Biochem Test 2 Groppe

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general term for molecules with the same formula but different structure

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isomers

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isomers that differ in order of attachements of atoms

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constitutional isomers

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isomers that are connected in the same order but differ in spatial arrangement

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stereoisomers

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2 kinds of stereoisomers

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enantiomers (mirror images)

diastereomers (not mirror)

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two kinds of diastereomers and difference between them

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epimers- differ at one of several asymmetric carbon atoms

anomers- differ at a new asymmetrical carbon atom formed on ring closure

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smallest monosaccharides

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glyceraldehyde and dihydroxyacetone

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Acyclic compounds drawn so that vertical bonds represent bonds pointing back and horizontal bonds are bonds pointing forward.

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Fischer projection

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Isomer of glyceraldehyde that rotates plane polarized light clockwise.

What's special about it?

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D-glyceraldehyde isomer (enantiomer)

all natural sugars derived from this- usable by animals (unlike L form)

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To determine the D- or L- configuration of a carbohydrate

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look at carbon furthest from aldehyde or ketone

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how anomers are differentiated

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alpha or beta
differ at the carbon that carries the aldehyde or ketone (rapidly changing)

alpha: -OH goes below sugar ring
Beta: -OH goes above sugar ring

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anomeric carbon for aldoses

ketoses?

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C1

C2

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Sugars with both carbonyl and carboxylic acid functional groups.

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uronic acids

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join the anomeric carbon of a carbohydrate to other molecules, including carbohydrates.

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glycosidic bonds

O, N, S- glycosidic bonds if it's bound to another group via Oxygen, Nitrogen, or Sulfur ion espectively

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Highly branched polymer of glucose found in plants. Soluble in water.

how is it linked? branched?

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amylopectin
Glucose units linked in a linear manner with α-1,4-glycosidic bonds.
Branching via α-1,6-glycosidic bonds every 24 to 30 glucose units

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Non-branching polymer of glucose linked mainly with α-1,4-glycosidic bonds. Can be several thousand units of glucose in length.

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amylose

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how glucose differs from amylopectin

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same composition but more extensive branching (every 8-12 glucose units)

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Branched homopolysaccharide made of many glucose molecules joined into chains of varying lengths.
Straight chains consists of α-1,6-glycosidic between glucose molecules, whereas branches are α-1,3-glycosidic bonds. Rotates plane polarized light to right

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Dextran

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how dextran is synthesized and where it's found

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synthesized from glucose moiety of sucrose by bacteria and yeast

dental plaque

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how levan is synthesized

where is it found

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synthesized from fructose moiety of sucrose by made by a few species of bacteria found in dental plaque including Strep. sanguis, Strep. salivarius and Actinomyces naeslundii but not by Strep. mutans.

in dental plaque

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lipopolysaccharide complex of the outer membrane of the cell wall of Gram-negative bacteria.

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endotoxin

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a heavily glycosylated glycoprotein

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proteoglycan

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functions of glycoproteins

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lubricants, adhesion of extracellular matrix, factor binding, impart structure to connective tissue.

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Polysaccharide chains consisting of a repeating disaccharide unit attached to protein to form a proteoglycan.

what do they contain? and what are they an important part of?

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glycosaminoglycan

contain an amino sugar- amino group in place of hydroxyl

important in cartilage

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sucrose is made up of

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glucose and fructose

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belief that the fermentation of sugars to alcohols was inextricably tied to living cells

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vitalistic dogma- Pasteur 1860

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what Hans and Eduard Buchner discovered in 1897 and what it meant

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cell-free yeast extracts that fermentation could take place outside the cell

metabolism became chemistry

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Gustav Embden, Otto Meyerhof, Carl Neuberg, Jacob Parnas, Otto Warburg, Gerty Cori and Carl Cori > 1940 discovered what

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many of the reactions of lactic acid fermentation were shared with alcoholic fermentation

underlying unity in biochemistry

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products of glycolysis

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break down of glucose to two pyruvate, four ATP and two NADH molecules

Net gain of 2 ATP and 2 NADH

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3 basic stages of glycolysis

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1: glucose undergoes 2 phosphorylations

2: F-1,6 BP is split to DHAP and GAP and isomerized to all GAP

3: Energy is harvested gaining a net 2 ATP. Pyruvate is end product

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why is glucose phosphorylated in the first step? What enzyme does it?

