Conversion of glucose to glycogen for storage - glucose can be used by the liver & other cells for energy or stored as glycogen for later use

Decomposition of fats - if glucose supply is low the liver can use glycogen ( lasts 12-16hrs) & other substrates to raise blood glucose concentration - glycerol from triglycerides - lactic acid from skin & muscle - amino acids

Aka adrenaline Produced by adrenal medulla Increases glucose production by: - inhibiting insulin secretion - increasing glycogenolysis ( breakdown of glycogen) - promoting lipolysis ( breakdown of fat )

Primarily cortisol Secreted by adrenal cortex when stimulated by ACTH Increases plasma glucose by - decreasing intestinal entry into cell - increasing gluconeogenesis, liver glycogen & lipolysis

Produced by anterior pituitary gland Increases glucose production by: - decreasing entry of glucose into the cells - increasing glycolysis ( metabolism of glucose to pyruvate / lactate)

Glucose testing methods Flashcards by Victoria Penny

Metabolism of glucose (4)

Converted to glycogen via glycogenesis & stored ( mainly in liver & muscle )
Metabolized to CO2, H2O & energy via Tricarboxylic acid cycle, electron transport chain & Oxidative Phosphorylation
Converted to ketoacids, amino acids & proteins ( transmission)
Converted to fat & stored in adipose tissue as triglycerides ( via acetyl CoA)

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Glycolysis

Metabolism of glucose to pyruvate or lactate for production of energy ( important for muscle tissue )

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Glycogenolysis

Breakdown of glycogen to glucose for energy

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Glycogenesis

Conversion of glucose to glycogen for storage

glucose can be used by the liver & other cells for energy or stored as glycogen for later use

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Gluconeogeneisis

Formation of glucose from non carbohydrate sources

Ex. Conversion of amino acids by the liver

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Lipogenesis

Conversion of carbohydrates to fatty acids

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Lipolysis

Decomposition of fats

if glucose supply is low the liver can use glycogen ( lasts 12-16hrs) & other substrates to raise blood glucose concentration
- glycerol from triglycerides
- lactic acid from skin & muscle
- amino acids

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Hormonal control of glucose

Increase blood glucose

glucagon
Adrenalin ( Epinephrine)
glucocorticoids ( cortisol & cortisone )
growth hormone
adrenocorticotropic hormone ( ACTH)
thyroxine
somatostatin

Decreases blood glucose
- insulin

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Glucagon

Primary hormone responsible for increasing glucose

Produced by alpha cells of islets of Langerhans in the pancreas

Released during stress & fasting states

Promotes glycogenolysis & gluconeogensis

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Epinephrine

Aka adrenaline

Produced by adrenal medulla

Increases glucose production by:

inhibiting insulin secretion
increasing glycogenolysis ( breakdown of glycogen)
promoting lipolysis ( breakdown of fat )

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Glucocorticoids

Primarily cortisol

Secreted by adrenal cortex when stimulated by ACTH

Increases plasma glucose by

decreasing intestinal entry into cell
increasing gluconeogenesis, liver glycogen & lipolysis

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Growth hormone

Produced by anterior pituitary gland

Increases glucose production by:

decreasing entry of glucose into the cells
increasing glycolysis ( metabolism of glucose to pyruvate / lactate)

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Adrenocorticotropic Hormone ( ACTH)

Produced by anterior pituitary gland

Increases release of cortisol

Increases plasma glucose by:

converting liver glycogen to glucose
promoting gluconeogenesis

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Thyroxine

Produced by thyroid gland

Increases glucose production by :
- increasing glycogenolysis, gluconeogenesis & intestinal absorption of glucose

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Somatosatin

Produced by the alpha- cells of the islets of Langerhans in the pancreas

Increases plasma glucose by :
- inhibiting insulin, glucagon & growth hormone

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Insulin

Primary hormone responsible for decreasing glucose

Produced by beta - cells of islets of Langerhans
In the pancreas

Promotes the storage of glucose as glycogen

Promotes the formation of lipids from glucose

Increases the permeability of glucose to cell

Theory of insulin action

Beta cells detect an increase in glucose, they release insulin
The insulin causes glucose to move into the cells ( muscle & adipose tissue ) via transport receptors Pg.98

Sodium dependent glucose transporters

Promote uptake of glucose form lumen of the small bowel

Promote reabsorption of glucose from urine I’m the kidney

Facilitative glucose transporters ( GLUTs)

Located on the surface of all cells

Designated GLUT1- GLUT14

Eleven mediate glucose transport

Divided into 3 subfamilies

class l ( GLUT1-4)
class ll ( GLUT 5,7,9,11)
class lll ( GLUT 6,8,10,12,14)

