
  • GRAS – 1976 by FDA
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37
Q

Why was it believed that Carbs caused weight gain?

A

1980s – CHO consumption increase, therefore lowering the %fat → But OVERALL energy consumption increased

  • REFINED (bad) CHO did increase, but FAT contributes more kcals to the total amount of energy consumed;
  • Because carbs went up, this DILUTES the amount of FAT as a percentage
  • Weight gain not necessarily due to CHO consumption, especially if you consume the RIGHT kind of COMPLEX CARBS
  • All depends on CALORIES!
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38
Q

What are MONOSACCHARIDES?

A
  • Natural or digestion product;
  • 3-7 Carbons (trioses-heptoses)
  • Building blocks polysaccharides → Natural state as single units or as breakdown products of digestion;
  • ALL CHO breakdown to Mono’s;
  • Functional group is a CARBONYL (C=O)
  • Aldehydes or ketones;
  • Glucose, Fructose, Galactose
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39
Q

What are ALDEHYDES?

A
  • Make Aldoses – carbonyl on the end of the Carbon chain
  • Based on D- or L- glyceraldehyde (3 carbons)
  • EX: Glucose, Galactose
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40
Q

What are KETONES?

A
  • Make Ketoses – carbonyl in the middle of the Carbon chain
  • Based on D- or L- ertyhrulose (3 carbons), but built up of dihydroxyacetone units (3 carbons)
  • EX: Fructose (very important metabolic intermediate in phosphorylated form)
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41
Q

What is a CHIRAL carbon?

A
  • Having 4 different atoms/groups attached to a single Carbon;
  • A molecule with “N” chiral carbons can have 2N stereoisomers;
  • Causes OPTICAL ACTIVITY
  • Glucose – 4 chiral carbons = 16 stereoisomers (8 D-glucose + 8 L-glucose)
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42
Q

What are Diastereomers?

A

-Compounds or stereoisomers have different configurations at one or more of the stereocenters (can be chiral carbons) and not NOT mirror images → Like our hands

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43
Q

How is the Stereoisomerism of a compound determined?

A
  • Being optically active is what determines the stereoisomerism and chirality of a compound;
  • How the compound reacts in polarized light;
  • Yields Enantiomers and Diastereomers (R/S or D/L)
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44
Q

What is Optical Activity?

A
  • The degree to which a molecule rotates in polarized light;

- D of one compound can be “+” optical rotation and “-“ another compound

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45
Q

What are the stereoisomer configurations of Monosaccharides?

A

-D or L configuration is based on the HIGHEST number chiral carbon → Farthest Carbon from functional Carbonyl group
-D = -OH on highest chiral on the RIGHT
-L = -OH on highest chiral on the LEFT;
Note: ALL -OH groups are flipped b/w D and L

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46
Q

What are Epimers?

A

-Type of stereoisomer;
-Structure of compound varies only by the orientation around a SINGLE Carbon (-OH on the left vs. the right);
-2 stereoisomers at EACH CHIRAL carbon;
-Glucose Epimers=
•D-Mannose – C-2 epimer → -OH left
•D-Galactose – C-4 epimer → -OH left

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47
Q

Why is the D configuration the most important?

A

-Metabolized form due to digestive enzymes being stereospecific for D isomers (WON’T breakdown L-configurations)

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48
Q

What is is the predominate form of Monosaccharides?

A
  • RINGS are much more STABLE than open chain form;
  • Forms when a bond forms between C1 for aldoses or C2 for ketoses and the highest numbered chiral carbon
  • Carbonyl carbon (C1) becomes a NEW chiral carbon in ring form (ANOMERIC Carbon)
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49
Q

What is Mutarotation?

A
  • Conversion between the alpha and beta ring structures = Alpha, Open, Beta;
  • Open chain form is the conversion state;
  • Equilibrium between Alpha and Beta ring structures;
  • Alpha = anomeric –OH is DOWN
  • Beta = anomeric –OH is UP
  • Glucose: ~36% Alpha-D-glucose; ~64% Beta-D-glucose; <0.01% open chain
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50
Q

What are the types of rings structures?

A
  • Pyran – 6-membered ring (EX: Glucose, dominant form)

- Furan – 5-membered ring (EX: Fructose, only form that exists in metabolism as phosphorylated intermediates)

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51
Q

What is an Anomer?

A
  • Epimers that are defined by differing at the ANOMERIC carbon;
  • One of two sterreoisomers of a cyclic saccharide that differs ONLY at the hemiacetal or hemiketal (ANOMERIC Carbon)
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52
Q

What are Reducing Sugars?

