Biochem (no cycles) #2

photoautotroph

energy source = light

carbon source = inorganic CO2

photoheterotroph

energy source = light

carbon source = organic compounds

chemoautotroph

energy source = inorganic compounds

carbon source = inorganic CO2

chemoheterotroph

energy source = organic compounds

carbon source = organic compounds

catabolism

breakdown of fuels to generate ATP and reducing power (NADH, FADH2); exergonic 

anabolism 

building of molecules; requires ATP; endergonic 

Why is ATP a major energy-coupling agent?

couples exergonic and endergonic reactions by transferring a terminal gamma phosphoryl group; has high transfer potential 

ATP —> ADP + Pi

exergonic

high phosphoryl transfer potential examples:

PEP, 1,3-BPG, phosphocreatine, & ATP

creatine phosphate in muscles:

phosphocreatine + ADP ↔ creatine + ATP

enzyme: creatine kinase 

NADH/NADPH group carried is ___ and its vitamin precursor is ___.

electrons; niacin (vitamin B3)

FADH2/ FMNH2 group carried is ___ and its vitamin precursor is ___.

electrons; riboflavin (vitamin B2)

Coenzyme A group carried is ___ and its vitamin precursor is ___.

acyl; pantothenate (vitamin B5) 

Thiamine pyrophosphate group carried is ___ and its vitamin precursor is ___.

aldehyde; thiamine (vitamin B1)

Biotin group carried is ___ and its vitamin precursor is ___.

CO2; biotin (vitamin B7)

Tetrahydrofolate group carried is ___ and its vitamin precursor is ___.

one carbon units; folate (vitamin B9) 

S-adenosylmethionine group carried is ___ and its vitamin precursor is ___.

methyl; N/A

Lipoamide group carried is ___ and its vitamin precursor is ___.

acyl; N/A

function of CoA

-SH allows it to have high acyl-transfer potential —> more thermodynamically favorable

structure of CoA

3’-phosphoadenosine diphosphate + pantothenic acid + B-mercaptoethylamine 

oxidation-reduction

transfer of e-, OILRIG; dehydrogenases

group transfer

transfer of function groups like phosphates, methyl or acyl; kinases

hydrolysis

breaking of bonds by the addition of water; peptidases 

lyase 

addition/removal of double bonds; aldolase

isomerization

rearrangement of atoms within a molecule; triose phosphate isomerase

ligation with ATP cleavage

formation of a new covalent bond using ATP; pyruvate carboxylase 

lactose

enzyme: lactase

—> glucose + galactose

sucrose

enzyme: sucrase

—> glucose + fructose

maltose

enzyme: maltase

—> 2 glucose

starch + glycogen

enzyme: amylase

SGLT1

secondary active transport; powered by movement of sodium down its concentration gradient 

GLUT1

found in most tissues (including brain and RBCs); 1 mM; high glucose affinity 

GLUT3

mostly found in neurons; 1 mM; high glucose affinity 

GLUT2

liver and pancreatic B cells; 15-20 mM; regulates insulin, removes excess glucose from the blood; low glucose affinity

GLUT4

muscle and fat cells; 5 mM; amount in muscle plasma membrane increases with endurance training; insulin dependent

GLUT5

small intestine; primarily a fructose transporter

glycolysis: stage 1

investment phase, use 2ATP

glycolysis: stage 2

payoff phase, 4 ATP, 2 NADH

kinetically "perfect” enzyme:

triose phosphate isomerase

rate-determining step:

PFK-1

galactosemia:

deficiency in galactose-1-phosphate uridyl transferase causes accumulation of galactose-1-phosphate; toxic, liver damage, cataracts

lactase deficiency:

inability to hydrolyze lactose; diarrhea, gas; can be managed by lactase supplements

hexokinase is stimulated by ___ and ___ and inhibited by ___ and ___.

insulin; glucose; glucagon; G6P

glucokinase is stimulated by ___ and ___ and inhibited by ___ and ___.

insulin; glucose; glucagon; F6P

PFK-1 is stimulated by ___ and ___ and inhibited by ___ and ___.

ADP; F-2,6BP; ATP; citrate

pyruvate kinase is stimulated by ___ and ___ and inhibited by ___, ___, and ___.

insulin; F-1,6BP; ATP; alanine; acetyl-CoA

F2,6BP inhibits ___.

