diabetes

<5.6mmol/L

>7mmol/L

0mml/L (you should avoid glucose because cancer cannot survive if there is no glucose source!)

>7mmol/L

<5.6mmol/L

I don't believe in pathology testing it's a scam by big pharma they just want you to get hooked on their drugs. wake up sheeple

just goes straight through, no worries mate

*Insulin binds to its receptor (tyrosine kinase linked) causing it to self- phosphorylate. This starts many signalling cascades.
* the final effect of these signalling cascades is translocation of the Glut-4 transporter to the plasma membrane, allowing influx of glucose into the cell

it asks nicely

it spent all it's birthday money on a fake I.D. so it could get in with it's friends who are older, but forgot it's star sign according to the I.D. card and had it taken away like, the second time it tried to use it. so, glucose can't get into the cells for another year.

100% - it is all reabsorbed

90% - about 10% is excreted in the urine

50% - half goes back into circulation, the other half is excreted

ketoacidosis is a pathological metabolic state, marked by uncontrolled ketosis. Free fatty acids are oxidised to ketones. They are b-hydroxybutyric acid, acetoacetic acid and acetone. In ketoacidosis, the body fails to adequately regulate ketone production causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased. In extreme cases ketoacidosis can be fatal.

Ketoacidosis should be the goal of anyone trying to lose weight because it means you are burning fat and its super healthy and really good for you because all you have to do is eat some kale or drink some lemon juice and you can alkalise back to get your blood really alkaline and its so good for you.

glut-4 transporter

glut-c3.37 transporter

WE SHOULDN'T BE LETTING GLUCOSE INTO OUR CELLS! WAKE UP SHEEPLE!

hypoglycaemia

hyperglycaemia

hyperglycaemia

hypoglycaemia

Type 1 Diabetes, Type 2 Diabetes, and, 'other' (primarily gestational diabetes)

the one thats just some extra sugar and then the one where you don't make enough of that thing. these are the technical names.

Biguanide
First line treatment for DMII
Works by inhibiting gluconeogenesis, hence reducing release of glucose from the liver. Also reduces glucose absorption from GIT, and increases glucose uptake in fat tissue and muscle tissue.
Take with meals or directly after. Start low dose and increase slowly.
DOES NOT CUASE HYPOGLYCAEMIA
WEIGHT NEUTRAL
AEs
GIT upsets, lactic acidosis (serious but rare – kidney issues increase risk)
*********
• May initially cause GI distress
Contraindicated: undergoing testing using IV dye, kidney problems.
• Lactic acidosis

Usually only used when sulphynlurea dose maxed out.
Works by reducing insulin resistance, especially in peripheral tissues. They increase sensitivity to insulin. They also reduce the amount of glucose released from the liver into the blood stream. Do so by working on PPAR gamma to affect metabolism of nutrients.
Doesn’t matter if taken with food.
Will NOT cause hypoglycaemia as monotherapy.
IF DUAL THERAPY WITH INSULIN SECRETAGOGUES CAN CAUSE HYPOGLYCAEMIA OR WHEN TAKEN WITH SULPHNYLUREA AND METFORMIN
********
Heartfailure – do not use
Liver disease – do not use

Provides instant burst of glucose goodness so the brain can function

Sulphnylurea
It works by increasing the amount of insulin produced and released by beta cells of the pancreas. They do so by blocking the exit of potassium from the beta cell at the ATP sensitive potassium channel. Excess potassium in the cell leads to the depolarisation of the membrane. There is a subsequent influx of calcium. The raised intracellular calcium causes the emptying of insulin granules and the release of insulin.
Needs residual function in beta cells to be effective
Take just before a meal.
CAN CAUSE HYPOGLYCAEMIA
LINKED WITH WEIGHT GAIN
AEs
Hypoglycaemia
********
Weight gain, hypoglycemia

Incretin Mimetic
Acts like GLP-1, activating GLP-1 receptor, releasing hormone from the GIT to pancreas, ordering the release of insulin when glucose levels in blood are high. Will only work in the presence of glucose, so no risk of hypoglycaemia. It also reduces the amount of glucose released from the liver and slows gastric emptying. Delayed gastric emptying can also help decrease appetite and prolong feeling of fullness.
Given by subcut injection.
CAN CAUSE HYPOGLYCAEMIA IF TAKEN WITH SULPHONYLUREAS
AEs
N&V
Do not use in patients with kidney problems
*********
Given by injection
Severe kidney problems – do not use

Thiazolidinediones
Usually only used when sulphynlurea dose maxed out.
It works by reducing insulin resistance, especially in peripheral tissues. They increase sensitivity to insulin. They also reduce the amount of glucose released from the liver into the blood stream. Do so by working on PPAR gamma to affect metabolism of nutrients.
Doesn’t matter if taken with food.
Will NOT cause hypoglycaemia as monotherapy.
IF DUAL THERAPY WITH INSULIN SECRETAGOGUES CAN CAUSE HYPOGLYCAEMIA OR WHEN TAKEN WITH SULPHNYLUREA AND METFORMIN
********
Heartfailure – do not use
Liver disease – do not use