A

0-Cyclic ring structure that may undergo a reaction to become a disaccharide
-MUST have an UNBOUND anomeric –OH to be involved in glycosidic bonds and undergo MUTAROTATION

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53
Q

What is the predominate form of FRUCTOSE?

A
  • In water, exists as 67% Beta-D-fructopyranose (6), 27% Beta-D-fructosefuranose (5);
  • BUT Beta-D-frutofuranose is the form in metabolism as phosphorylated intermediates and glycosidic links for disaccharides
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54
Q

What are disaccharides?

A
  • Glycosides bound together by a glycosidic bond, which is an acetal link;
  • Acetal link = from the hemiacetal at the anomeric carbon to -OH of another group, such as an alcohol
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55
Q

What are the disaccharides and their composition?

A
  • Maltose – glucose + glucose → Digested, reducing;
  • Lactose – galactose + glucose → Digested, reducing;
  • Sucrose – glucose + fructose → Digested, NON-reducing because BOTH anomeric carbons are bound in glycosidic bonds to make the disacch.
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56
Q

What are the Oliogosaccharides?

A
  • Less than 10 sugar units;
  • Raffinose, Stachyose, Verbascose;
  • others on the market, mainly as fructose (FOS) and (GOS);
  • All are NOT digestible
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57
Q

What are Polysaccharides?

A
  • More than 10 sugar units;

- Starch, Glycogen, Cellulose (fiber with beta bonds that can’t be digested)

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58
Q

What is Amylose?

A
  • Starch (plant glucose);
  • Linear glycogen chain of Alpha-1,4 glycosidic bonds;
  • Digested SLOWER due to linear structure; “Resistant” to digestion
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59
Q

What is Amylopectin?

A
  • Starch (plant glucose);
  • Branched glycogen chain of Alpha-1,4 glycosidic bonds (backbone) and Alpha-1,6 glycosidic bonds (branches);
  • Most starches are ~80% Amylopectin;
  • Digested much FASTER than Amylose due to enzymatic reactions working at each branch
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60
Q

What is Glycogen?

A
  • Animal storage form of starch;
  • HIGHLY branched form of glucose molecules of both Alpha-1,4 and Alpha-1,6 glycosidic bonds;
  • Digested the FASTEST due to extremely high number of branches
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61
Q

What Carb digestion takes place in the MOUTH?

A
  • Digestion of BOTH amylose and amylopectin by Alpha-Amylase enzymes;
  • Forms dextrins
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62
Q

What Carb digestion takes place in the STOMACH?

A
  • NO DIGESTION
  • Stomach acids destroy Alpha-amylase activity;
  • Dextrins pass to small intestine
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63
Q

What Carb digestion takes place in the SMALL INTESTINE?

A
  • AMYLOSE = Pancreatic Alpha-Amylase hydrolyzes Alpha-1,4 glycosidic bonds of the dextrins to produce the disaccharide Maltose;
  • AMYLOPECTIN = Pancreatic Alpha-Amylase hydrolyzes Alpha-1,4 glycosidic bonds to dextrins, maltotriose, isomaltose, and maltose; DOES NOT hydrolyzes any Alpha-1,6, but stops 4 units away
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64
Q

What Carb digestion takes place in the Brush Border of the Small Intestine?

A
  • Maltase enzyme in the microvilli hydrolyzes Maltose all the way down to single Glucoses;
  • Alpha-dextrinase is the main enzyme for hydrolyzing Alpha-1,6 glycosidic bonds;
  • DIGESTION MUST GO ALL THE WAY TO MONOSACCHARIDES;
  • CANNOT ABSORB DISACCHARIDES
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65
Q

What was the original belief toward carb digestion?

A
  • In VIVO (in the body) digestion = ONLY 1,4 and 1,6 CHO bonds; Also, 1,3 was found to be digested
  • In VITRO (in the lab; experimental NOT in the body) = 1,3 CHO bond not digested
  • 1970s, Complex carbs were ALL slowly digested, unlike sugars and DID NOT have much effect on blood glucose levels → Though branches made them harder to digest (Complete OPPOSITE of truth)
  • TRUTH = REFINED Starches found to have High Glycemic effect on blood glucose
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66
Q

What is the difference in glucose and fructose absorption?

A
  • More absorption capacity of glucose than fructose;
  • Glucose 5400g/day;
  • Fructose 4800 g/day
  • Intestinal distress seen with high doses of fructose (50g)
  • Fructose absorption limited in ~60% of adults
  • Most dietary Fructose does NOT pass liver make it into systemic blood
  • Highly efficient digestion means all carbs typically absorbed BEFORE jejunum of SI
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67
Q

How do Monosaccharides enter into cells?