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1) glucose 6-phosphate has negative charge, cannot pass back out through the membrane and leave cell
2) destabilizes glucose for further breakdown

Hexokinase- takes 1 ATP

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enzyme for fructose-6-phosphate conversion to fructose-1,6-bisphosphate that completes the first step of glycolysis

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phosphofructokinase- takes 1 ATP and can be allosterically affected

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splits fructose 1,6-bisphosphate to DHAP and GAP (glyceraldehye 3 phosphate)

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aldolase

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2 steps in 3rd stage of glycolysis that generates ATP

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conversion of 1,3 BPG to 3-PG (by phosphoglycerate kinase)

phosphoenopyruvate to pyruvate (by pyruvate kinase)

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3 irreversible steps of glycolysis and their enzymes

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1st step: Glucose to G3P by hexokinase

Fructose-6-P to Fructose-1,6-BP by phosphofructokinase

Phosphoenolpyruvate to pyruvate by pyruvate kinase

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3 mechanisms by which glycolysis is regulated

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- allosteric effectors
- covalent modification (e.g. phosphorylation)
- modulating level of transcription/expression of enzymes (insulin)

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activated and inhibitors of phosphofructokinase

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activated by:
AMP, insulin (means you have sugar in your blood you need to breakdown), and Fructose 2,6 BP (a product of F6P)

inhibited by: ATP (allosteric inhibitor/ lowers affinity for F6P), citrate of citric acid cycle, H+ ion

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allosteric affectors of pyruvate kinase

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activated by F-1,6-BP and Insulin

inhibited by Alanine and by being PHOSPHORYLATED by ATP when blood glucose is low

active when NOT phosphorylated

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why entry into glycolysis via fructose 1-phosphate pathway is less regulated

what enters this way?

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it enters after the phosphofructokinase regulation step at the level of DHAP/GAP

fructose from the liver enters here

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where does galactose enter glycolysis?

where does fructose from fat enter glycolysis?

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G-6P level

F-6P level (next step)

Front 40

why is more fructose converted to fat than enter glycolysis cycle?

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Hexokinase (Stage 1, Step 1) preferentially utilizes glucose, producing glucose 6-phosphate, rather than fructose to yield fructose 6-phosphate.

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what converts galactose to G-6-P and what is caused when this enzyme is working improperly?

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galactose 1-phosphate uridyl transferase

Galactosemia: vomiting and diarrhea after consumption of milk by infants; can eventually lead to mental retardation

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enzyme missing in those that are lactose intolerant

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lactase

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alternative source of energy under anaerobic conditions, and what it produces

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Cori Cycle
reduces pyruvate to lactic acid and one NAD+ is made (to put into glycolysis) (fermentation)

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cori cycle enzyme

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lactate dehydrogenase

reduces pyruvate, oxidized NADH to NAD+

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how is glycolysis maintained under oxygen debt

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Cori cycle sends lactate to the liver to be converted back to glucose, then sent back to the muscle for more glycolysis

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overall reaction of cori cycle

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Glucose + 2Pi +2ADP --> 2 lactate +2ATP + 2H2O

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can utilize lactate for use in the citric acid cycle and oxidative phosphorylation

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tissues not deprived of oxygen, like cardiac cells. Share metabolic burden

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where gluconeogenesis occurs

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mostly in liver, some in kidney

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sources of precursor molecules for gluconeogenesis

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amino acids (from muscle), lactate (lactic acid), glycerol (from fat)

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where the first step of gluconeogenesis occurs and the enzyme needed

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mitochondria, pyruvate carboxylase (pyruvate to oxaloacetate)

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where the last reaction of gluconeogenesis occurs and the enzyme needed

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membrane bound in the endoplasmic reticulum (Glucose-6-phosphatase)

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oxaloacetate is shuttled across the mitochondrial membranes by turning into

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malate (then oxidized back to oxaloacetate)

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important regulatory steps in gluconeogenesis

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pyruvate carboxylase (pyruvate -->oxaloacetate)

phosphoenolpyruvate carboxykinase(oxaloacetate -->phosphoenolpyruvate)

fructose 1,6 bisphosphatase (F 1,6-BP to F6P)

glucose 6-phosphatase (G6P to Glucose)

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inhibitors and activators of gluconeogenesis

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Acetyl CoA activates pyruvate carboxylase
ADP inhibits it

ADP inhibits phosphoenolpyruvate carboxykinase

F,2,6-BP and AMP inhibit fructose 1,6 bisphosphatase and citrate activates it

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family of transporters that enable glucose to enter and leave cells

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GLUT 1-5

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regulate transport of glucose at a normal basal level

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GLUT 1 & 3

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regulates transport of glucose at a high blood glucose level

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GLUT 2 in liver and pancreas- liver removes excess and pancreas is stimulated to release insulin into blood stream

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non-protein chemical compound that is bound tightly to an enzyme and is required for catalysis. Can be considered "helper molecules/ions" that assist in biochemical transformations

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cofactor : divided into small organic molecules called coenzymes 2)metals

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any of a number of freely diffusing organic compounds that function as cofactors with enzymes in promoting a variety of metabolic reactions. A small organic molecule required for the activity of many enzymes; vitamins are often components of coenzymes.

