Since becoming a Diabetes and Obesity "specialist" this past week, I have began to notice the presence of information on Diabetes and inflammation everywhere. I came across an interesting article recently published in Time titled "Why Inflammation Matters for Diabetics". I always find it interesting to come across articles discussing topics being taught in my physiology courses, so this article complimented these two weeks of diabetes and obesity discussion perfectly.
The article briefly discusses the role of inflammation in diabetes, as we were able to examine together as a group. What I found interesting was the article cites a research study performed by the American Heart Association, showing that anti-inflammatory drugs may be a new way to prevent cell damage and blood vessel disease in diabetics. Further researching the study, cells from the aorta were cultured and the ability to metabolize glucose was examined under normal conditions versus conditions of inflammation. In the condition where inflammation was mimicked in the cells, by the addition of interleukin-1 (IL-1), more glucose entered the cells compared to when there was no inflammation present. What I found interesting was when glucose entered the inflamed cells, the pathway to metabolize glucose created even more inflammation. Once an anti-inflammatory drug, anakinra, was added the inflammation was reduced and the negative effects on glucose metabolism reversed.
I found this study and article interesting because it highlighted yet another proposed method for treating the condition of Type II diabetes. Choosing to directly target inflammation associated with type II diabetes, with the use of anti-inflammatory drugs, may be a step in the right direction for the future treatment of diabetic patients.
References:
http://time.com/3329225/inflammation-diabetes/
http://newsroom.heart.org/news/inflammation-may-be-key-to-diabetes-heart-disease-link?preview=e861
The article briefly discusses the role of inflammation in diabetes, as we were able to examine together as a group. What I found interesting was the article cites a research study performed by the American Heart Association, showing that anti-inflammatory drugs may be a new way to prevent cell damage and blood vessel disease in diabetics. Further researching the study, cells from the aorta were cultured and the ability to metabolize glucose was examined under normal conditions versus conditions of inflammation. In the condition where inflammation was mimicked in the cells, by the addition of interleukin-1 (IL-1), more glucose entered the cells compared to when there was no inflammation present. What I found interesting was when glucose entered the inflamed cells, the pathway to metabolize glucose created even more inflammation. Once an anti-inflammatory drug, anakinra, was added the inflammation was reduced and the negative effects on glucose metabolism reversed.
I found this study and article interesting because it highlighted yet another proposed method for treating the condition of Type II diabetes. Choosing to directly target inflammation associated with type II diabetes, with the use of anti-inflammatory drugs, may be a step in the right direction for the future treatment of diabetic patients.
References:
http://time.com/3329225/inflammation-diabetes/
http://newsroom.heart.org/news/inflammation-may-be-key-to-diabetes-heart-disease-link?preview=e861
This article makes me think of GLUT 4 and how it works with inflammation. It also makes me curious about if/how the bodies of a non-diabetic versus a diabetic would attempt to regulate themselves.
ReplyDeleteThanks for sharing the article it is interesting so see something we're talking about in class out in the real world, especially one written so recently. What i found really interesting was that this time article doesn't seem consistent with one of the article we had to read for today's class. In the paper talking about inflammatory cytokines in women with cardiovascular disease their findings were that IL-1 was not significantly different among women with or without CVD or diabetes. This makes me wonder why the researchers in the study presented by the time article are looking at IL-1 in a diabetic model.
ReplyDeleteHello Dan and Alison!
ReplyDeleteThank you for your comments! I agree with you Dan that the findings of this study are not consistent with the findings of the paper discussed in class about inflammatory cytokines (IL-1) in women with cardiovascular disease. I hadn't read the paper on IL-1 and women when I wrote this blog post or else I would have commented on the inconsistencies between the findings of the two. The study from the American Heart Association does not provide much detail on the logistics or types of patients used in the study. I would be curious to know what type of patients were being studied that allowed them to find that correlation.
Madison, your comment that more glucose enters the cells under the inflammatory state surprised me; my understanding is that generally type II diabetes causes high blood glucose levels because the glucose is not being taken into cells efficiently. Glucose uptake is inhibited when insulin signaling is disrupted, like in insulin insensitivity associated with type II diabetes. I wonder if there is a mechanism for glucose entry into cells that is independent of insulin which inflammation specifically activates. Within the heart at least, glucose transport is less reliant on insulin because contraction stimulates GLUT4 translocation - maybe inflammation mimics some of the cellular effects of contraction?
ReplyDeleteFor more about glucose metabolism in the heart:
http://www.ncbi.nlm.nih.gov/pubmed/14766360