A
  • Transporter carries MONOSACCHARIDES into the enterocytes from the intestinal lumen ;
  • CANNOT absorb anything but Monosaccharides (Glucose, Fructose, Galactose);
  • Will then leave cells for the PORTAL BLOOD
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68
Q

How are Glucose/Galactose ACTIVELY Transported INTO Cells?

A
  • Sodium ATPase membrane proteins pump Glucose/Galactose and Sodium through cell membrane;
  • ATP (energy) and Na+ requiring!
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69
Q

How do Glucose/Galactose go through FACILITATED Diffusion INTO Cells?

A
  • GLUT2 (glucose transporter) moves Glucose/Galactose into cell when lumen levels are high (High to low concentrations)
  • NO ENERY, just need the transporter
70
Q

How does Fructose go though FACILITATE Diffusion INTO Cells?

A

-GLUT5 moves Fructose into the cells

71
Q

How are Glucose/Galactose ACTIVELY Transported OUT of cells?

A
  • Sodium is sent into blood by Sodium/Potassium ATPase pump;
  • Allows Potassium from the blood into the cell;
  • GLUT2 facilitates Glucose/Galactose out of the cell
72
Q

How do Glucose/Galactose go through FACILITATED Diffusion OUT of cells?

A

-GLUT2 continues to carry Glucose/Galactose out of the cell into the bloodstream

73
Q

How does Fructose go through FACILITATED Diffusion OUT of cells?

A

-GLUT2 also carries Fructose from the cell to the blood

74
Q

What happens to water-soluble nutrients when absorbed?

A
  • Enter the portal vein and go to the liver;
  • Portal Vein – moves blood from the spleen and gastrointestinal tract to the liver’s capillary beds
  • Enter by facilitated diffusion;
  • Most of fructose/galactose converted to glucose in the liver
75
Q

How is Galactose utilized and converted to Glucose-1-PO4?

A
  • Utilizes UDP-glucose – nucleotide sugar that allows for the glucose transferase reaction to occur
  • Transferase reaction = Galactose-1-phosphate displaces Glucose-1-phosphate from UDP-glucose leaving UDP-glucose 4 epimerase;
  • Can now react at C4 and take on more glucose molecules
  • Coenzymes = NAD+/NADH – transfer electrons through oxidation/reduction reaction at C4
  • Remaining UDP-glucose is recycled and used again to make more Glucose-1-Phosphate
76
Q

How is Fructose utilized by the body?

A
  • Fructokinase (liver, kidneys, and intestine) – phosphorylates Fructose to Fructose-1-phosphate;
  • Fructokinase NOT effective on Glucose, NOT affected by fasting or insulin (blood glucose levels);
  • Glucose limits fructose metabolized for energy because it is better for glycolysis as the substrate for Hexokinase
77
Q

What is Glucokinase?

A
  • Hexokinase isozyme found in the liver
  • IS affected by blood glucose levels and its indicators of fasting and insulin;
  • Facilitates phosphorylation of glucose to glucose-6-phosphate, but ONLY when the brain and blood glucose levels are supplied first!
  • Keeps liver from metabolizing glucose first
78
Q

Why does ingesting high levels of fructose cause intestinal distress?

A
  • Bypasses the regulatory steps (Phosphofructokinase) that glucose undergoes in Glycolysis
  • Enters glycolysis at later stage therefor it is not as highly regulated;
  • Greatly effects blood sugar and metabolism by such a quick conversion to glucose
79
Q

What is the problem with fructose creating trioses so quickly?

A
  • When glycolysis trioses are OUTSIDE the liver (Extrahepatic tissues) they are precursors for Glycerol-3-phosphate, which creates the backbone of fatty acids;
  • AKA: Fructose turns to fat in tissues other than the liver;
  • Leads to increased VLDL secretion and ultimately LDL cholesterol
80
Q

What are GLUT isoforms?

A
  • Glucose transporters;
  • Membrane proteins with specific binding sites (different locations/molecules)
  • Use conformational changes to bind and transport;
  • Reverts to original form when not bound so may be recycled
81
Q

GLUT1

A
  • Basic supply of glucose to cells;

- Erythrocytes

82
Q

GLUT2

A
  • Low affinity transporter;
  • Found in tissues where cytoplasmic vs. blood glucose levels regulate transport;
  • Cytoplasmic glucose concentration in cells REFLECT blood glucose
83
Q

GLUT3

A
  • High affinity;

- Supplies BRAIN and others glucose-dependents

84
Q

GLUT4

A
  • INSULIN DEPENDENT!!;
  • Regulated by Insulin for muscle, heart, adipose;
  • Synthesized in the trans-golgi network (TGN)
85
Q

GLUT5

A

-Fructose ONLY into cells

86
Q

What is Insulin?

