"Young adult obese
subjects with and without insulin resistance; what is the role of chronic
inflammation and how to weigh it non-invasively?"
Giovanni Tarantino*1, Patrizia Colicchio1, Paolo
Conca1, Carmine Finelli1,
Matteo Nicola Dario Di Minno1, Marianna Tarantino2,
Domenico Capone3
and
Fabrizio Pasanisi1
In the
above titled paper, the authors claim that both increased spleen diameter and
CRP (C-reactive Protein) are valid tools to utilize in diagnosing insulin
resistance. While the authors affirm that obesity is the leading risk factor
for metabolic syndrome which further expresses into non-alcoholic fatty liver disease,
they are sure to keep their experimental population within a range of people
that do NOT drink alcohol. They mention that this was strictly enforced by
utilizing the MAST (Michigan Alcohol Screening Test) and CAGE (Cut down,
Annoyed, Guilty, and Eye Opener) so that alcohol abused fatty liver acid would
be ruled out according to DSM-IV diagnostic criteria.
Since the
authors were so strict in enforcing the non-alcoholic form of fatty liver
disease (NAFLD), it came to my attention to question if the alcoholic form of
fatty liver disease (ALFD) was a better or less severe form of the disease, or
if it was indeed worse. Searching through some valid research articles, I found
this one to be helpful, yet with some grey areas still:
http://www.biomedcentral.com/content/pdf/1471-2458-10-237.pdf
Do
you think that it actually convinces us that one is better than the other
depending on the health situation of the person? Also, correlating to our theme
of obesity/diabetes, which type of fatty liver disease is more
"favorable" to have?
After doing a little further research on the progression and prevention of both Alcohol Related Liver Disease and Non-alcoholic Fatty Liver Disease, I have made the conclusion that neither type is more favorable than the other. It seems to me that the stage that each condition is at is more important in terms of reversibility of the condition.
ReplyDeleteFor example, with alcoholic induced liver disease, this condition often begins with fatty liver disease, and then progresses to alcoholic hepatitis, and finally alcoholic cirrhosis. Out of these stages, only fatty liver disease and mild alcohol hepatitis are reversible by utilizing a low fat diet, elimination of the diet, and possible medications. Severe alcoholic hepatitis and alcoholic cirrhosis result in permanent scarring of the liver and are not reversible.
Similar to Alcohol Induced Liver Disease, Non alcoholic Fatty Liver Disease also progresses in stages. This condition often begins as Fatty Liver Disease among people that are overweight or present with diabetes and can progress to Non-alcoholic steatohepatitis and eventual cirrhosis of the liver, which is not reversible as fatty liver disease is.
In relation to this paper, I think it would be very interesting to learn more about the reversibility of spleen enlargement related to Metabolic Disease and compare that to the reversibility of fatty liver disease.
http://www.liverfoundation.org/abouttheliver/info/alcohol/
http://www.liverfoundation.org/abouttheliver/info/nafld/
Thank you for you input April! It makes sense that both AFLD and NAFLD start out with a "base" if you will, of fatty liver disease. Evidently neither of these are favorable, and I think that your conclusion of neither one being more favorable over the other is the only one we can make in present time.
DeleteThe fact that the initial stages of both types of fatty liver disease are reversible makes me realize that diet control is simply the ultimate way to steer clear of liver disease period.
In regards to your inquiry of the reversibility of spleen enlargement in Metabolic Disease, I also thought that would be interesting to research. After a little browsing I found that it also depends on the stage in terms of enlargement that the spleen is at during the time of treatment. The problem I found was that the original paper talked about spleen diameter increase in metabolic disease, but most papers I researched related spleen enlargement to length and not specific to metabolic disease. I think that the paper "Young adult obese subjects with and without insulin resistance; what is the role of chronic inflammation and how to weigh it non-invasively" is too recent in order for there to be much research done on the spleen enlargement subject.
