Term
What is the IDF critera for > FBG?
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Definition
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Term
| What two scientists have questioned the MS as a syndrome? |
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Definition
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Term
| For MS to be a S it must be greater than the sum of its parts and there must be an underlying biological aetiology, T/F? |
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Definition
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Term
| The IRSsPI3 kinase pathway mediates insulins metabolic actions and is overactive when obesity is present, T/F? |
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Definition
| F. It is the pathway that mediates insulins metabolic action but it is underactive when obesity is present. |
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Term
| The second unaffected pathway is the Sch Sos Ras pathway, T/F? |
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Definition
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Term
| Draw the whole pathway that starts with obesity |
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Definition
Obesity
Imparied PI-3 Kinase signalling
> Glucose
> Insulin = Hypertension
> MAP kinase signalling
> cytokine production
> 11B - HSD-1 expression
> corticosterone production
> Hepatic VLDL production
> Plasma triglycerides. |
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Term
| Explain in 1 sentence how insulin resistance and MS fit together. |
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Definition
| The MS may be secondary to an obesity induced, pathway selective defect in insulin signalling. |
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Term
| What is a normal blood glucose level? |
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Definition
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Term
| Where is insulin secreted from and how? |
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Definition
| Insulin is secreted by the beta cells of the pancreatic islets of Langerhans is response to > blood glucose. The glucose enters the cell from the blood via the GLUT2 transporter and is metabolised to > ATP that then blocks the ATP gated K channel that means K cant get in therefore depolarising the membrane, allowing Ca2+ to get in that then triggers the exocyotosis of insulin and thus insulin levels are raised. |
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Term
| How are glucose levels lowered? |
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Definition
| Glucose is converted to glycogen and this is stored in both muscle and liver. There is an increased uptake of glucose into cell and gluconeogenesis is inhibited. When insulin is present there is a favouring to make the excess blood glucose into fatty acids for storage. |
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Term
Insulin is a peptide hormone that has 3 stages.
What are the 3 stages and what identifies them? |
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Definition
Preproinsulin. Still has signal sequence.
Proinsulin. No signal sequence but still has C peptide chain.
Insulin. No C peptide, only A and B chain. |
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Term
| What is glucagon and where does it come from? |
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Definition
| Glucagon is a peptide hormone secreted from the alpha cells of the pancreas and they raise blood glucose levels (opposite of insulin). |
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Term
| GLUT4 expression increases with endurance training and when insulin is present GLUT4 transporters are sent to the membrane. When insulin levels drop these transporters are endocytosed. |
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Definition
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Term
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Definition
Glucose uptake by muscle decreases so blood glucose remains high. Glycogen systhesis is inhibited so stores are depleted. This make the hyperglycaemia worse.
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Term
| Hyerglycemia is defined as ... |
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Definition
| excessive amount of glucose circulating in the blood plasma, usually > than 10mmol/l |
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Term
| Glucose and adipose tissue (fat): |
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Definition
| Glucose is not taken up and therefore there is an incresed lipolysis or triglycerides. This then makes FFA (free fatty acids). These then make ketones that make ketone bodies that lead to diabetic ketoacidosis. This is when glucose appears in the urine and takes water with it that leads to dehydration. |
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Term
| Why are ketone bodies used? |
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Definition
| Do to the insufficnt glucose in the cell and the depletion of glycogen the 'starvation' energy source is used, this being the ketone body. |
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Term
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Definition
1. BGL low. Insulin high. The tissue develops a resistance and so an increase in insulin is made by the body. This is Hyperinsulineamia.