A
  • From pancreatic Beta-cells;
  • ANABOLIC (building) hormone;
  • Stimulates muscle and adipose cells to take on glucose, fatty acids, and amino acids as needed;
  • Regulates glucose absorption by binding membrane receptor and activating GLUT4
87
Q

What happens when Insulin is activated to LOWER blood glucose?

A
  • Insulin stimulates the activity of GLUT4;
  • GLUT4 enters plasma membrane of the cell from its storage compartments (GSVs);
  • Moves to the site where glucose needs to be bound and brought into the cells;
  • NO insulin, GLUT4 remains inactive in storage form
88
Q

Mechanism of Insulin Action

A
  • Reacts/binds with membrane receptor that stimulates GLUT4 transfer proteins that bring compounds into cells
  • ANABOLIC, so storage and synthesis promoting of glycogen, lipids and proteins;
  • INHIBITS CATABOLISM of glycogen, lipids and proteins
89
Q

What occurs in T1DM or T2DM?

A
  • NO insulin (T1) or too little insulin (T2) NO glucose taken into insulin-regulated cells or those that ue GLUT4;
  • Excess glucose will enter cells that have GLUTs not controlled by insulin
90
Q

What hormones OPPOSE the actions of Insulin?

A
  • Glucagon – b/w meals, releases stored glycogen to glucose-dependent cells
  • Cortisol and epinephrine – stress, breaks down glycogen for muscles
  • Growth hormone – amino acid intake when blood glucose/insulin levels drop; but regarding glucose, opposes insulin-promoted uptake
91
Q

What is Glycemic Index?

A

-Rate of glucose absorption (%)
-Graphed as “Blood glucose level per Hour after eating”
-Calculated by a reference food (White bread)
= Area under the curve for test food/Area under the curve for reference food)

92
Q

What is Glycemic Load?

A

-Takes into account actual carb content of food

= (decimal X grams carbs/serving)

93
Q

What is Glycogenesis?

A

Making glycogen

94
Q

What is Glycogenolysis?

A
  • Breakdown of GLYCOGEN (stored)→ back into to glucose;

- Used to raise blood glucose levels or give muscles energy

95
Q

What is Glycolysis?

A
  • Oxidation of glucose to pyruvate (3C) and H+;
  • Free energy released is used to form of high-energy ATP and NADH;
  • Followed by the TCA cycle
96
Q

What is Gluconeogenesis?

A
  • Making glucose from a NON carb source;

- Intermediate must have at least 3 carbons to generate glucose

97
Q

What are the NON-Carb sources that can be used to make Glucose?

A
  • MUST HAVE 3 CARBONS:
  • Glucogenic amino acids;
  • pyruvate
  • PEP;
  • OAA
98
Q

What CANNOT be used to make glucose?

A

-LESS than 2 carbons;
-Ketogenic amino acids and acetyl CoA (from fatty acids) CANNOT be used to make glucose
•Conversion of Pyruvate to Acetyl CoA is IRREVERSIBLE and the commitment AWAY from glucose synthesis and TO the TCA cycle

99
Q

What is the Hexose Monophosphate Shunt?

A
  • Making 5-carbon monosaccharides and NADPH;
  • Products used for SYNTHETIC pathways (such as making glucose, instead of Glycolysis and metabolizing);
  • NADPH is the reduced coenzyme of carb synthesis
100
Q

What is the Tricarboxylic Acid Cycle (TCA)?

A
  • Oxidation of pyruvate and acetyl CoA;
  • Provides glycolysis with needed electrons and then to proceed onto the ETC to produce energy
  • Products per glucose (2 cycles) =
  • 2 ATP/GTP (energy)
  • 6 NADH (goes to ETC);
  • 2 FADH2 (goes to ETC);
  • 4 CO2
101
Q

What are Glucogenic Amino acids?

A
  • Amino acids and their derivatives can enter the TCA at various intermediates and proceed through the cycle to be turned in to glucose;
  • IF they have 3 carbons!!
102
Q

What happens in ANAEROBIC Respiration?

A
  • NO oxygen;
  • Lactate in the muscle and glycerol backbones (NOT acetyl-CoA of fatty acids) are converted to Pyruvate and on to OAA and PEP;
  • Pyruvate is 3C so need 2 to combine to make OAA and on to PEPE for one glucose
103
Q

What steps of the TCA cycle are IRREVERSIBLE?

