Glucose Hormone Regulation Flashcards
Define regulate in terms of glucose lebels
Maintaining a variable (glucose blood levels) constant in face of disturbances
Rates for Glucose
Glucose 70-1– mg/dl
Post meal- 140mg/dl
What are hormones that increase blood glucose
Glucagon, Epi, Cortisol. Growth, Thyroid hormones
Distribution of cells in islet in pancrease
65%- beta- insulin
25%- Alpha- glucagon
10%- delta- somatostatin
The human islets are 100-150um and are mostly spherical
Explain the relationship between the liver and the pancreas
The liver is the first organ exposed to the pancreatic secretions and takes in about 50% of the insulin secreted and then regulates systemic concentrations
Explain insulin synthesis
It’s intial a pre-proinuslin and then disulfide bonds are added making it a proinsulin.
From the proinsulin- the C peptide is cleaved making insulin (a and b peptide with disulfides)
The C-peptide is still secreted with the insulin. The C-peptide is not absorbed by the liver so a good indicator of the amount of insulin released. May also have growth hormone
What are the error dectectors
Control Center
Effectors
And varaible
in the glucose regulation system
Error detector- Beta cells in pancreas
Control center- insulin
Effectors- liver, adipose, muscle
Variable- glucose
What does insulin do? What are the two exceptions?
Controls the rate glucose is taken up. Exception is the bran and the liver.
HOHow does glucose affect the Beta cells?
It enters through the glut 2 receptors (glucose independent) and and when it hits the cells glucose is degraded.
Te degradation increase the levels of ATP, NADP, and NADPH
Explain entire mechanism of increase in blood glucose to insuling secretion
- Blood glucose taken up by Glut 2
- It’s degraded when it hits the beta cells and produces ATP, NADH, NADPH
- the ATP binds to a K+/ATP channel closing the channel. Causing a depolarization
- There is an influx of Ca2+ due to that depol
- Ca2+ causes insulin release
CCK/Ach can also cause increase of Ca2+ through IP3, PKC, PKA mechanism
GIP, GLP and glucagon also increase insulin release through cAMP and PKA phos of Ca2+ channels
AA increase ATP/NADPH and thus close K-ATPase channels.
Explain the SUR receptors
The SUR receptors are attached to the K-ATP channels and inhibit it(close it) and causes Ca2+ influx and insulin release.
SUR can be used in diabetics!
Purpose of Mg-ADP
It opens the K-ATPase channel which inhibits insulin release. Important for ppl with hyperinsulinism
Explain the incretin effect
Oral and IV glucose in the same amounts cause different changes in insulin secretion.
The oral causes a higher secretion of insulin due to other effects influcing GLP(intestinal L-cells) and GIP (intestinal K-cells)– these both causes insulin secretion before the blood gluocse has even risen
What happens to the incretin effect in diabetics?
It is much smaller. The pancreas isn’t reponsing to the GLP and GIP
Explain the insulin autocrine functions?
Insulin binds to tyrosine kinase and activates phos of the IRS and P13K and stimulates secretion.
this is important for regulation of cell survival and cell growth.
Explain the insulin spike
It’s biphase. An initial peak is due to the immediate pool of insulin that is right next to the Ca2+ channels.
It then declines and slowly rise using the ready releasable pool and the reserve pool
Difference in impaired fasting and impair glucose tolerance
impaired fasting glucose (predominant liver insulin resistance)
impaired glucose tolerance (predominant muscle insulin resistance, impaired insulin secretion)
Division of glucose
33% to CNS
34% to liver
33% to muscle
Which organs have glut 2 glut 1?
INsulin non-senstive
RBC and brain= Glut 1
Intestines
Cornea
Kidney
Liver
Effects of insulin deficiency
Hyperglycemia- and decreased glucose uptake by organs
Electrolyte imbalacne (K channels stays open?) Increase protelysis and lipolysisso loss of nitrogen in urine (urea cycle can’t keep up with protein degradation) and an increase in plasma FFAs, increase in ketogensis, ketouria, and Ketoemia
Dehydraion acidosis and death!
Glucagon in response to a high carb meal? HIgh protein meal?
Insulin suppresses the glucagon after high carb
Protein increase glucagon
Function of Amlyin
It’s co secreted with insulin and promtoes fullness and decrease food intake. Slows down gastric emptying and inhibits secretion of digestive fluids
Leptin function
Satiety hormone primarily in adipose. Permeates the BBB.
When high food intake leptin stimulates energy expenditure and does the opposite when food intake is low (cnserves)
Leptins mechanism? what opposes it?
- Cross the BB
- Stimulates ARC which projects to hypothalamus
- This inhibits proteins and neurons that stimulate food intake
4
Affects opposed by ghrelin
