Dems Exam 2

Front 1

Resting Metabolic Rate (RMR): What is it and how do you measure it?

Back 1

75% f total energy expenditure, the energy cost of keeping Na and K where they belong. Primary determinant of RMR is lean body mass. RMR can be measured by indirect calorimetry.

Front 2

Thermic Effect of Food (TEF)

Back 2

8% of total energy expendature. TEF is the cost of digesting food and getting and distributing their nutrients. Protein has the highest energy cost of digestion, hense the Atkins diet.

Front 3

Energy Expenditure of Physical Activity (EEPA)

Back 3

30-40% of daily energy expenditure. Includes non exercise activity thermogenesis (unconscious movement) and working out. EEPA is estimated by TEE -(TEF+RMR)

Front 4

Effect of obiesity on RMR, TEF and EEPA?

Back 4

EEPA is higher but the thermic effect of food is about constant and as you don't have much lean muscle mass the RMR is still low. Thus it takes more calories to sustain a larer weight, more weight to move around.

Front 5

What is indirect calorimetry and what does it measure?

Back 5

CAlorimetry measures respiratory gas composition to estimate BCO2 estimating the rate of energy consumption in a resting participant, thus the Resting metabolic rate is measured (RMR).

Front 6

C6H12O6; aldehyde group on top of a five-carbon chain, each carbon of which has a hydroxyl group attached to it. Recall that this can be thought of either as a linear (6-carbon) or an etherized 5-carbon ring structure with a carbon hanging off it: What structure is this?

Back 6

glucose

Front 7

What molecule: hydrocarbon chain with a carboxylic acid group on one end (COOH) and a methyl group (CH3) at the other

Back 7

fatty acids. Triglyceride has 3 faty acids esterified to glycerol C3(OH)3H5

Front 8

What molecule: central carbon with a hydrogen and a side chain attached to it with an amino group on one end (NH2) and a carboxylic acid group (COOH) on the other.

Back 8

amino acid with a C and a N terminal end

Front 9

catabolism

Back 9

break down stored material for energy, catabolism - cut up molecules for energy

Front 10

anabolism

Back 10

store material when in positive energy balance, anabolism = add molecules together.

Front 11

This process occurs when glucose is present in excess following a meal, it occurs in teh cytoplasm and breaks down glucose to 2 pyruvate with a net of 2 ATP formed

Back 11

glycolysis occurs when glucose is present in excess following a meal, it occurs in teh cytoplasm and breaks down glucose to 2 pyruvate with a net of 2 ATP formed

Front 12

This process occurs in the mitochondria breaking down pyruvate to CO2 and H20 in the presence of oxygen.

Back 12

Krebs cycle/ TCA cycle

Front 13

This process occurs when the body is in negative energy balance in order to provide glucose only tissues ie RBC and the brain glucose. This occurs in the liver mostly (somewhat in the kidneys) and converts a variety of carbon skeletons to glucose starting in the mitochondria and ending in the cytoplasm.

Back 13

Gluconeogenesis

Front 14

Occurs in teh cytoplasm when glucose is high, forms glucose polymers.

Back 14

Glycogenesis

Front 15

occurs when glucose is present in excess and drives NADPH generation which drives de novo lipogenesis from glucose derived acetyl CoA. Occurs in cytoplasm

Back 15

Hexose monophosphate shunt (Pentose phosphate shunt)

Front 16

In glucose rich positive energy state glucose can be broken down to pyruvate, enter TCA cycle to form acetyl CoA but instead of being fully oxidized the acetyl CoA instead forms chains that are esterfied to glycerol. What process is this?

Back 16

De Novo lipogenesis

Front 17

In a negative energy state triglycerides are broken down into fatty acids and glycerol and released into lymphatics where they are taken up by non glucose exclusive tissue and broken down two carbons at a time. These 2 carbon usits make CoA which will be fed into the TCA cycle to form acetyl CoA.

Back 17

This is beta oxidation and it is used to provide energy for non glucose exclusive tissue and can also be used to produce ketone bodies .

Front 18

What is the rate limiting step of glycolysis?

Back 18

Phosphofructokinase1
glucose 6P to glucose 1,6 P

Front 19

What are the 3 regulated steps of glycolysis?

Back 19

1)hexokinase: glucose to G6P (costs 1 ATP)
2)PFK1: G6P to G1,6BP (costs 1 ATP)
3)pyruvate kinase: PEP to pyruvate (produces 2 ATP)

Front 20

What is the rate limiting step of gluconeogenesis?

Back 20

PEPCK (phosphenolpyruvate carboxykinase) OAA to PEP

Front 21

What are the 4 regulatory steps of gluconeogenesis?

Back 21

1) pyruvate to OAA via pyruvate carboxylase
2) OAA to PEP via PEP CK
3) F 1,6 BP to F6P via F 1,6 bisphosphatase
4) G6P to glucose via glucose 6 phosphatase

Front 22

What step traps glucose inside the cytosol for glycolysis?

Back 22

hexokinase traps glucose in the cell by phorphorylating it into G6P

Front 23

What enzyme traps pyruvate inside the mitochondria for the TCA cycle?

Back 23

pyruvate dehydrogenase removes a carbon (CO2 and NADH are products)producing acetyl CoA traping the 2 carbon structure in the mitochondria.

Front 24

How does OAA get outside the mitochondria in order to become pyruvate and ascend the chain of glyconeogenesis?`

Back 24

malate dehydrogenase is necessary to transform OAA to malate then back to OAA once its outside the mitochondria.

Front 25

What is the rate limiting step for glycogenesis?

