• Ketone formation
• Storages as triacylglycerols (fatty liver)
• Cholesterol synthesis
• Lipoprotein synthesis
• Bile acids/salts synthesis
• Beta-oxidation
• Fatty acid synthesis 

• Pentose phosphate pathway (NADPH or nucleotides)
• Maintaining blood glucose homeostasis- GNG
• Glycogen: storage
• Glycolysis: pyruvate 

• AA catabolism
• Synthesis of apoproteins
• Synthesis of plasma proteins
• Synthesis of nitrogen contraining compounds
• Urea cycle 

• Fat predominant source (80-90%)
• CHO (5-18%)
• Proteins (2-5%) 

• Muscle glycogen
• Plasma glucose
• Plasma fatty acids
• IMTG 

• Increase activity of PFK (positive allosteric effector)
• Increase activity of glycogen phosphorylase b (positive effector)
• Increase the activity of AMP-activated protein kinase (AMPK)- phosphorylate GS (making it inactive) 

Glycogen phosphorylase

Glycogen synthase

Glycogenesis, glycogenolysis

Glucagon, epi, Ca2+

Covalent- GPK- phosphorylation = active

Allosteric- [AMP], Pi, ATP, Glucose (G 6-P)

Protein phosphatase 1

Glycogenesis, glycogenolysis

Covalent- GSKa, GPKa, PKA, CaMK, AMPK- phosphorylation = inactive

Protein phosphatase 1

Pyruvate carboxylase

PEPCK

Fructose 1,6 bisphosphatase

Glucose 6-phosphatase

Pyruvate carboxylase- allosteric activation by acetyl CoA

PEPCK- transcriptional regulation via PKA

Hexokinase

PFK1

Pyruvate kinase

• PFK1- allosteric regulation
• AMP/ADP (+)
• Pi (+)
• F-2,6-bis P (+)- when glucose level is low, glucagon is released into the bloodstream, triggering a cAMP signal cascade. Protein kinase A thus activated phosphorylates the bifunctional enzyme, activating FBPase2 which lowers frustose 2,6-bisphosphate (F-2,6-BP) levels. Because F-2,6-BP normally stimulates phosphofructokinase-1 (PFK1), the decrease in its concentration leads to the inhibition of glycolysis and the stimulation of gluconeogenesis
• ATP (-)
• Citrate (-1)
•  Pyruvate kinase (PK)
• Phosphorylation inhibits PK by PKA

Citrate synthase

Isocitrate dehydrogenase

a-ketogluterate DH

Perilipin

HSL

1. Following a meal in which there is food fat found in chylomicrons
2. Following a meal in which there is CHO, providing a source of glucose to produce glycerol 3-P in adipocytes
3. An increase in blood insulin concentration facilitates TAG synthesis

• helps get glucose into fat cells
• increased LPL activity in adipose tissue
• helps get fatty acids into cells (FAT/CD36)
• opposes the reverse process- lipolysis or TAG breakdown 

FA entry into the mitochondria, this is favored when CPT1 is not inactivated by malonyl CoA from ACC reaction

MCD breaks down Malonyl CoA to remove this inhibition

ACC

*Citrate is a positive allosteric effectors

*Malonyl CoA and LCFA CoA are negative allosteric effectors

*ACC1 is inhbited by phosphorylation by AMPK and PKA

FAS

*Gene expression

• BCKAD
• Phosphorylation by BCKAD kinase decreases activity
• Dephosphorylation by BCKAD phosphatase increases activity
• The products allosterically inhibit BCKAD
• Starvation, prolonged exercise, and poorly controlled diabetes inhibit kinase
• Cortisol (a glucocorticoid) will inhibit the kinase

*increasing the oxidation of BCAA (AA catabolism)

•  Insulin increases BCKAD kinase activity

*Reducing the oxidation of BCAA and promoting their inclusion in proteins (an anabolic process)

• CPS1

*The enzyme is allosterically activated by N-acetyl glutamate (NAG)

-NAG formed by N-acetyl glutamate synthetase

__dependent on Arg- if Arg builds up from the urea cycle (it is going to slow), it increases the production of NAG

No.

With overnutrition you generate more FAs

Fed state- ~3 hours after meal

Post-absorptive or early fasting- 3 to 18 hours following a meal

Fasting state- 18 hours- 2 days without additional food

Starvation state- fully adapted state of food deprivation lasting as long as several weeks

RBCs have no mitochondria and burn glucose anaerobically

CNS cannot store energy

3 ways:

RBCS

Adipose tissue (glucose becomes glycerol which becomes TAG)

Muscle is stored as glycogen

Amino acids from muscle are the primary substrate, glycerol and lactate

These are stimulated by glucagon and cortisol due to lower glucose levels in the blood

Insulin production willl rapidly decrease

Muscle and adipose tissue will become resistant to insulin

Glucagon will continue to stay elevated, cortisol will increase initially and decrease, and thyroid hormone decreases

Proteins need to be conserved to live, and fuel ulization changes as result from gluconeogenesis to lipolysis... FAs become predominant energy source as well as ketones

As a result of switch to lipolysis glycerol becomes gluconeogenic precursor to spare AAs

In fasted state, insulin is no longer a regulator but the catecholamines are

*glucagon

*epinephrine

*norepinephrine

Acute,

glucagon in the liver

epinephrine

norepinephrine

glucagon

epinephrine

norepinephrine

What is happening with adipose tissue in a fed state with:

Lipolysis

TAG synthesis

What are the important hormones?

Lipolysis- inactive

TAG synthesis- active

Hormones- insulin, will suppress lipolysis and increase TAG

What is happening with adipose tissue in a fasted state with:

Lipolysis

TAG synthesis

What are the important hormones?

Lipolysis- active

TAG synthesis- inactive

What are the important hormones for regulation?

glucagon

epinephrine

norepinephrine

What is happening in skeletal muscle in a fed state?

Glycolysis

Beta-oxidation

Glycolysis- active

Beta oxidation- inactive

What is happening in skeletal muscle in a fasted state?

Glycolysis

Beta-oxidation

Glycolysis- inactive

Beta oxidation- active

What is happening in the liver during a fed state?

Glycogen metabolism

Gluconeogenesis

Lipid synthesis

Glycogen metabolism- inactive

Gluconeogenesis- inactive

Lipid synthesis- active

What is happening in the liver during a fasted state?

Glycogen metabolism

Gluconeogenesis

Lipid synthesis

Glycogen metabolism- active

Gluconeogenesis- active

Lipid synthesis- inactive