A
  • Acetyl-CoA to citrate;
  • Isocitrate to Alpha-Ketoglutarate;
  • Alpha-Ketoglutarate to Succinyl-CoA
104
Q

What happens in the Propionyl-CoA Carboxylase Reaction?

A
  • Prionyl-CoA results from the breakdown of beta-oxidation of odd-chain fatty acids, the metabolism of isoleucine and valine and also a product alpha-ketobutyric acid, which in turn is a product of digestion of threonine and methionine;
  • Becomes Succinyl-CoA, an intermediate in the TCA cycle
  • Propionyl-Coa → D-Methylmalonyl-CoA → L-Methymalonyl-CoA → Succinyl-CoA
105
Q

What are Phosphorylation and Dephosphorylation?

A
  • Key regulators of the enzymes and signal transduction in Carb metabolism!;
  • Adding or removing –PO4;
  • Turns some enzymes on and some off; Makes some more active and others less active
106
Q

What are the 5 phases of Glucose homeostasis?

A
  1. Absorptive → just ate
  2. Post-absorptive → all meals digested and absorbed (Most people don’t go past this stage, unless skipping breakfast)
  3. Early Fast → Blood glucose levels decreasing and need stored supply
  4. Intermediate Supply → Using up stores
  5. Long-term starvation → All glucose stores (as glycogen, amino acids, etc.) have been utilized
107
Q

What occurs in the Absorptive or Fed State?

A
  • Hyperglycemia due to having just ate;
  • “Fed” so body is storing fats and using dietary glucose for energy and to lower blood glucose levels;
  • Will use up exogenous glucose first!;
  • Can store alot of fat, but very limited glucose in the liver and muscle
108
Q

What occurs in the Post-Absorptive State?

A
  • All meal is digested and absorbed;
  • Blood glucose returned to normal;
  • Typically don’t go past unless missing breakfast!;
  • Meals supply glucose for ~4 hours;
  • If insulin overshot or blood glucose drops, Hypoglycemia will trigger glucagon to catabolize glycogen stores
109
Q

What occurs in the Early Fast State?

A
  • Hypoglycemia and need to used stored glycogen to raise blood levels;
  • Glycogen will provide glucose for about hour 4-24;
  • Gluconeogenesis will be activated ~ hour 16 to provide glucose from other source;
  • ATKINS = Gluconeogensis will move up into phase 2 due to no carb consumption
110
Q

What occurs in Intermediate Starvation?

A

-All sources of glucose (carb and non-carb) are being utilized and depleting

111
Q

What occurs during Long-Term Starvation?

A

-NO MORE storage of anything

112
Q

What does the Brain utilize in times of glucose depletion?

A
  • Brain will utilize fatty acids and ketogenic amino acids that have been converted to ketone bodies (from the acetyl-CoA);
  • Ketosis is meant to lower the need for Gluconeogenesis and slow glucose use
113
Q

What is normal blood glucose?

A

70-105 mg/dl

114
Q

What is hypoglycemia?

A

(LOW blood glucose) = 45-60 mg/dl

115
Q

What are Adregeneic symptoms of Hypoglycemia?

A
  • Related to Adrenalin;

- Release of epinephrine/norepinephrine and stimulation of the sympathetic nervous system

116
Q

What are Neuroglucopenic symptoms of Hypoglycemia?

A

Brain dysfunction caused by low blood glucose

117
Q

What is Fasting Hypoglycemia?

A

-Drugs induced; Insulin, sulfonylureas (increase insulin), insulinomas (Beta-cell tumors) or excessive alcohol

118
Q

What is Fed (reactive) hypoglycemia?

A
  • Impaired glucose tolerance and then excessive insulin release which intakes too much glucose;
  • Idiopathic, postprandial;
  • OR consumption of low, simple, refined carbs and small amounts of balance macros
119
Q

What is dietary fiber?

A
  • Nondigestible carb and lignin found in plants;
  • Nonstarch polysaccharides – Cellulose, pectin, gums, hemicellulose, Beta-glucans, and fibers in wheat and oat bran
  • Plant carbs not recovered by alcohol precipitation – inulin, oligosaccharides, fructans
120
Q

What are Functional Fibers?

A
  • Nondigestible carb isolated and extracted or manufactured;
  • PROVEN health benefits
  • Cellulose, pectin, lignin, gums, beta-glucans, fuctans, chitin/chitosan, polydextrose/polyols, psyllium, resistant dextrins, resistant starches
121
Q

What are Potential Functional Fibers?

