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Diabetes
Diabetes
o Adipose (fat) – to increase glucose uptake, promote lipid synthesis from glucose, and decrease lipid
breakdown
o Liver – to decrease glucose production, and promote glycogen and lipid synthesis from glucose
· Process:
o Insulin binds to specific receptors on the cell surface.
o Secondary messengers initiate a signal cascade to stimulate glucose uptake.
o A drop in blood glucose level leads to decrease release of insulin.
o Combinations:
Ultra-long-acting insulin + rapid acting insulin analogue e.g., Ryzodeg 70/10
Administered once daily with main carbohydrate meal
· Risk factors:
o Overweight/ obesity
o Physically inactive
o Hypertension
o Low high-density lipoprotein (HDL) or high trigylcerides
o Age, 45 or older
o Family history
o History of gestational diabetes
o Ethnicity – African American, Hispanic, Pacific Islander
o AGEs and retinopathy – diabetic related damage to the blood vessels of the retinal.
Role of AGEs:
Increase vessel permeability causing leakage and breakdown of the blood-retinal barrier
Increase vascular stiffness
Upregulate VEGF which stimulates angiogenesis and neovascularisation
o AGEs and nephropathy – diabetic related damage to the kidney which leads to haemodynamic changes
(hyperfiltration and hyperperfusion), proteinuria, poor glomerular filtration rate and eventually renal failure.
Role of AGEs:
Reduce glomerular filtration capacity by altering normal structure of ECM proteins and basement
membrane permeability
Stimulate growth factors and cytokines which induce hyperfiltration and hyperperfusion
o AGEs and neuropathy – diabetic induced nerve damage. Typically, affects peripheral tissues e.g., legs and
feet.
Role of AGEs:
Modified axon proteins leading to nerve fibre atrophy
Increased micro vessel permeability and reduced nerve blood flow, inducing hypoxia.
Paramacular capillary
non-perfusion