Visceral fat and insulin resistance – causative or correlative?

Having been introduced to "the English guy" aka Keith Frayn, I've discovered a rather extensive, as well as diverse, body of work by this researcher.   I'm sure to be sharing more in the coming weeks.  

The association between abdominal fat accumulation and risk of chronic diseases, including type II diabetes and coronary heart disease, has long been recognized. Insulin resistance may be a key factor in this link. Many studies have pointed to an association between insulin resistance and intra-abdominal fat accumulation (visceral obesity). However there is no clear proof of a causal link between visceral fat accumulation and insulin resistance. In assessing the probability of a causal link, it is useful to consider potential mechanisms. One such potential causal link is the release of non-esterified fatty acids from visceral fat into the portal vein, so that they have direct effects on hepatic metabolism. Visceral fat has been shown in many studies to exhibit a high rate of lipolysis compared with subcutaneous fat depots. However, if the idea that visceral fat releases fatty acids into the portal vein at a high rate is examined critically, a number of difficulties appear.  Not least of these is the fact that continued high rates of lipolysis should lead to the disappearance of the visceral fat depot, unless these high rates of fat mobilization are matched by high rates of fat deposition. There is far less evidence for high rates of fat deposition in visceral adipose tissue, and some contrary evidence. Evidence for high rates of visceral lipolysis in vivo from studies involving catheterization of the portal vein is not strong. If this potential link is discounted, then other reasons for the relationship between visceral fat and insulin resistance must be considered.  One is that there is no direct causal link, but both co-correlate with some other variable. A possibility is that this other variable is subcutaneous abdominal fat, which usually outweighs intra-abdominal fat several-fold. Subcutaneous fat probably plays the major role in determining systemic plasma non-esterified fatty acid concentrations, which are relevant in determining insulin resistance. In conclusion, there is at present no proof of a causal link between visceral fat accumulation and insulin resistance, or the associated metabolic syndrome. The possibility of co-correlation with some other factor, such as subcutaneous abdominal fat accumulation, must not be forgotten.
Hmmmm.... Co-correlation.  

This article discusses essentially 5 types of "central adiposity", so I might suggest an alternate title of "Central fat and insulin resistance".
  • Intra-abdominal, aka Visceral Fat:  mesenteric and omental (pot-belly) in the front, and perirenal/retroperitoneal (as you see on my diagram these are different depots but described as the same in the article, so I take their intention to be non-subQ back fat).
  • Subcutaneous:  anterior (paunch) and posterior (love handles)
Here is a good diagram of where each of the various adipose depots are located:
Some excerpts:

A number of studies have been aimed at identifying which of these various abdominal depots is most closely associated with insulin resistance. This is problematic since the subcutaneous and intra-abdominal depots are themselves correlated ...
One approach used specifically to examine the contribution of the intraabdominal depots has been to select subjects with large or small amounts of intra-abdominal fat, but to match them for total body fat and for subcutaneous abdominal fat.... this approach seemed to show that intraabdominal fat accumulation is associated with insulin resistance ... [but in this] study the groups did also differ in subcutaneous abdominal fat (by 11% on average) ...  the complementary experiment, matching for intra-abdominal fat and comparing people with high and low amounts of subcutaneous abdominal fat, has not been done. 
Another approach is to study a large number of people and use correlation analysis.  Studies using this technique show that the closest correlation with insulin resistance is seen with the subcutaneous abdominal depots.   Interestingly, these studies seem to show that the posterior subcutaneous depot is more closely associated with insulin resistance than is the anterior depot ... perirenal depot in these studies is clearly not associated with insulin resistance.
There is, then, a clear association between abdominal obesity and insulin resistance. Some studies suggest that the intra-abdominal or visceral depots show the closest link with insulin resistance, although others do not, and more evidence on this point is needed. However the observation of a link between abdominal obesity and insulin resistance does not mean that the former causes the latter. It could mean that insulin resistance causes abdominal obesity, or that both abdominal obesity and insulin resistance co-correlate with some other factor. 

Here's a summary of the results/conclusions for each of the five fat types:

1.  Anterior SubQ (aka paunch, muffin top, belly roll, over the belt flop):  Associated with IR

2.  Posterior SubQ (aka love handles, haunches):  Associated with IR, stronger than ASQ

3.  Omental (aka beer belly, pot belly) & 4.  Mesenteric:   Associated with IR but the Portal Theory (that these depots release NEFA into the portal vein therefore have a direct effect on the liver is not born out by in vivo studies.  "Some studies suggest that the intra-abdominal or visceral depots show the closest link with insulin resistance, although others do not"

5.  Perirenal:  Not associated with IR


Matt Stone said…
Definitely correlative. In fact, blood sugars can be decreased (all postprandial readings and fasting levels) quickly and reliably even WHILE abdominal fat is increasing. I perfected my glucose metabolism while gaining fat, most of it around the middle, which - a year later, is very much reduced.
CarbSane said…
Frayn seems to have looked only at one causal direction ... that being visceral fat --> IR. The alternative being that VF & IR are correlated with (and or perhaps caused by) some common third factor.

Not sure what to make of your experience there. I don't have BG issues yet my remaining fat is far more centralized than my "normal" (all my adult life until losing weight on Atkins in the late 90's) fat distribution. Would like to do something about this, and it would be nice to know if I have visceral fat correlating with my subQ belly fat.
Matt Stone said…
I believe the VF and IR are caused by elevated cortisol and 11 Beta HSD activity. Induced primarily by the stresses of chronic infection, chronic inflammation, mental and emotional stress, and subtle nutrient inadequacy.

The drop in postprandial and fasting BG is not just a personal experience, but one repeated now with very high success percentage amongst over a dozen people who have followed my basic template and tested BG throughout.
Matt, so that solves the mystery of why you increased your insulin sensitivity even you had a large belly.
CarbSane said…
Matt, on that list of cortisol elevators, I don't have any infection or inflammation that I'm aware of. Stress? Sure, but no more than I dealt with during some periods before I tried LC the first time. Maybe nutrient inadequacy would have to be the culprit. To be fair, I'm not sure if my shift to central fat is VF or SubQ, but not sure it matters either. I don't like it, or the possible health implications. My BG's would indicate I'm not insulin resistant. Puzzling :)
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