A

-Isolated, nondigestible plant, animals or commercially produced
oPlant – resistant starch, pectin, and gums
oAnimal – chitin and chitosan
oCommercial – resistant starch, polydextrose, inulin and indigestible dextrins

122
Q

Why are health benefits not included in the definitions of fibers?

A

Health benefits are not included in these definitions due to the continuing research and new knowledge as to their physiological effects would lend the definitions to be quickly out dated

123
Q

Where is most of the fiber found?

A
  • More that 95% of fiber in plant cell walls;
  • Plants species, part of the plant, and maturity influence the fiber composition
  • Starch “within” the cell wall means the interior of the kernel is NOT between the primary and secondary cell walls
124
Q

What are the fiber-related plant components?

A
  • Cellulose;
  • Hemicellulose;
  • Lignin;
  • Pectins;
  • Suberin;
  • Cutin;
  • Waxes
125
Q

What is the Primary Cell Wall?

A
  • Thin envelop that surrounds the contents of the growing cell;
  • Contains small amount of unorganized cellulose
126
Q

What is the Secondary Cell Wall?

A
  • Develops as the cell matures;

- Contains many strands of cellulose arranged in an orderly fashion with a matrix of non-cellulosic polysaccharides

127
Q

What is Cellulose?

A
  • Dietary or added fiber → NONdigestible, but some is fermented by intestinal bacteria (plant source better fermented)
  • High molecular weight
  • Beta-1,4 glycosidic bonds b/w glucose (D-glucopyranosyl homopolymer);
  • Hydrogen bonding between stands
  • Major secondary cell wall component;
  • INSOLUBLE in water, but can be increased with water-soluble additions to the glucose chain
  • Common food additives = carboxymethylcellose, methylcellulose (Citrucel fiber supplement), and hydroxypropylcellulose
128
Q

What is methylcellulose used for?

A

-Fiber supp Citrucel

129
Q

What is Hemicellulose?

A
  • Dietary fiber;
  • Plant cell wall component (~20-30%; varies with plant);
  • Heterogeneous polysaccharide;
  • Linear or highly branched
  • Most water-soluble due to acidic side chain
  • NONdigestible, but fermented by large intestine bacteria
130
Q

What are the sugars that can make up Hemicellulose?

A
  • Backbone = Xylose, mannose, galactose
  • Chains = Arabinose, glucoronic acid, galactose
  • Glucoronic acids comes from Redox rxn of glucose
131
Q

What are Pectins?

A

-Dietary or potentially functional;
-Just about totally fermented by intestinal bacteria;
-Found in cell wall and middle lamella where allows cell walls of neighboring cells to stick together and give stability;
-Large group from pectins to pectic acids to pectinic acids;
-Water-SOLUBLE, gel-forming, high ion-binding potential
•Low pH stable → Good source of fiber in acidic foods

132
Q

What are the sources of Pectins?

A
  • Dietary = Apples, Strawberries, Citrus
  • Functional = extracted from citrus peels and apples to add to jams and jellies
  • *Source of fiber in enteral nutrition
133
Q

How do Pectins and Pectic Acids vary?

A
  • Vary in methyl ester content → Carboxylic acid mostly esterified with methanol
  • Possible side chains= Rhamnose, Arabinose, Xylose, Fucose, and Galactose → or methylated forms
134
Q

What are Lignins?

A

-Made of Phenol units with other substituents;
(Phenol unit = Carbolic acid)
-Secondary plant cell walls and some algae;
-Component of ALL Vascular plants
-One of most abundant organic polymers, second only to Cellulose → BUT NOT A CARB

135
Q

What makes Lignins so important in vascular plants?

A

-Allows plant stems to conduct water → Lignin is HYDROPHOBIC (unlike polysaccharide cell wall components);
o-Allows vascular tissues to conduct water by crosslinking with polysaccharides;
-Fills space between cellulose, hemicellulose, and pectin;
-Covalently bounds to hemicellulose yielding mechanical strength to the plant

136
Q

What are Gums (Hydrocolloids)?

A
  • Highly fermentable dietary fibers;
  • Composed of a variety of sugars and their derivatives
  • Secreted from plants at the site of injury by specialized secretory cells and exuded or forced from the plant tissues;
  • Very commonly used in the processing of food and candies;
  • Natural sources = oatmeal, barley, legumes
137
Q

What are the Tree/Shrub Exudates?

A
  • Tree = Gum arabic (food additive to gel, thicken or stabilize), gum karaya , and gum ghatti;
  • Shrub = Gum tragacanth
138
Q

What are Hydrocolloids?