Although not always reliable, WebMD did bring to my attention that spleen enlargement in general is able to be treated by surgically removing it using laparoscopy. If it comes to this treatment, you would also need be put on medications and/or vaccines so that you can fight potential infections that are normally cleared by the spleen. So spleen enlargement (in general, not necessarily specific relation to metabolic disease) technically is reversible at any stage since it is possible to live without a spleen!
http://www.webmd.com/digestive-disorders/enlarged-spleen-causes-symptoms-and-treatments?page=2
I was just reading through the adiponectin + leptin post and I couldn't help, but think that a possibility of the cause of the spleen enlargement could be due to lipid oxidation. As Christian said in the first comment to the original post, lipid oxidation damages cells, which, in turn, causes an immune response and inflammation. So, that was my initial thought.
ReplyDeleteAfter that, I decided to look up some of the causes of splenomegaly on the Mayo Clinic website. I brought up, in class, that I would like to see if there is a direct connection between a fatty liver and splenomegaly and, of course, how they likely lead to insulin resistance. Well, it turns out, according to the Mayo Clinic website, that cirrhosis and other liver diseases can cause splenomegaly. That brought me to look at causes of cirrhosis. According to WebMD, a fatty liver is amongst the few most common causes of cirrhosis in the U.S.. I also looked at the causes of cirrhosis on the Mayo Clinic website as well, just for consistency, and accumulated liver fat is on the list of causes of cirrhosis there too. Just from those connections (not that I had ever doubted it, mind you), it would seem that one thing leads to another, which leads to another, until we have a chain reaction of unfortunate causes and diseases. Namely, something leads to cirrhosis, which leads to splenomegaly, which leads to something else, which possibly leads to insulin resistance.
Now, what I really like to know is- Where does the path start? If a fatty liver leads to splenomegaly and we can find a link to splenomegaly leading to insulin resistance, I would really like to know just what it is that starts this whole cascade.
I also looked up non-alcoholic fatty liver disease on the Mayo Clinic website and there's not a clear cause of the issue. They just state that the general issue is that the liver is having problems breaking down fats. I would have to do a good bit of more research before I came to any clear idea as to what is the actual cause of this disease, but I feel that this is a very good place to start looking in order to find more or more efficient ways to battle insulin resistance; at the very least, in terms of prevention.
Anyways, that's all I've got for now. I really loved all of the discussion for this topic and I'm really looking forward to more topics!
Adiponectin + Leptin post: http://inflammablog6.blogspot.com/2013/02/leptin-adiponectin-inflammation.html
Mayo Clinic on splenomegaly: http://www.mayoclinic.com/health/enlarged-spleen/DS00871/DSECTION=causes
Mayo Clinic on cirrhosis: http://www.mayoclinic.com/health/cirrhosis/DS00373/DSECTION=causes
Mayo Clinic on Nonalcoholic Fatty Liver Disease: http://www.mayoclinic.com/health/nonalcoholic-fatty-liver-disease/DS00577/DSECTION=causes
WebdMD on Cirrhosis: http://www.webmd.com/digestive-disorders/cirrhosis-liver
Thanks for that insight...that was actually something I had been thinking about as well when researching fatty liver disease in general. I agree with you that by finding a definitive cause for fatty liver disease (in the relation of it leading to splenomegaly and then insulin resistance)would be highly beneficial for insulin resistance prevention.
DeleteI did a little research to see if I could find more than Mayo Clinic's definition for the cause of fatty liver disease as you mentioned. I found that on top of just malnutrition and struggles of the liver to break down fats, other possibilities include certain metabolic and nutritional diseases as well as toxins. Some of these diseases that induce fatty liver were glycogen storage diseases, acute fatty liver of pregnancy, jejunoileal and gastric bypass, inflammatory bowel diseae, HIV, hepatitis C, and many more!
The following paper helped me realize all the possibilities that could be associated with the onset of fatty liver disease. As with basically any disease, it's near impossible to single out one definitive cause for the general population. I guess that's science for you haha.
http://www.ncbi.nlm.nih.gov/pubmed/16770927