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coenzyme

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the link between glycolysis and the citric acid cycle

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pyruvate dehydrogenase complex

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what is synthesized by the pyruvate dehydrogenase complex?

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2 pyruvate are oxidatively decarboxylated to

2 acetyl CoA

irreversible

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2 potential fates for acetyl CoA

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oxidation to CO2 via citric acid cycle/ ox phor or conversion to fat by lipid biosynthesis

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why can't fat be mobilized for gluconeogenesis to provide the brain with glucose during fasting?

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production of acetyl CoA (fat precursor) is irreversible. Therefore, can't get acetyl CoA or fat back to glucose.

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3 enzymes of pyruvate dehydrogenase complex

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pyruvate dehydrogenase component

dihydrolipoyl transacetylase

dihydrolipyl dehydrogenase

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function and prosthetic group of pyruvate dehydrogenase component (PDH complex)

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TPP- oxidative decarboxylation of pyruvate

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function and prosthetic group of dihydrolipoyl transacetylase (PDH complex)

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Lipoamide- transfer of acetyl group to CoA

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function and prosthetic group of dihydrolipoyl dehydrogenase

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FAD- regeneration of the oxidized form of lipoamide

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role of NAD+ and FAD in pyruvate dehydrogenase complex

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electron acceptors- oxidizing agents

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key means of regulation of PDH complex

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phosphorylation (inactive form)

dephosphorylation (active)

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how are the phosphatases/kinases of PDH complex regulated

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insulin activates phosphatase, so acetyl CoA can be produced and ged into citric acid cycle

ATP activates Kinases that inactivate it (feedback inhibition keeps it from continuing too long)

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the energy driving the formation of citrate

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thioester bond of CoA

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multienzyme complex formed by all enzymes in citric acid cycle and what's the point?

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Metabolon- allows product from one reaction to be channeled directly to the next reaction as a substrate- more efficient

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2 key control point of the citric acid cycle

how're they regulated?

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isocitrate dehydrogenase

alpha-ketoglutarate dehydrogenase

negatively regulated by ATP and NADH (alpha-keto regulated also by succinyl CoA)

isocitrate dehydrogenase activated by ADP

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dual roles of citric acid cycle

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step in generating energy (NADH, FADH2, GTP), but also source of biosynthetic precursors (fatty acids, amino acids, purines, sterols, glucose)

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TPP is a cofactor for which complexes

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Pyruvate dehydrogenase (complex)
α-ketoglutarate dehydrogenase (complex)

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acids found in the citric acid cycle are

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oxaloacetic acid and a-ketoglutaric acid

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the chemiosmotic hypothesis

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Oxidation of NADH and FADH2 used to create a gradient of proton concentration that powers formation of ATP (61- not accepted til 78)

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what causes the proton motive force in oxidative phosphorylation?

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high proton concentration on cytosolic side of mitochondrial membrane pH gradient and transmembrane potential

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where oxidative phosphorylation occurs

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mitochondrial matrix

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in ox phos, the respiratory chain consists of:

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3 proton pumps and one physical link to the citric acid cycle

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in ox phos, the two electron transfers that mediate transfer between pumps

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coenzyme Q and cytochrome C

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component of citric cycle that is in oxidative phosphorylation

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succinate dehydrogenase from TCA (produces FADH2) is part of the succinate Q reductase complex within the mito innermembrane

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reduces coenzyme Q in ox phos

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FADH2

electrons removed by succinate Q reductase

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component of all the complexes of ox phos and cytochrome c

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Iron

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final electron acceptor of ox phos

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O2 (reduced to H20)

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how the proton gradient in the inner membrane space is used to make energy

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the protons want to come into the matrix and are used by ATP synthase to make ATP (takes 3 protons to make one ATP)

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how does ADP get into the matrix/ ATP get out once made?

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through ATP-ADP translocases (takes 1 proton to use)

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per pair of electrons from NADH, how many protons are pumped into the inner membrane space?

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10

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per pair of electrons from FADH2, how many protons are pumped into the inner membrane space

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6

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3 main components of cellular respiration

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electron motive force of NADH and FADH2

proton motive force in inner membrane space

phosphoryl transfer potential in ATP

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how are electrons from NADH made through glycolysis shuttled into the mitochondria?

where are these located?