FBPase-1 (gluconeogenesis)

cancer (warburg effect):

rapid ATP production; aerobic glycolysis (glycolysis —> pyruvate —> lactate) even in the presence of O2

HIF-1a:

activates genes that promote the warburg effect; inhibits the PDH complex

PDH complex enzymes:

1. pyruvate dehydrogenase 

2. dihydrolipoyl transacetylase 

3. dihydrolipoyl dehydrogenase 

PDH complex importance:

coverts pyruvate into acetyl-CoA to go into Kreb’s cycle 

PDH is stimulated by ___, ___, and ___ and inhibited by ___, ___, and ____

ADP; NAD+; CoA; ATP; NADH; acetyl-CoA

glucose-alanine cycle:

amino acid loses amine group to make glutamate, also making pyruvate 

cori cycle: 

glycogen —> pyruvate —> lactic acid (in muscle), then lactic acid travels through bloodstream to liver cell, lactic acid —> glucose-6-phosphatase —> glucose, travels through blood stream back to muscle cell

triose phosphate isomerase deficiency:

accumulates DHAP/GAP; hemolytic anemia, metabolic problems

pyruvate kinase deficiency:

decreased ATP in RBCs; hemolytic anemia, blocks final ATP production in glycolysis 

pyruvate carboxylase deficiency:

impairs gluconeogenesis; leads to lactic acidosis, hypoglycemia

stimulates PDH kinase = inhibits PDH complex

NADH, acetyl-coA, ATP

inhibits PDH kinase = stimulates PDH complex

pyruvate, ADP

PDH phosphate deficiency

decreased pyruvate; lactic acidosis; can be treated by ketogenic diet

Beriberi (thiamine deficiency)

neuropathy, lactic acidosis; treat with thiamine 

mercury/arsenic poisoning:

bind lipoamide and inhibit PDH complex and a-KG D.H; chelation can be used as treatment

increased PDH kinase activity, inhibits PDH, which leads to ___.

aerobic glycolysis (aka warburg effect)

citrate synthase is stimulated by ___.

ADP

citrate synthase is inhibited by ___, ___, ___, and ___. 

succinyl- CoA; ATP; NADH; citrate 

glucose-6-phosphate D.H =

rate determining step

glucose-6-phosphatase deficiency = 

inability to release free glucose from G6P—> Von Gierke’s disease (hypoglycemia)

role of glycogen in liver

maintain blood glucose

role of glycogen in muscle 

supply G6P for local ATP production during activity 

glycogenesis

forming glycogen from glucose for storage (high blood glucose/insulin)

glycogenolysis

breaking down glycogen into glucose for when the body needs energy (low blood glucose)

glycogenesis stimulated by

insulin

glycogenolysis is hormonally stimulated by 

glucagon, epinephrine 

in muscle, ___ activates glycogen phosphorylase and ___ and ___ inhibit. 

AMP; G6P; ATP

saturated fats

no double bonds, pack tightly together, higher BP

unsaturated fats

double bonds, kinked, lower BP

synthesis:

cytosol, cofactor NADPH is used, consumes ATP/GTP, uses ACP

oxidation:

mitochondrial matrix, cofactor NADH/FADH2 is produced, produces ATP, uses CoA

palimate (16-C):

primary end product of fatty acid synthesis in humans; requires NADPH for PPP as a reducing agent 

odd-chain fatty acids:

not made in human fatty acid synthesis; starts with propionyl-CoA instead of acetyl-coA

palmitate synthesis costs ___and yields ___.

7 malonyl-CoA + 14 NADPH; 106 ATP

malonyl-CoA inhibits ___ from simultaneous synthesis and oxidation.

CPT1

carnitine palmitoyltransferase I

helps transport long-chain fatty acids into the mitochondria 

ACC is stimulated by ___ and ___ and is inhibited by ___ and ___.

citrate; dephosphorylated insulin; AMPK/AMP; glucagon 

cholecystokinin (CKK)

satuety signal from gut; reduces food intake

GLP-1

enhances insulin secretion and satiety

Leptin

produced by adipose; signals long-term energy stores and reduces appetite

Adiponectin

enhances insulin sensitivity and fatty acid oxidation 

lipogenesis is stimulated by __.

insulin

gluconeogenesis and B-oxidation are stimulated by ___.

glucagon/epinephrine 

gluconeogenesis

creates new glucose molecules from non-carbohydrate sources

AMPK activation ___ fatty acid synthesis and ___ fatty acid oxidation.

inhibits; stimulates 

AMPK decreases fatty acid synthesis in the ___. 

liver 

AMPK increases fatty acid oxidation in the ___.

muscle 

Type I Diabetes

autoimmune destruction of B-cells; insulin deficiency

Type II Diabetes

insulin resistance

alcohol consumption leads to high levels of ___ and ___. 

NADH & acetyl-CoA

alcohol consumption inhibits ___ and promotes___, causing fatty liver. 

gluconeogenesis; glyercol-3-p

excess acetyl-CoA + low OAA favors ___ and ___.

ketogenesis; fatty acid synthesis

ketogenesis

formation of ketone bodies