Secretie:
Verschillende producten stimuleren verschillende wegen (er zijn 3 wegen)
1. GLUT2 -> oxidatieve fosforylatie: ATP -> sluiten ATP-gevoelige K-kanalen -> openen
voltage-gated Ca-kanalen: Ca influx -> depolarisatie cel: exocytose insulinegranules
a. glucose, AZ, ketonzuren, VVZ, fructose, sulfonylurea
! GLUT 2: alleen in lever, pancreas, dunne darm
2. PL-C -> IP3 + DAG
IP3: release Ca uit ER = depolarisatie = insulinesecretie
DAG -> PK-C: insulinesecretie
a. CCK, Ach
3. Adenylaatcyclase -> cAMP -> PK-A: insulinesecretie
a. glucagon, beta-adrenerge agonisten, GLP-1, GIP, secretine
FIRST PASS EFFECT: 60% v insuline w via v portae in lever geëlimineerd
Bij IV-glucose toediening:
-fase 1: FPIR = first phase insuline response (2-5min) -> vrijstellen opgeslagen insuline
-fase 2: duurt zolang glycemie gestegen is -> vrijstellen opgeslagen + nieuw gevormde
insuline
Diabetes: verlies FPIR
, a. Insuline – alfa -> tyrosine-kinase thv bèta -> fosforylatie tyrosine-residues ->
insulinewerking
b. Maar 5% v rec w gebruikt bij max effect
Aantal rec afh v synthese rec, endocytose rec, + recycling/degradatie
Blootgesteld aan veel insuline = daling rec (type 2 DM)
Hepatic glucose output = gluconeogenese + glycogenolyse in lever
Bij vasten: verminderd glucoseverbruik door spieren
Bij beweging: hogere glucoseverbruik door spieren, hogere glucose-opname uit bloed
(insulineonaf!)
2. Lever = first pass effect + doelorgaan via GLUT2
3. Spier: via GLUT4: in myocyt bijna geen gluconeogenese
4. Adipocyt: via GLUT4: geen glycogeensynthese, wel synthese v LPL, alfa-glycerol
fosfaat
GLUT2 = insuline-onaf: in lever, pancreas, dunne darm
GLUT4 = insulineafh: in spier + vetcel
Functies
- groeibevorderend + meer genexpressie
- glucose-opslag: glycogeensynthese, eiwitsynthese, lipogenese, glycolyse,
antiketogeen
- kaliumopname in cel (! hypokalemie bij te weinig insuline)
- anti-inflammatoir: daling oxidatieve stress, bescherming endotheel
Glucagon
AZ stimuleren glucagonsecretie
Doel: lever zet glucose vrij
Preproglucagon -> proglucagon
Glucagon door proteasen in alfa cellen
Glicentine, GLP-1, GLP-2, IP-2 door proteasen thv neuroendocriene cellen (L-cellen
thv ileum + colon)
SST
<deltacellen in eilandjes v Langerhans
<D-cellen GI
<hypothalamus (CZS)
Inhibitie: GH, insuline, glucagon, G, VIP, TSH
HOOFDSTUK 2: Diabetes mellitus type 1 en 2
= hyperglycemie door stoornissen in metabolisme en met langetermijnscomplicaties op
micro/macro-niveau
Type 1: absoluut insulinetekort
Type 2: relatief insulinetekort (met/zonder insulineresistentie)
75-80% v bèta-cellen venietigd = insulinetekort, hyperglycemie en diagnose
Insulitis = lymfocyten + macrofagen in eilandjes gericht tegen bèta-cellen (vooral jong)
Transfer v ziekte via milt, BM
Omgevingsfactoren: virussen (coxsackie B, CMV, bof, rubella, EBV, enterovirussen…), dieet
(nitrosamine…), levensstijl (stress), borstvoeding + melk algemeen beschermt moeder + baby
Type 2 DM
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