Alright, so we know that when a person with diabetes has a bacterial infection their metabolic control becomes difficult, but why?
Well a bacterial infection will get our cells producing more TNF-a and IL-1b. These cytokines, in particular TNF-a, will attach to insulin receptors on cells.
What happens now? Insulin cannot bind to that receptor and so glucose cannot be accepted into that cell for metabolism. In other words, cytokines prevent insulin from binding to cells which = insulin resistance and consequently increased BGL.
Where does perio fit in? LPS (in periodontopathogen cell walls) --> stimulate monocytes/macrophages --> lots of cytokines --> bind to insulin receptors --> insulin resistance --> stops glucose moving into cells --> high BGL.
One more thing,
Insulin resistance = persistent hyperglycaemia = AGE (remember this from class) = attachment to macrohpages --> synthesis of more TNF-a and IL-1b = insulin resistance = high BGL. It’s like a vicious circle!
So really, in periodontitis cytokines are produced which inhibit the action of insulin; resulting in hyperglycaemia. When there’s hyperglycaemia we amplify the amount of cytokines because.. now AGE is involved in generating even more proinflammatory mediators.
Okay, so this is my understanding of how periodontitis influences metabolic control. Not 100% certain because I got a bit confused when I was researching :)
So basically: pro-inflammatory cytokines prevent insulin from binding to cells and thus glucose is not taken into cells effectively. During periodontitis, LPS causes host response from macrophages and monocytes to produce increased amount of pro-inflammatory cytokines, inhibiting insluin in higher numbers limiting glucose uptake further.
Alright, so we know that when a person with diabetes has a bacterial infection their metabolic control becomes difficult, but why?
ReplyDeleteWell a bacterial infection will get our cells producing more TNF-a and IL-1b. These cytokines, in particular TNF-a, will attach to insulin receptors on cells.
What happens now?
Insulin cannot bind to that receptor and so glucose cannot be accepted into that cell for metabolism. In other words, cytokines prevent insulin from binding to cells which = insulin resistance and consequently increased BGL.
Where does perio fit in?
LPS (in periodontopathogen cell walls) --> stimulate monocytes/macrophages --> lots of cytokines --> bind to insulin receptors --> insulin resistance --> stops glucose moving into cells --> high BGL.
One more thing,
Insulin resistance = persistent hyperglycaemia = AGE (remember this from class) = attachment to macrohpages --> synthesis of more TNF-a and IL-1b = insulin resistance = high BGL. It’s like a vicious circle!
So really, in periodontitis cytokines are produced which inhibit the action of insulin; resulting in hyperglycaemia. When there’s hyperglycaemia we amplify the amount of cytokines because..
now AGE is involved in generating even more proinflammatory mediators.
Okay, so this is my understanding of how periodontitis influences metabolic control. Not 100% certain because I got a bit confused when I was researching :)
Maria
ReplyDeleteIt makes perfectly good sense to me.
Well done
So basically: pro-inflammatory cytokines prevent insulin from binding to cells and thus glucose is not taken into cells effectively. During periodontitis, LPS causes host response from macrophages and monocytes to produce increased amount of pro-inflammatory cytokines, inhibiting insluin in higher numbers limiting glucose uptake further.
ReplyDeleteWell done guys.
ReplyDelete