GLUT 1&3

GLUT 1& 3 provide the glucose requirements of the brain

GLUT 2 are found in

hepatocytes

B-cells of the pancreas

basolateral membranes of intimal & renal cells

allows the movement of glucose into & out of these cells

GLUT 4

catalyzes a rate-limiting step for glucose uptake and metabolism in skeletal muscle
-skeletal muscle is the major organ of glucose consumption

when insulin concentration in the blood are low, GLUT 4 is localized in intracellular compartments & is inactive

insulin is released after a meal & stimulate the translocation of GLUT 4 to the plasma membrane
-this promotes uptake of glucose into skeletal muscle & fat

measurement of blood glucose

serum, plasma, whole blood, urine, & CSF can be analyzed

serum & plasma should be separated from cells within 1 hour of collection

if delayed analysis, collect in sodium fluoride tube ( grey)
this will prevent glycolysis

fasting blood glucose tests should be performed in the morning after an 8 - 10 hour fast

higher in the morning than the afternoon ( diurnal)
diabetes may be missed in patients tested in afternoon

glucose results based on sample type

serum& plasma values will be higher than whole blood values

venous whole blood ( lowest)
capillary/arterial
serum/plasma ( highest )

whole blood concentrations are approx. 10-12% lower than plasma

methods for glucose testing

oxidation/reduction reaction methods aromatic amines methods enzymatic methods - glucose oxidase - hexokinase electrode methods

oxidation/reduction reaction- Copper Reduction

Cupric copper is reduced to cuprous copper by a reducing sugar ( glucose ) used in urinalysis ( clinitest) ( blue) (red) 1. cuprous copper + reducing sugar ---------> cuprous copper 2. cuprous copper + Phosphomolybdic acid--------------------------------->phosphomolybdous acid ( blue ) blue color measured using spectrophotometer and is related ti the sugar concentration recorded as 1+ 2+ 3+ 4+ positive for all reducing sugars used for determining genetic disorders -ex. galactosemia urine dipstick neg ( no glucose in urine) urine flintiest pos ( galactose detected )

glucose oxidase

most specific enzyme for glucose only reacts with ß- D glucose method: glucose + O2--->Gluconic acid + H2O2 H2O2 + chromagen ---> oxidized chromagen + H2O chromagen is colorless until oxidized conc of glucose is proportional to color

what are 2 step reaction called

Trinder Reactions

chromagens in glucose oxidase

chromogens are colourless chemical compounds that can be converted to a dye or color compound through a chemical reaction o-dianisidine ( brown) o-tolidine( blue) 4-aminophenizone( red) ** two other common chromogens: 3-methyl-2-benzothiazolinone hydrazone N,N-Dimethylalaniine

alpha & beta glucose | & what converts one to the other

Blood glucose : alpha-D glucose ( 36%) beta -D glucose ( 64%) glucose oxidase can only cause oxidation of the Beta for, Mutarotase can be added to convert alpha to beta forms extend incubation time will allow spontaneous conversion

interfering substances in glucose oxidase

in 2nd step other substances in the sample can be oxidized instead of the chromagen - results in a decrease of color & a false decrease in glucose reading other reducing substances : uric acid bilirubin ascorbic acid ( vitamin C) glutathione ( anti-oxidant) a false increase in glucose conc. can be caused by strong oxidizing substances ( bleach )

glucose oxidase -CSF

CSF glucose is a STAT ( freeze if cant do ASAP & freeze after) CSF levels will be ~60% of blood glucose levels ( plasma ) reference range : 2.2-3.9 mol/L decreased : - bacterial meningitis - fungal infection increased : - hyperglycaemia - traumatic tap

whats in the glucose reagent

BUFFER | NOT GLUCOSE

what is the reference method for glucose

Hexokinase - more accurate than glucose oxidase - less interferences ( not affected by uric acid & ascorbic acid ) - can be performed on serum, plasma , urine, CSF &serous fluid

what causes a false decrease in hexokinase results

grosss hemolysis & very high bilirubin

steps of hexokinase

Glucose + ATP --> glucose- 6-phosphate + ADP G-6-P + NADP+ ----> 6- phosphogluconate + NADPH + H+ NADP+ no absorbance at 340 nm NADPH absorbance at 340 nm increase in absorbance is read @ 340 nm

enzymatic methods- Glucose dehydrogenase

Glucose + NAD+ ----> Gluconolactone + NAD + H+ increased absorbance at 340 nm( form NADH) is measured NADH generated is proportional to glucose conc not widely used

polarographic electrode methode ( oxygen electrode)

measures the rate of oxygen consumption ( depletion ) after sample is added to a solution containing glucose oxidase glucose + O2 --> gluconic acid + H2O2 H2O2 needs to be eliminated through two side reactions with catalase & molybdate ( to prevent the reaction from reversing ) suitable for serum, plasma & CSF NOT WHOLE BLOOD ( blood cells consume oxygen)