L10 - Energy balance p2

vagal nerve

important sensory signals

• cephaluc stage of digestion

• stomach desgation

• nutrient detection in stomach

signals to NTC through afferent signals by mechanorecptors

afferent and efferent signals of vagus nerve

afferent saitety signals to :

• chemorecptors in gut

• metaborecptor to stomach

efferent signals to:

• liver and pancresae to modulate insulin release

gut-brain signalling

have stretch and tension recptors in stomach

GU tract also signals when empty

once in bowl get absorption of nutrients by SGLT1 and GLUT2 into blood stream

lipids own way through lymph then into normal circulation

ways of getting increatin released by entroendocrine cells

1-

• high glucose

• more ATP

• ATP be used to activate adenyl syslase

• make more camp

• INCREASE Ca

• then activate releaseof GLP1 and GIP

2-

• memebrane depolarization

• activation of Ca channles

• more ca inside

• actiavtion of GLP1 and GIP

Gut-Brain signalling

• can have hormone bind to receptor

• or this happens in tissue and blood hormones bind to vagal afferents that signal to NTS in brain to then initiate a response

• can also have hormone that cross blood brain barrier and bind to their recptors on hypothallmus

glucoprivic feeding

• recpors in 4th ventricle in lower brain stem

• when given 5TG ((5-thioglucose) - stops glycise form being ohsophylated

• have inclease insulin and blood glucose

• these recptors control the rpeosne

when there is glucose what happens to KATP channels

they close to allow depolarization

how do sulphonylurea drugs work

bind to KATP channels causing them to close stiulating release of insulin in type 2 diabetics

have 2 nuclotide binding domains once nucelotides binds e.g ATP causes inhbition of channel activity

hypoglucemia on vagus nerve

• when have glucose constant Action potential firing

• when no glucose activty decraeses less ap firing

• see that cell hyperpolarizes due to opening of ATP sensitive channles

• when add glucose again AP increases

however what was found about Katp channels

that 40% of dorsal vagal neucleus express Katp but do not respond to hypoglycemia so doesnt emna if have channels repond to it

leptin

• coded by ob gene

• released by adipocytes

• leptin released is proportional to adipocyte mass

• acts on CNS

• low leptin → starvation (more important)

• too high leptin → predation

• obesity loss in leptin or leptin recptor

• leptin helps stop eating (low leptin makes incrase appertite) opposiet for high leptin

• of resisnat like in obesity just keep eating

what happens in these mice