The Endocrine Pancreas - Insulin Flashcards
what peptide hormone suppresses hunger
leptin
what two hypothalamic centres control food intake
feeding centre and satiety centre
two theories suggest what controls food intake centres . How do they differ
glucostatic theory is blood glucose based whereas lipostatic is fat store based.
where is leptin released from
fat stores
3 types of energy output
cellular work, mechanical work and heat loss
what is the absorptive state
where ingested nutrients supply body energy needs and the excess is stored
post-absorptive phase is anabolic/catabolic
catabolic
absorptive phase is anabolic/catabolic
anabolic
what is the post-absorptive phase
when we break down our body energy stores
what sources of energy can the brain use
glucose and ketones
in what situation does the brain use ketones for energy
starvation
glycogen release –> fatty acids turned into ketones
long term consequence of hypoglycaemia
coma and death
in normal metabolism, what happens to excess ingested glucose
it undergoes lipogenesis to fat stores
ways that glucose can be made by body
breakdown of glycogen
amino acids into glucose (gluconeogenesis)
normal BG level
5mmoles
what BG is defined as hypoglycaemic
<3mmoles
what BG prick test is defined as hyperglycaemic
> 11mmoles
what fasting BG is defined as hyperglycaemic
> 7mmoles
two chief hormones of blood glucose control
insulin and glucagon
4 types of pancreas cells and what they secrete
alpha - glucagon
beta - insulin
delta - somatostatin
F - pancreatic polypeptide
what does pancreatic polypeptide do
we don’t really know, probably helping nutrient absorption
trigger of insulin release
blood glucose and amino acid levels increasing
what other hormones lower blood glucose
none. only insulin lowers blood glucose
what two forms is glucose stored as
glycogen and triacylglycerols
where is glycogen stored
in the liver and muscle
where is TAG stored
in the liver and adipose tissue
mechanism of insulin secretion
glucose –> into cell by GLUT transporter –> metabolism increases –> ATP increases –> Katp channels close –> depolarised –> voltage Ca2+ channels open –> insulin exocytosed
what is special about K+ ion channels of B-cells
sensitive to ATP within the cell
what channels close in the secretion of insulin
Katp
what channels open in the secretion of insulin
Ca2+
what does closing Katp channels do to the cells polarity
depolarises it
GLUT transporter of glucose into cells of muscle and fat
GLUT-4
what receptors does insulin bind to GPCR or tyrosine kinase
tyrosine kinase
effect of insulin stimulation of cell
GLUT-4 migrates to cell membrane from cytoplasm and transports glucose
what types of tissues need insulin for glucose uptake
muscle and adipose
what are the non-insulin dependent tissues
Kidneys, brain, rbc and b-cells of pancreas and liver
what GLUT transporter takes up glucose in the liver
GLUT-2
how does insulin indirectly effect glucose uptake in liver
insulin release –> hexokinase activated –> converts glucose to glucose 6 in cell–> creates a concentration gradient over membrane –> glucose moves into cell by GLUT-2
how does glucose move into liver cells
moves down a concentration gradient
effect of insulin on glycogen synthesis
stimulates its synthesis and inhibits its phosphorylase
effect of insulin on amino acid uptake
increases it
effect of insulin on protein synthesis
increases it and inhibits its lysis
effect of insulin on TAG synthesis
increases
effect of insulin on gluconeogenesis
inhibits enzymes of gluconeogenesis
effect of insulin on K+ ions
promotes entry into cells by stimulating Na+/K+ ATPase
where is insulin degraded
mostly liver and kidneys
what happens to insulin bound receptors after
they are ENDOcytosed and destroyed.
some are recycled
stimuli of insulin release
increased BG and aa.
glucagon (to take up the glucose that glucagon causes to be made)
vagal nerve activity
GI secretory and motility hormones
inhibitor of insulin release
low BG.
somatostatin
stress
sympathetic alpha2 effects?
what has greater effect on insulin secretion. intravenous or oral delivery of glucose
oral. because vagus nerve is stimulated to release GI hormones and insulin in addition to the B-cells being directly stimulated
