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Flashcards in Glucose Hormone Regulation Deck (26):

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
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

1. Blood glucose taken up by Glut 2
2. It's degraded when it hits the beta cells and produces ATP, NADH, NADPH
3. the ATP binds to a K+/ATP channel closing the channel. Causing a depolarization
4. There is an influx of Ca2+ due to that depol
5. 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



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?

1. Cross the BB
2. Stimulates ARC which projects to hypothalamus
3. This inhibits proteins and neurons that stimulate food intake

Affects opposed by ghrelin


What happens to leptin in obesity

It increase with adipose cels but its permeability to BBB decrease especially with a high fat diet


Disscuss Prader Willis

Genetic defect in chromosome 15 where they have impaired brain stomach feedback due to a lack of leptin