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malate-aspartate shuttle- heart and liver only

or

glycerol 3 phosphate shuttle -muscle

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ATP potentials of NADH and FADH2

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2.5 ATP
1.5 ATP

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total ATP made from glycolysis and citric acid cycle

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32

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how brown adipose tissue generates heat

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by uncoupling oxidative phosphorylation through UCP-1

allows protons to flow into the matrix freely disrupting the proton gradient ~generates heat~

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reduces O2 to H20

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cytochrome c oxidase

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enzymes that deactivate reactive oxygen species that can be accidentally made by cytochrome c oxidase

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Superoxide dismutase and catalase

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source of NADH and FADH2 for ox phos

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glycolysis
TCA cycle
fatty acid oxidation

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names of 4 protein complexes in ox phos

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NADH-Q oxido-reductase
sucinate-Q reductase
Q-cytochrome c oxidoreductase (or just cytochrome reductase)
cytochrome c oxidase

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drives reaction between oxaloacetate and acetyl CoA

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Aconitase (makes citrate)

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number of electrons sent to oxidative phosphorylation from the TCA cycle

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8

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the anomeric carbon for aldoses

ketoses?

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C1

C2

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predominant linkages in glycogen between glucose units

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alpha 1,4

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NADPH is required for

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reductive biosynthesis (such as lipid synthesis)

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ribose 5-phosphate is needed for

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RNA, DNA, ATP, NADH, FAD, coenzyme A

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2 purposes of the nonoxidative phase of the pentose phosphate pathway

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nucleotide biosynthesis
conversion into intermediates to feed into the glycolytic pathway

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where pentose pathway occurs

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cytosol

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pathways requiring NADPH

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-fatty acid, cholesterol, neurotransmitter, nucleotide biosynthesis

- reduction of oxidized glutathione
- cytochrome p450 monooxygenases

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basic oxidative phase or pentose pathway and main product

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glucose 6 phosphate --> ribulose 5-phosphate

2 NADPH produced, CO2 by product

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overall reaction of non-oxidative phase of pentose pathway

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3C5 --> 2C6 + C3

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ribulose 5-phosphate is converted into these 2 products via what enzymes

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ribose 5-phosphate (via isomerase

xylulose 5-phosphate (via epimerase)

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rate limiting step of oxidative phase

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NADP+ (cofactor for first enzyme- inactive without it)

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action of pentose pathway in mode one

need ribose 5-phosphate more than NADPH

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products of glycolysis feed into:

oxidative path
non-oxidative path in reverse

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action of pentose pathway in mode 2

need both NADPH and ribose 5P

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oxidative portion only

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action of pentose pathway in mode 3

need NADPH more than R5P

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gluconeogenesis forms glucose 6 phosphate to feed into oxidative portion

nonoxidative products feed back into gluconeogenesis

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action of pentose pathway in mode 4

needs NADPH and ATP

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oxidative and non-oxidative run normally.

nonoxidative products feed into glycolysis to make pyruvate & eventually ATP

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necessary to reduce oxidized glutathione

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NADPH generated by glucose-6P dehydrogenase (pentose pathway)

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purpose of reduced glutathione

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combat oxidative stress and maintain normal reduced state of cytoplasm

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how does glucose 6-P dehydrogenase deficiency cause hemolytic anemia

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can't clear ROS caused by anti-malarial drug

hemoglobin sulfhydryls aren't reduced, form heinz body aggregates on cell membrane

deformity causes cell to undergo lysis

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principle enzyme in glycogen breakdown

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glycogen phosphorylase

- removes glucose 1 at a time til 4 remain before the 1,6 linkage

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after initial removal of glucose from a glycogen branch, these 2 enzymes remove the last 4 pieces

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transferase moves all but the last to the main chain

alpha-1,6 Glucosidase removes the last residue of the 1,6 linkage

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type of glucose removed from glycogen & what converts it to G6P

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glucose 1-phosphate

phosphoglucomutase

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converts G6P to glucose and where it's located

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glucose 6-phosphatase on interior of the smooth ER membrane (mainly in liver-not in muscles)

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necessary coenzyme for glycogen phosphorylase

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PLP- containing B6

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holds glycogen phosphorylase b in a T state in the muscle

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presence of ATP and glucose-6-phosphate (plenty of supplies, no need to dip into reserves)

Front 125

can cause glycogen phosphorylase b to turn to phosphorylase a in the muscle

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epinephrine activation of PKA--> cascade to activate phosphorylase kinase

Ca2+ released from Sarcoplasmic reticulum

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shifts glycogen phosphorylase a to T state in the liver

