Type 2 DM: Epidemiology & pathogenesis
26 important questions on Type 2 DM: Epidemiology & pathogenesis
Why has their been an increase in Type 2 Diabetes Mellitus (T2DM) in the past decades in the Netherlands?
What is expected in the trends in T2DM prevalence in the coming years?
Why is the disease burden of people with T2D high?
Because of its association with other diseases: dementia, cardiovascular diseases, hypertension, etc.
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How is the life expectancy of someone with T2D?
- and when someone has T2D + cardiovascular disease, the life expectancy is about 5 years shorter.
What is the role of genetics in T1D and T2D?
Mutation in what kind of genes are associated with T2D (in GWAS studies)?
- Mutation in these genes only explains 10% of genetic predisposition.
Besides beta-cells, what types of genes also are associated with T2D?
What three organs play a role in the pathogenesis of hyperglycemia, and what is their role in healthy individuals?
- Pancreas (produces insulin in beta-cells)
- Muscle (stores glucose → glucose production by liver goes down → glucose levels go down)
What three factors cause hyperglycemia (think about the 3 important organs)?
- increased glucose production by the liver
- decreased glucose uptake in muscle
What can be shown by a glucose tolerance test, and what is the difference in that test between people with a normal glucose tolerance and people with impaired glucose tolerance?
- Obese, with normal glucose tolerance: less glucose uptake in muscle, compensated with higher insulin levels → glucose levels in the blood are normal.
- Obese, with impaired glucose tolerance: muscle cells are even more insulin resistant. Despite really high insulin levels, the glucose levels in the blood are higher than normal.
When someone develops diabetes, what does the glucose tolerance test show?
- somewhat lower insulin levels (due to beta-cell dysfunction),
- high blood glucose levels.
How can the high hepatic glucose production in people with T2D be shown?
Treatment strategies are often focused on these 3 aspects of T2D development. What does Metformin do?
What other organs are also involved in the pathogenesis of T2D?
- Adipose tissue
- Gut
- Kidney
- Brain
How does insulin lead to glucose uptake in the muscle?
- A cascade, in which PI 3 kinases are involved, is activated
- The cascade leads to translocation of GLUT receptors
- Those receptors facilitate the uptake of glucose in the muscle cell
What does a defect in this pathway lead to, and what is the most common point of defect in this pathway?
- and this defect is very common at the level of PI 3 kinases.
What organ plays a role in disturbing the insulin signaling cascade, and by which substances?
- by the release of pro-inflammatory cytokines and free fatty acids.
- These substances lead to insulin insensitivity in the muscle.
Besides disturbing the insulin signaling cascade, what can free fatty acids from adipose tissue also cause?
What is a potential mechanism for the development of cardiovascular diseases in people with T2D?
- When insulin binds on these receptors, 2 pathways that lead to NO production (vasodilation) and ET-1 production (vasoconstriction) occur.
- In healthy individuals, there is a balance between NO and ET-1.
- In people with T2D, the NO pathway is impaired, leading to high ET-1 levels (also because of the extra high insulin levels).
- These high ET-1 levels may cause cardiovascular disease.
What is the role of the gut, and gut hormones, in T2D?
So their insulin levels are about the same after an oral or an intravenous load.
What drugs can be given to counteract incretin resistance?
What is another possible role of the gut in the pathogenesis of T2D?
What role does the kidney play in the pathogenesis of T2D?
- In T2D, the SGLT-2 reabsorption is higher (although some glucose ends up in the urine).
How can this effect in the kidney possibly be targeted?
What is the role in the brain in the pathogenesis of T2D?
What is a possible target for this brain effect?
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