A
  • Colloid system with colloid particles that are hydrophilic polymers in water;
  • Creates a gel/sol
139
Q

What are Galactomannans?

A
  • Polysaccharide with a mannose backbone and galactose side groups;
  • Stabilizers in foods that increase viscosity;
  • Guar gum (2:1, mannose:galactose) is the most commonly used stabilizer in foods
140
Q

What are Beta-Glucans?

A
  • Dietary or potentially functional → Purified form shown beneficial
  • Dietary = Cereal brans, oats, barley
  • *Very common Functional Fiber due to effect on lowering serum cholesterol and reducing postprandial (after eating) blood glucose levels
  • Homopolymers of glucopyranose units (Lots of glucose) → Beta-1,4 with some Beta-1,3
  • Water-SOLUBLE, highly fermentable
141
Q

What are Fructans?

A
  • Dietary and potential functional;
  • NOT in food composition databases;
  • Added to foods to increase fiber content;
  • Poly fructose = varying chains of fructose units;
  • Dietary = Chicory, asparagus,garlic, agave (makes tequila);
  • Inulin, Oliogofructose, Fructooligosaccharides (FOS)
142
Q

What is Inulin (fructan)?

A
  • 2-60 units of Beta-2,1 links and glucose at the C2 position of the terminal end (NONREDUCING);
  • Storage form of energy in plants (don’t store starch);
  • Smalest are Fructoligosaccharides w/ 1-ketose the smallest (2 fructose + glucose)
143
Q

What are Oligofructose (fructan)?

A

-Formed by the partial hydrolysis of Inulin; 2-8 fructose units and might have an end glucose

144
Q

What are Fructooligosaccharides (fructan)?

A

-2-4 fructose units

145
Q

Fructans and fermentable fibers are potential…

A
  • PREBIOTICS – promote growth/activity of beneficial intestinal bacteria
  • Probiotics – actual beneficial bacteria → Ex: Bifidobacteria spp.
146
Q

What are Galactooligosaccharides?

A
  • Chain of galactose units made from repeated transgalactosylation reactions with a terminal (end) glucose;
  • If an end galactose hydrolysis occurred;
  • Varying degress of polymerization;
  • Not natural
147
Q

What is Resistant Starch?

A
  • Not easily enzymatically digested and makes it all the way through to the large intestine;
  • Bond are NOT accessible to Alpha-Amylase → But ARE fermented;
  • Recommended consumption 20g/day (Americans consume 3-8g/day)
148
Q

What is RS1?

A
  • Dietary;
  • Plant cell walls;
  • Unprocessed whole grains
149
Q

What is RS2?

A
  • Dietary;
  • Ungelatinized starch GRANULES;
  • high amylose cornstarch;
  • GREEN bananas
150
Q

What is RS3?

A
  • Functional;
  • Retrograde starch from cooking/cooling or extruding foods;
  • Cooked and COOLED Potatoes, sushi rice;
151
Q

What is RS4?

A
  • Functional;

- Chemically modified starch – added fatty acids, cross linked starch strands

152
Q

What is Chitin?

A
  • Modified, nitrogen-containing polysaccharide made from N-acetylglucosamine;
  • Beta-1,4 links (like cellulose);
  • “chitin is cellulose with one hydroxyl (-OH) group on each monomer replaced with an acetyl amine group”;
  • Increased H-bonding due to amine groups on adjacent polymers → Increased molecular strength
153
Q

How does Chitin occur in animals?

A
  • Arthropods exoskeleton as the modified form embedded in sclerotin;
  • Not typically found pure in animals, but apart of composite materials (stronger);
  • EX: Combined with Calcium Carbonate produces a much stronger (crustaceans or mixed with sclerotin of beetles)
  • EX: Pure form might be as the body wall of a caterpillar which is mainly chitin
154
Q

What is Chitosan?

A
  • Deacetylated (acetyl amine group has been removed) form of chitin
  • Linear polysaccharide with randomly arranged Beta-1,4 D-linked glucosamine (deacetylated) and N-acetyl-D-glucosamine (acetylated)
  • High molecular weight, viscous, and INSOLUBLE similar to Chitin → Can be manufactured to be lighter and more soluble
  • Health benefits = lowers cholesterol, improved immune functions (enhances natural killer cells) and minimizes side effects of some chemotherapy
155
Q

What is Polydextrose?

A
  • Glucose + sorbitol units polymerize at high temps in a partial vacuum;
  • Added to foods as a bulking agent or sugar sub;
  • NOT digested, but fermented in large intestine
156
Q

What are Polyols?