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glucose allosteric inhibition

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type of phosphorylase that isn't affected by glucose

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muscle phosphorylase a

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type of phosphorylase that isn't affected by AMP

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liver phosphorylase b

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activates cascade of activation of phosphorylase b in the LIVER

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glucagon

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how epinephrine or glucagon (in liver) activates cascade of events in glycogen metabolism

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bind to 7TM receptor, activates adenylate cyclase to get cyclic AMP--> activate PKA -->activate phosphorylase kinase--> phosphorylates phosphorylase B to A

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different jobs of muscle and liver for glucose homeostasis

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Muscle consumes glucoses
ATP/AMP regulates phosphorylase activity and glycogen breakdown in the muscle

Liver maintains glucose homeostasis for whole body

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catalyzes transfer of glucose from UDP to a growing chain of glycogen (glycogenesis)

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glycogen synthase

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1st step of glycogenesis

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glucose 1-phosphate activated by addition to UDP (PPi kicked off) - after being isomerized from G6P

makes UTP-glucose

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3 jobs of protein phosphatase 1

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shuts down glycogen phosphorylase (from A to B) and phosphorylase kinase

activates glycogen synthase to A form

removes phosphoryl groups from ALL

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how does insulin affect glycogen synthesis

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stimulates it- wants to remove glucose from blood stream and store it.

Insulin causes insulin receptor substrates to be phosphorylated which will
inhibits glycogen synthase kinase that would normally inactive it.

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common theme to all glycogen storage diseases

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excess amount of glycogen in liver- unable to get to glucose

Front 137

how triglyceride melting point is affected by lengthening chain

increasing double bonds?

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melting point is increased with length

melting point is decreased with more double bonds

Front 138

components of a phospholipid

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choline +phosphate glycerol make up head
linked to hydrocarbon tail

Front 139

steroidal lipid and its purpose

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cholesterol- help membrane fluidity

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energy produced from 1 gram of fatty acids

Back 140

9 kcal

Front 141

2 reasons fat stores more energy

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hydrocarbons in fat are more reduced than in carbs and protein

carbs and proteins are hydrated/water bound. less energy per unit weight. fat stores are a purely lipid environment

Front 142

requires aqueous solution for activity and what enables this solvation

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lipases

bile salts made by liver promote solvation of triglycerides for hydrolysis to free fatty acids and monoacylglycerol.

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lipases breakdown triacylglycerides to

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monoacylglycerides and free fatty acids

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carry triacylglycerides to lymph system and eventually blood

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chylomicrons

Front 145

regulates triacylglycerol lipase

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cAMP dependent PKA

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Utilization of triacylglycerides from adipose tissue requires these three stages of processing

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1. hydrolysis by cAMP regulated kinases

2. Fatty acid activation and transport into mitochondria

3. Rounds of oxidation of fatty acids to acetyl CoA

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products of triacylglycerol hydrolysis

Back 147

glycerol (absorbed by liver, made into glyceraldehyde 3 phosphate)

free fatty acids

Front 148

free fatty acids are bound to _____ to travel to other tissues for oxidation

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albumin

Front 149

catalyses fatty acid activation and what are the products

energy used?

Back 149

Acyl CoA Synthetase

fatty acid --> acyl adenylate --> Acyl CoA

equivalent of 2 ATP used

Front 150

needed to transfer acyl CoA into mitochondrial matrix

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carnitine bound to the acyl CoA

goes through translocase

Front 151

4 steps of beta oxidation and where does it occur

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1. oxidation (FAD)
2. hydration
3. oxidation (NAD)
4. thiolysis

on B carbon of Acyl CoA -->forms acetyl CoA

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net ATP from palmitate fatty acid

Back 152

106 ATP

Front 153

in addition to the mitochondrial matrix, fatty acids are also oxidized here

Back 153

peroxisomes

Front 154

oxidizing fatty acids with double bonds at odd numbered carbons requires an

Back 154

isomerase

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oxidizing polyunsaturated fats with even double bonds requires

Back 155

reduction, then isomerization

Front 156

final thiolysis product of odd numbered carbon acyl CoA

Back 156

acetyl CoA and propionyl (converted to succinyl CoA)

Front 157

ketone bodies are caused by

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Acetyl CoA build up in the liver due to no available oxaloacetate (being used in gluconeogenesis)

conversion of acetyl CoA to ketone bodies

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can be converted to acetyl CoA in muscle and renal cortex

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acetoacetate (ketone body)

Front 159

3 pathophysiological states associated with ketone bodies

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ketosis

ketouria

acidosis