Back 25

glycogen synthase is the commited step in glycogen synthesis. By changing G1P to UDP glucose the enzyme glycogen synthase makes it possible to keep adding glucose molecules in a 1-4 orientation. The other essential enzyme of glycogen synthesis is the branching enzyme which adds 1-6 linkages.

Front 26

What two enzymes are needed to cleave the 1-4 and the 1-6 bonds of glycogen during glycogenolysis?

Back 26

1-4 = glycogen phosphorylase
1-6 = debranching enzyme

Front 27

After glycogenolysis the G1P is rearranged to G6P which then is dephosphorylated so it can exit the cell as glucose. What 2 enzymes are needed?

Back 27

1) phosphoglucomutase
2) glucose 6 phosphatase

Front 28

What is the purpose of the Pentose phosphate shunt? What is its main product?

Back 28

PP Shunt generates NADPH via the first irreversible reaction of G6P to 6 phosphogluconolactone via glucose 6 phosphate dehydrogenase. NAPH is needed for many synthesizing reactions especially fatty acid biosynthesis. The PPP is also needed for five carbon ring generations for nucleotide synthesis.

Front 29

What are the 4 counterregulatory hormones when glucose levels are low?

Back 29

1) glucagon
2) catecholamines
3) cortisol
4) growth hormone
These counter-regulatory hormones promote glycogenolysis and gluconeogenesis.

Front 30

maltose =

Back 30

glucose + glucose, starch breakdown product

Front 31

Lactose =

Back 31

glucose + galactose, milk sugar

Front 32

Sucrose =

Back 32

glucose + fructose , table sugar

Front 33

Where does glycolysis take place?

Back 33

Glycolysis takes place in the cytosol. Glucose 6 P is no longer able to leave the cell.

Front 34

Glucagon causes intracellular 2nd messenger signaling via what two molecules?

Back 34

Increased glucagon increases cAMP and protein kinase A which lead reactions to facvor gluconeogenesis and inhibit glycolysis as you are in a fasting stage.

Front 35

What are the products of aerobic glycolysis?

Back 35

4 ATP (net 2), 2 NADH, 2 pyruvate

Front 36

What is the product of glycolysis if there is no oxygen present?

Back 36

pyruvate becomes lactate due to pyruvate dehydrogenase reducing a NADH to NAD+. Thus The net products would be 2 ATP, 2 lactate, 2 NAD+. These NAD+ are essential to the oxidation of glyceraldehyde 3 phosphate to keep glycolysis going.

Front 37

At what 3 locations do teh cells undergo lactic acid fermentatino even in the presence of O2?

Back 37

RBC, sperm and the retina

Front 38

What are the 3 fates of glucose as it enters the cell?

Back 38

1) G6P generated via hexokinase for glycolysis
2) oxidized to pentoses via PPP and generate NADPH
3) stored as polyxaccharide or sucrose

Front 39

This is the first energy payoff reaction of glycolysis where the fist NADH is generated via the first oxidation reaction. Note that it is at this step that glycolysis stops if NADH is not oxidized to NAD+, what is the enzyme?

Back 39

glyceraldehyde 3P is reduced to 1,3 bisphosphoglycerate via glyceraldehyde 3 phosphate dehydrogenase producing 2 NADH.

Front 40

What are the first and second substrate level phosphorylation reactions in glycolysis both leading to a payoff of 2 ATP?

Back 40

1) 1,3 bisphosphoglycerate to 3 phosphoglycerate + 2 ATP via phosphoglycerate kinase (net = 0 ATP)
2) PEP to pyruvate + 2ATP via pyruvate kinase (irreversible)

Front 41

What are the regulatory influences on pyruvate kinase?

Back 41

Neg- Inhibited by ATP, alanine and PKA. During fasting glucagon dependent inactivation of liver pyruvate kinase occurs via phosphorylation by PKA preventing glycolysis.
Positive- F1,6 BP

Front 42

What are the two enzyme deficiencies that most commonly lead to hemolytic anemia?

Back 42

1) G6PDH deficiency (glucose 6 phosphate dehydrogenase is the rate limiting step of PPP)
2) pyruvate kinase deficiency

Front 43

Compare glucokinase and hexokinase.

Back 43

glucokinase- selective for glucose, only in liver and pancreas, high Km and high
Vmax- slower then hexokinase but more enzyme activity at higher glucose loads. Inhibited by F6P.
Hexokinase- nonspecific, in all cells, inhibited by G6P. Low Km and Vmax. Very vast at low concentrations of glucose but quickly saturated.

Front 44

What are the regulatory effectors of glucokinase/hexokinase?

Back 44

glucokinase = F6P
hexokinase = G6P

Front 45

The rate limiting step of glycolysis is PFK1. What regulates this enzyme?

Back 45

ATP and citrate (TCA) inhibit PFK1 and encourage gluconeogenesis.
GF 2,6 BP via PFK2 activity is the most potent activator of PPFK1 encouraging glycolysis.

Front 46

F 2,6 Bis phosphate levels are what drive PK1 the main regulator of glycolysis. When is PFK2 active, when it is phorphorylated or unphosphorylated? What enzyme controls this?

Back 46

PFK2 is active in its unphosphorylated state, If PKA or cAMP are high (2nd messengers present) the PFK2 is phosphorylated and its activity is inhibited.

Front 47

What happens to PFK2 in its inactivated form?

Back 47

When cAMP and PKA are high PFK2 is phosphoryalted causing a conformational change to fructose 2,6 bisphosphatase which removes the P and results in F6P to be used in gluconeogenesis.