In this week’s discussion the class is covering the topics of Obesity, Type 2 Diabetes, and Metabolic Syndrome based from the articles posted on the 495 website. An interesting point that reoccurs in all of the articles is about Insulin Resistance. The development of insulin resistance is not yet known. However, we know it is a precursor of type 2 diabetes and increases amongst the obese population. There are no genetic connections that can be determined yet about insulin resistance. Do you think that understanding the development of insulin resistance is the goal in helping eliminate and control Type 2 diabetes and metabolic syndrome amongst the obese population?
It appears that once scientists are able to fully understand the pathway of insulin resistance, a big advancement will be made in these three inflammatory diseases. Obesity, a state of chronic inflammation, is the root cause for these inflammatory diseases which links insulin resistance amongst them. Adipose tissue is now known as a major endocrine organ. Some of the chemicals excreted here adiponectin, leptin, TNF-a, resistin, IL-6, and CRP. These chemicals have a direct affect upon obesity, diabetes, and metabolic syndrome. The one process that seems to be interconnected amongst all of these is insulin resistance. Once this process is determined, doctors will be able to control the inflammation pathways that cause these diseases to get out of control. What I propose is that once the scientists and doctors figure out this pathway, they will be able to control diabetes, metabolic syndrome, as well as other inflammatory diseases amongst the obese. One will be able to be obese without these health concerns.
05 September 2007
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It's interesting to look at where the cytokines are being produced in obesity...TNF-alpha seems to be made by macrophages that have infiltrated the adipose tissue, whereas the adipose tissue itself is making leptin and adiponectin. It seems that the body is doing everything it can to decrease the fat load, but we just keep over-riding it with another trip to McDonalds!!
TNF-α can also be produced by adipose tissues, fibroblasts, and cardiac myocytes. TNF- α can also act as a appetite suppressant in the hypothalamus which makes it's link to the obesity issue kind of tough to deal with...if you keep increasing this particular appetite suppressant, you'd be ramping up the inflammation response and perpetuating the problem.
I think we should get working on that miracle pill - that way we can all retire after graduation fat and happy...and wealthy.
TNF alpha promotes inflammatory responses which causes diseases like Crohns and asthma as well as some other serious diseases. If TNF a was used to supress appetite issues there would be a sudden increase in other diseases such as the ones listed above. So, we are still in search of that miracle pill.
Dear Nathan,
I would like to briefly post some remarks on your intriguing question, "Do you think that understanding the development of insulin resistance is the goal in helping eliminate and control Type 2 diabetes and metabolic syndrome amongst the obese population?"
I fully believe that understanding insulin resistance, and more importantly, helping PEOPLE UNDERSTAND insulin resistance will go a long way to helping attenuate the concurrent epidemics of T2DM and the metabolic syndrome. Because insulin action varies about 6-fold amongst healthy people, and because "insulin resistance" is largely a SYMPTOMLESS condition, the condition is abstract and difficult for lay people to understand because they do not necessarily feel bad. So our biggest challenge beyond understanding it ourselves (as scientists) will likely lie in translating that message to the public.
While the typical assumption is that all obese people are insulin resistant, remember that this profile can be misleading. Ruderman and colleagues have identified "metabolically healthy obese" (MHO) people who, in fact, are quite obese but are remarkably insulin sensitive and with a normal lipid profile. On the flipside, there are people (in Finland) who are lean but are insulin resistant. These deviations from the typical profile will make it difficult for us, as health care providers and scientists, to concisely convey our messages about insulin resistance to the public. Overall though, you've captured the profile of insulin resistance quite nicely: overweight or obese, inactive, and consuming a diet high in saturated fats.
A most interesting commentary...thank you.
Terih- It is interesting that you brought up the point about certain populations being lean while still having insulin resistance or being fat with a properly working insulin system. This goes to help show one how little is still known about the full affects of this system on one's body. If scientists are able to decode this pathway there may be an explanation for these certain populations. Insulin resistance may even be more of a broad problem than we know of. Since it is symptomless, there very well could be a large part of the general population walking around with this problem and never will know it.
Nathan, please forgive my late response. Yes! I believe you have stated the problem quite well: there is a substantial proportion of the population with insulin resistance (and remember that those people presumably do not know they have it, or that there is anything wrong with it). In fact, the most recent data from NHANES (a large epidemiologic health surveillance mechanism) revealed a 35.1% increase in hypersinsulinemia among non-diabetic adults between 1994 and 2002 (See Ford et al, 2006). Striking, isn't it? TeriH
Nathan, please forgive my late response. Yes! I believe you have stated the problem quite well: there is a substantial proportion of the population with insulin resistance (and remember that those people presumably do not know they have it, or that there is anything wrong with it). In fact, the most recent data from NHANES (a large epidemiologic health surveillance mechanism) revealed a 35.1% increase in hypersinsulinemia among non-diabetic adults between 1994 and 2002 (See Ford et al, 2006). Striking, isn't it? TeriH
They will still have plenty of non-insulin based health concerns. Heart disease is a big one.
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