1. only carbs/fat metabolized directly for energy use

2. only excess carbs/fat stored

major tissues for interconversion = adipose, muscle, liver

during the absorptive state

1. what is done with structure/storage forms of substrates?

2. what's the main energy source?

3. what is done with excess calories?

1. storage/structure 

2. main energy source is glucose

3. excess calories are stored

how is insulin stored in the pancreas? 

what happens to it upon release?

how long is it's half life?

stores as proinsulin in secretory granules

the chain is cleaved to form insulin & c-peptide

half life of 6 minutes

what 3 things enhance insulin release?

what inhibits it's release from the pancreas?

very high plasma glucose concentration

high plasma amino acid concentration

hormones from GI tract

sympathetic neurons & epinephrine

glucose attach to receptor -> used to make ATP

the ATP inhibit an ATP sensitive K channel

more K in the cell -> depolarize cell

Ca channels open -> Ca influx trigger vesicles to secrete insulin

temporal effects of insulin on a cell

rapid effect?

intermediate effect?

long term effect?

rapid: 1-5 min, increased activity / insertion of GLUT receptors in membrane

intermediate: 10-20 min, alters metabolistic enzyems

long term: hours to days, altered gene transcription

what excretes glucagon?

what 2 things cause it?

main effects?

pancreatic α-cells

1. decr in plasma glucose

2. incr in plasma amino acids 

glycogenolysis, lipolysis

βcells secrete a lil insulin at first to prevent muscles from hogging all the glucose to allow the CNS to get glucose first

cellular mech of glucagon intake

what type of receptor?

effect in liver?

effect in adipose tissue?

G-protein coupled receptor

makes cAMP -> activate protein kinase A

liver - conversion of phosphorylase b to a, breaks down glycogen

adipose tissue - PKA mediated activation of a lipase, for lipolysis

what effect do these hormones have on energy metabolism:

1. epinephrine

2. GH & cortisol

3. cortisol

1. similar to glucagon

2. lipolysis, gluconeogenesis, inhibit insulin effects on glucose uptake at skeletal muscle (to allow CNS to get glucose first)

3. lipolysis, gluconeogenesis, protein catabolism

type I diabetes what goes wrong?

what about in type II?

type I - impairment of insulin production

type II - lack of insulin sensitivity

chronic complications of diabetes mellitus?

name 4

atherosclerosis (cuz of high lipidemia - body breaks down lipids for energy)

small blood vessel disease (eye -> blindness), vessels become permeable, leak blood

nerve damage

infection

type I diabetes effect on:

breath

weight

urine

blood

breath - acidosis

weight loss

ketoneuria & glycosuria

blood - hyperglycemia, ketoacidosis, islet cells antibodies

type II diabetes effect on:

eyes

heart

weight

urine

blood

feet

eyes - cataracts, diabetic retinopathy

heart - ischemic, heart diseasae

weight - obese

urine - glyco/proteinuria

blood - hyperglycemia

feet - peripheral neurophathy

Dx for diabetes

what should plasma glucose be?

urine glucose?

what's the glucose tolerance test?

plasma glucose should be 80-90 mg/dl

no glucose in urine

test - give 1g glucose/kg body weight -> levels should return to normal after 2 hours

acute hypoglycemia

what's usually the cause?

at what level of glucose do we see CNS sensitization

at what level do we see seizures, coma etc

what's the Rx?

taking insulin w/o a meal

50-70 mg/dl

20-50 mg/dl

give large amounts of glucose 

give epinephrine

common type of islet cell tumor

can cause hypoglycemic attacks

due to excess insulin secretion

very rear alpha cell tumors

usually asymptomatic but can cause diabetes