Alpha-glucosidase inhibitor.
Works on the surface of the small intestine to slow absorption of glucose into the blood by preventing the breakdown of carbohydrates from dimers to monomers.
Take just before a meal. Start low dose, increase slowly.
AEs
Flatulence, bloating and diarrhoea due to undigested carbohydrates in colon.
ON IT’S OWN DOES NOT CAUSE HYPOGLYCAEMIA
If dual therapy, and hypoglycaemia occurs, will need to treat with pure glucose.
*******
Abdominal distension and bloating Take just prior to meal

Alpha-glucosidase inhibitor.
Works on the surface of the small intestine to slow absorption of glucose into the blood by preventing the breakdown of carbohydrates from dimers to monomers.
Take just before a meal. Start low dose, increase slowly.
AEs
Flatulence, bloating and diarrhoea due to undigested carbohydrates in colon.
ON IT’S OWN DOES NOT CAUSE HYPOGLYCAEMIA
If dual therapy, and hypoglycaemia occurs, will need to treat with pure glucose.
*******
Abdominal distension and bloating Take just prior to meal

Sodium-Glucose Transporter Inhibitor (SGLT2 Inhibitor)
It works by inhibiting the reuptake of glucose into the blood from the nephron. Glucose is excreted in the urine instead of going back into circulation.
USED ON ITS OWN WILL NOT CAUSE HYPOGLYCAEMIA
AEs
Thrush, UTIs
Not suitable for patients with kidney problems
********
Urinary tract infections
Severe kidney problems

DDP-4 Inhibitor
It works by preventing the cleavage of GLP-1, hence, increasing release of insulin from the pancreas (only when glucose is present). Reduces amount of glucose released by the liver. They inhibit glucagon release.
USED ON ITS OWN WILL NOT CAUSE HYPOGLYCAEMIA
Subcut injecton
AEs
Nausea and headache
*********
Do not cause hypoglycaemia
Given by injection
Severe kidney problems – do not use

Biguanide
First line treatment for DMII
It works by inhibiting gluconeogenesis, hence reducing release of glucose from the liver. Also reduces glucose absorption from GIT, and increases glucose uptake in fat tissue and muscle tissue.
Take with meals or directly after. Start low dose and increase slowly.
DOES NOT CUASE HYPOGLYCAEMIA
WEIGHT NEUTRAL
AEs
GIT upsets, lactic acidosis (serious but rare – kidney issues increase risk)
*********
• May initially cause GI distress
Contraindicated: undergoing testing using IV dye, kidney problems.
• Lactic acidosis

Incretin Mimetic
Acts like GLP-1, activating GLP-1 receptor, releasing hormone from the GIT to pancreas, ordering the release of insulin when glucose levels in blood are high. Will only work in the presence of glucose, so no risk of hypoglycaemia. It also reduces the amount of glucose released from the liver and slows gastric emptying. Delayed gastric emptying can also help decrease appetite and prolong feeling of fullness.
Given by subcut injection.
CAN CAUSE HYPOGLYCAEMIA IF TAKEN WITH SULPHONYLUREAS
AEs
N&V
Do not use in patients with kidney problems
*********
Given by injection
Severe kidney problems – do not use

Sulphnylurea
It works by increasing the amount of insulin produced and released by beta cells of the pancreas. They do so by blocking the exit of potassium from the beta cell at the ATP sensitive calcium channel. Excess potassium in the cell leads to the depolarisation of the membrane. There is a subsequent influx of calcium. The raised intracellular calcium causes the emptying of insulin granules and the release of insulin.
Needs residual function in beta cells to be effective
Take just before a meal.
CAN CAUSE HYPOGLYCAEMIA
LINKED WITH WEIGHT GAIN
AEs
Hypoglycaemia
********
Weight gain, hypoglycemia

Sodium-Glucose Transporter Inhibitor (SGLT2 Inhibitor)
It works by inhibiting the reuptake of glucose into the blood from the nephron. Glucose is excreted in the urine instead of going back into circulation.
USED ON ITS OWN WILL NOT CAUSE HYPOGLYCAEMIA
AEs
Thrush, UTIs
Not suitable for patients with kidney problems
********
Urinary tract infections
Severe kidney problems

Alpha-glucosidase inhibitor.
Works on the surface of the small intestine to slow absorption of glucose into the blood by preventing the breakdown of carbohydrates from dimers to monomers.
Take just before a meal. Start low dose, increase slowly.
AEs
Flatulence, bloating and diarrhoea due to undigested carbohydrates in colon.
ON IT’S OWN DOES NOT CAUSE HYPOGLYCAEMIA
If dual therapy, and hypoglycaemia occurs, will need to treat with pure glucose.
*******
Abdominal distension and bloating Take just prior to meal

>7%

≤5%

Glycosylated (or glycated) haemoglobin
Glycosylated (or glycated) haemoglobin (haemoglobin A1c, Hb1c , or HbA1c, A1C) is a form of haemoglobin used primarily to identify the average plasma glucose concentration over prolonged periods of time. It is formed in a non-enzymatic pathway by hemoglobin's normal exposure to high plasma levels of glucose.
HbA1c of 7% or less should be set for all patients with type 2 diabetes
Any reduction of HbA1c is of benefit even if the 7% target cannot be met
HbA1c indicates glycaemic control during preceding 2–3 months; there is an association between the risk of microvascular complications and level of glycated haemoglobin. Monitor every 3–6 months.

glycated haemoglobin is a pointless measurement for long term observations because if you don't eat before the test it will make it go right down and ruin the results