Sfm: Fed And Fasted States

Front 1

Critical organs during fasting

Back 1

Brain
Liver
Adipose
Skeletal Muscle

They communicate through Innervation, circulating metabolites (esp glucose), hormones and cytokines

Front 2

Hormones

Back 2

Insulin
Counterregulatory hormones: glucagon, catecholamines, growht hormone, glucocorticoids

Front 3

Insulin vs Glucagon/Epinephrine

Back 3

Insulin: increased in the fed state. Regulates via dephos.

Glucagon, epinephrine: Counterregulator hormones, increased in fasted. Regulate via phosphorylation.

Front 4

24 Hour Fed Fasting Cycle

Back 4

Post-absorptive: Using energy stores. In the morning after a long sleep.

Preprandial: Using energy stores. After or generally finished absorbing last meal.

Postprandial state: absorbing food you have eaten. Absorbing food. Greater energy utilization. After a meal.

Front 5

Organs that must function similarly under both energy states

Back 5

Brain and Heart

Front 6

PROInsulin

Back 6

Insulin consists of two peptides: A for acidic, B for basic

A and B joined by disulfides.
C must be cleaved by C-peptide.

Front 7

How is insulin synthesis and secretion regulated?

Back 7

Glucose enters the Bcell via nonhormone regulated glucose transporters (GLUT2). Well enter at a rate proportional to extracellular glucose range.

Once inside, glucose is phosphorylated by an isoform of glucokinase that has a high Km. Phosphorylation proportional to glucose entry.

After glucose phosphorylation, metabolism proceeds along aerobic pathways. This leads to an increase in the intracellular ATP:ADP ratio.

Higher ATP inhibits ATP sensitive K channel. Leads to activation of voltage gated calcium channel, calcium influx, and insulin secretion.

Again:
1. Glucose through transporter.
2. Glucokinase phosphorylates glucose.
3. Metabolism proceeds. More ATP.
4. ATP binds Calcium channel, leading to depolarization and insulin secretion.

Front 8

Insulin Actions

Back 8

Stimulates synthesis of glycogen, protein, fat, DNA, and RNA .Inhibits breakdown of glycogen, protein, and fat.

Mitogenic.

Front 9

Insulin Signalling

Back 9

Protein tyrosine kinase: Insulin receptor is protein tyrosine kinase. When bound, it increases its phosphorylative activity.

Front 10

How does insulin affect serum glucose production???

Back 10

Decreases hepatic glucose producition (inhibits glycogenolysis and gluconeogenesis)

Promotes glucose uptake.

Front 11

Hormonal Regulation in the Liver

Back 11

Glycolysis/gluconeogensis- acutely regulated by bifunctional enzyme, PFK/Fuctose26BP.

Fatty acid synthesis/degradation: regulated by acetyl CoA carboxylase. Catalyzes the formation of malonyl CoA.

Glycogen synthesis/degradation: regulated by phos/dephos of phosphorylase and glycogen synthase.

Dephosphorylated in response to insulin, phosphorylated in response to glucagon and insulin.

Front 12

Regulation in Liver by Substrates

Back 12

Fed: Glucose binds phosphorylase, inhibiting it.

Fed: Hexose monophosphate pathway: increase in NADPH: fatty acid synthesis promoted.

Fasted state: excess production of acetyl CoA. Exceeds capacity of acetyl CoA. Used for ketone body production.

Front 13

Adipose Tissue

Back 13

Brain: During fasting, glucose is important. Ketones are used.

Muscle: Major glucose repository. Fasting: gluconeogensis from muscle.

Glucose-->G6P--> Glycogen, Pyruvate, AcCoA

Early Starvation
Glycogen-->G6P-->Glucose
Late Starvation: Ketone bodies and shit.