The fact that obesity, a major risk factor for type 2 diabetes, and diabetes itself, are inflammatory conditions, led to investigations exploring whether inflammatory mediators
predict the development of type 2 diabetes in populations at risk. Several such studies have now confirmed that the presence of inflammation predicts the development of type 2 diabetes. The first of these studies by Schmidt et al. showed that the presence of inflammatory mediators predicted the future occurrence of type 2 diabetes in adults [11] and was part of the larger Atherosclerosis Risk in Communities Study (ARIC). A recent paper from the same study continues this theme by showing that elevated plasma concentrations of sialic acid, orosomucoid, IL-6 and CRP predict type 2 diabetes [12]. An overall inflammation score based on these four indices, the total leucocyte count and plasma fibrinogen concentration, provided an increased
risk of 3.7 (when comparing the highest and the lowest quintiles) in white non-smokers for the development of type 2 diabetes [13]. There are at least three other prospective studies confirming the fact that an increase in inflammatory indices at baseline predicts type 2
diabetes and insulin resistance [14–17]. Similarly, there is also a correlation between fasting insulin concentrations and CRP concentrations in plasma [5,18,19], indicating that insulin resistance and inflammatory processes are related and that in association with the other facts
discussed there might be a causal link. Novel data have now appeared showing that the concomitant presence of promoter polymorphisms of TNF-a (G-308A) and IL-6 (C-124G) in obese subjects with impaired glucose tolerance carry twice the risk of conversion to type 2 diabetes when compared with other genotypes. A G-308A mutation of the TNF-a promoter is associated with increased plasma TNF-a concentrations and a 1.8 higher risk of developing diabetes compared to noncarriers. A C-124G mutation of the IL-6 promoter increases the risk for insulin resistance [20].
TRENDS in Immunology Vol.25 No.1 January 2004
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So, what do think about what your wrote? Do you believe that a blood test can predict whether a person will become obese? Is this something that we could measure in school-age students and start interventions earlier?
ReplyDeleteIn my opinion the important part (clinical) in metabolic syndrome and diabetes is screening.
ReplyDeleteWe still don't know what kind of test can be useful for screening and early diagnosis.
On the other hand most of the cases are diagnosed after middle age and change the life style is so hard in that age.
In cellular mechanism which step occurs first,inflammation cause diabetes or diabetes cause inflammation?
If we know inflammatory pathways are involved in diabetes,why we don't use anti inflammatory drugs in diabetes?
Almost all articles talk about visceral adipose tissue,Is there any difference between adipose tissues?
In the article that I found and then posted, I did find that what the authors wrote was very interesting.
ReplyDeleteIn persons that are obese, they have overfilled their nutrients and are "over nutritious" to an extent of being "no longer nutritious." Lifestyle changes and changes to diet and exercise are the biggest changes that someone can make in order to "prevent" becoming obese but having the availability of blood testing as another tool in the toolkit in order to "prevent" becoming obese can not be ignored. Just because your lab results do not signal alarming inflammatory markers, it by no means makes you exempt.
Interesting post Rob, did the articles indicate whether the blood inflammation markers are specific for diabetes or would someone with an infection or a sprained ankle also test positive for those factors?
ReplyDeleteIn either case it presents an interesting clinical question: when do we test someone for these markers and how much weight do the test results carry.