A
  • Alcohol containing multiple hydroxyl groups; found in syrups
  • Polglycitol and malitol
157
Q

What are Sugar Alcohols?

A
  • Polyols commonly added to foods;
  • Lower caloric content than sugars;
  • Less sweet and thus combined with high intensity sweeteners;
  • Formed under mild reducing conditions from their analogue sugars
  • Used in chewing gum because not broken down by enzymes or bacteria in the mouth → No tooth decay
  • Malitol, sorbitol, xylitol, and isomalt
158
Q

What is Polyglicitol?

A
  • Corn products → HYSTAR 3375 Polyglycitol Syrup;
  • Syrup made from maltitol, sorbitol, and high weight polymers; Composed of polyols ;
  • Used in sugar free candy
159
Q

What is Psyllium?

A
  • FUNCTIONAL fiber – extracted and isolated FROM the foods, NOT still contained in the original dietary state;
  • SOLUBLE fibers
  • Mucilage from husk of psyllium seeds; Similar to gums;
  • Health claims related soluble fiber to reduced CHD;
  • Laxative (High water binding capacity, viscous, DO NOT consume if trouble swallowing, need plenty of fluids, choking could occur )
160
Q

What are Resistant Dextrins?

A
  • POTENTIAL Functional fiber → Made from heat and acid treated cornstarch followed by amylase
  • AKA - Resistant maltodextrins
161
Q

What are the Soluble Fibers?

A

Dissolves in hot water =

  • Fructans
  • Psyllium → Viscous
  • Beta-glucans → Viscous
  • Pectins → Viscous
  • Gums → Viscous
  • Hemicellulose (some)
162
Q

What are the Insoluble Fibers?

A

DON’T dissolve in hot water =

  • Lignin
  • Cellulose
  • Hemicellulose (some)
163
Q

What are the 2001 NAP recommendations for fiber?

A

Beneficial physiological properties of fiber that are highly noted relate to viscosity and fermentability → Recommended alternatives for soluble/insoluble to distinguish Dietary Fiber (those found already occurring in the foods) from Added Fibers (AKA: Functional fibers) that “modulate gastric and small bowel function (soluble) from those that provide substantial bulk to stool (insoluble)”

164
Q

What are the effects of Soluble Fiber?

A
  • Delayed gastric emptying;
  • increased transit time (take longer to pass);
  • Decreased nutrient absorption
165
Q

What are the effects of Insoluble Fiber?

A
  • Decreased transit time (passes much quicker than soluble);

- Increased fecal bulk

166
Q

What is Viscosity?

A
  • Fiber’s ability to bind water NOT related to solubility
  • Delayed gastric emptying (Non-viscous would shorten transit time)
  • Reduction in foods mixing with digestive enzymes
  • Reduced nutrient diffusion → Gradual blood glucose response, much less glycemic effect upon blood sugar levels due to controlled, release of the
167
Q

How does fiber effect absorption and binding of other nutrients?

A
  • Decreased absorption of lipids → Excreting bile which is needed for lipid absorption
  • Hypochoelsterolemic Properties→ Lowers cholesterol level by excretion of bile, causing the serum cholesterol to be utilized by the pancreas to make more bile;
  • Altered mineral (increase/decrease depends) and reduced carotenoid absorption
168
Q

What are Fermentable Fibers?

A
  • Prebiotics;
  • Generate short chain fatty acids – acetate, propionate, and butyrate
  • Butyrate = energy for colonocytes;
  • Other fermentation products – hydrogen, CO2, and methane
169
Q

What do the short chain fatty acids from fermentation cause?

A
  • Increase H2O and sodium absorption by the colon
  • Mucosal cell proliferation
  • Energy
  • Acidification of luminal environment
170
Q

What are Non-Fermentable Fibers?

A
  • Detoxification by microbes

- Increased fecal bulk → Act as a laxative and reduce intraluminal pressure

171
Q

What are the health effects of fiber?

A
  • AI – set for amount observed to reduce coronary heart disease (assume this amount will also promote GI health);
  • Need more evidence for cancers including colon;
  • Evidence DOES exist that TOTAL FIBER reduces the risk of DM, but this is seen as secondary due the amount to reduce CHD;
  • Might help weight maintenance due to slowed gastric emptying and lengthened satiety so consume less
172
Q

AI’s for Fiber

A 
Men = 38g;
Women = 25g;
Children (up to 8) = 25g;
Girls = 26g;
Boys = 38g

Spring 2014 (22 decks)

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