2. BGL high. Insulin High. the insulin doesnt fix the problem. hyperglycemia and hyperinsulinemia.
3. BGL high. Insulin low. beta cells die due to high glucose levels and this means there is less insluin made. |
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Term
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Definition
| Is all about insulin resisance that gets worse over time if things dont change. Result in metabolic changes in FFA level and high glucose levels that harm the function of the beta cell that cause it to die. |
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Term
| The insulin receptor is a ____ _______ with 2 ___ and 2 ___ subunits. The ____ subunit is a ___ |
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Definition
| preformed heterotetramer, alpha, beta, beta, tyrosine kinase. |
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Term
| The insulin receptor comes together from 2 monomers and is either active or inactive. T/F? |
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Definition
| F. It is preformed and has tonic, allosteric regulation |
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Term
| The insulin receptor is highly ____ and ____. This means it responds to a low conc of the ligand and only to that ligand. |
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Definition
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Term
| IRS1 stands for _________. Tyrosine phospholation of the insulin receptors, upon extracellular ligand binding, induces the cytoplasmic binding of IRS-1 to these receptors, through its ___. Multiple tyrosine residues of IRS-1 itself are then phosphorylated by these receptors. This enables IRS-1 to activate several signalling pathways, including the ____and the ___. |
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Definition
| Insulin receptor substrate 1, SH2 domains. PI3K pathway, MAP kinase pathway. |
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Term
| IRS1 is a _____ protien that provides a ___ function. |
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Definition
| Signalling scaffold, bridge/platform. |
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Term
| Insulin resistance is _____ |
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Definition
| a subnormal biological response to a normal amount of insulin. |
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Term
| A reason for insulin resistance is phosphorylation of additional (serine) residues on IRS1 will stop signalling for IRS1. |
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Definition
| This means insulin binds receptor but the scaffold protien is not working the way it should |
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Term
When there is low BG levels the pancreas...
Where there is high BG the pancreas... |
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Definition
releases glucagon from alpha cells and liver releases glucose into blood. Glyocgen to glucose and new synthesis of glucose.
releases insulin from beta cells and cells then take in glucose from blood. Glucose to glycogen and synthesis of glucose is slowed. |
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Term
| In type 2 diabetics, the 2nd insulin spike is missing, T/F? |
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Definition
| F, it is the first spike that is missing |
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Term
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Definition
Polyuria (excessive piss) = dehydration
Hyperglycaemia = high glucose blood levels
Macrovascular disease = Atherosclerosis
Microvascular disease = Retinopathy
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Term
T2D, carbohydrate and lipid metabolism is stuffed, the microcirculation is stuff so blurred yees, the mouth is dry from dehydration, the aim is to lower the blood glucose levels so they all stop. This is done with 3 types of drugs that fix
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___ |
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Definition
Insulin secretion
Insulin resistance
Limit glucose absorbtion
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Term
| Insulin secretion: This is fixed by using |
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Definition
| Sulfonylurea's. These increase endogenous insulin secretion from Beta cells by binding to KATP chanells and reduce K+ premeability thus depolarisation and Ca2+ entry and therefore insulin secretion. |
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Term
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Definition
Biguanides: Metformin.
This is the 1st line most common treatment for T2D.
Metformin improves hyperglycemia primarily through its suppression of hepatic glucose production (hepatic gluconeogenesis).[82] The "average" person with type 2 diabetes has three times the normal rate of gluconeogenesis; metformin treatment reduces this by over one third.[104] Metformin activates AMP-activated protein kinase (AMPK), a liver enzyme that plays an important role in insulin signaling, whole body energy balance, and the metabolism of glucose and fats;[105] activation of AMPK is required for metformin's inhibitory effect on the production of glucose by liver cell |
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Term
Limit glucose absorbtion:
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Definition
Alpha glucosidase inhibitors:
Block the enzymes that digest and promote absorbtion of starches in the small intestine. |
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Term
| How to DPP4 inhibitors and GLP-1 agonists work? |
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Definition
DPP4 or dipeptidly peptidase 4 inhibitors work by inhibiting the enzyme that breaks down the incretins like GLP1 and GIT. These incretins normally regulate blood glucose levels but when inhibited dont. So this stops the inhibition. The incretins can then have 2 actions
1. Stimulates insulin release
2. Inhibits glucagon release
These together work to lower blood glucose |
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