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insulin signalling. Neuro - anatomy of homeostatic regulation of food intake ; opposing actions of AgRP /NPY and POMC/CART containing neurons.

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Presentation Transcript
slide2
Neuro-anatomy of homeostaticregulation of foodintake; opposing actions of AgRP/NPY and POMC/CART containingneurons
slide4

Increased concentration of glucose in the blood, after a meal, leads to increased ATP production in the pancreatic b-cell and this in turnreduces K+ outflow, leading to membrane depolarisation. The subsequent C2+ entry constitutes the secretion signal

slide5
Release of insulin in response to glucose leads to glucose uptake and storage in the form of glycogen (in muscle and liver)
recruitment of adaptors and effectors through domains that bind phosphotyrosine containing peptides
Recruitment of adaptors and effectorsthroughdomainsthatbindphosphotyrosine-containing peptides

SH2 domain

(or PTB domain)

phosphotyrosine peptide

from IRS1 (or insulin receptor)

slide12

A downstreameffector of PI 3-kinase is the protein kinase PKB

PDK2 : phosphatidyl inositol-dependent protein kinase 2 was so named because the identity was unclear. It is now generally agreed that the mTOR/Rictor complex provides the initial phosphorylation

slide17
PKB stimulates the mTORpathway, whichalsoprovides a anorectic signal (via an as yetunclearpathway)
slide20

A lack of glucose blocks the mTOR-mediatedanorectic signal. This occursthrough an increase of 5’-AMP whichisproduced in a « rescue » pathwaywheretwo ADP are combined to raise the level of ATP

slide21
The global picture of insulin, leptin, glucose and amino-acid –mediatedregulation of foodintake via mTOR and AMPK