One of the things we’re hearing about more and more these days is how organ fat, particularly liver and pancreatic fat, may influence the pathology of type 2 diabetes, and while most of the talk is centered on liver fat, we don’t want to forget about the pancreas here, as it plays a pretty central role in our disease to be sure.
We do know that peripheral adiposity, what we commonly call the state of being fat, does contribute to diabetes quite a bit, but perhaps nothing like how fat in non adipose tissue, like in the pancreas, messes us up.
If you’ve read my series on The Heart of Diabetes, where we looked at some of the work of Dr. Roger Unger, who is far and away the most brilliant diabetes researcher of all time I might add, you’ll remember that he spoke about the ravages of lipotoxicity in pancreatic islets, and in particular, in the alpha cells of the pancreas, the ones that secrete glucagon, the opposite of insulin and what raises our blood sugar.
So as it turns out, our glucagon levels are way too high as type 2 diabetics, and bringing these levels down is fundamental to fixing the problem and improving our glucose metabolism to a non diabetic state. Excess glucagon even can be said to equal diabetes itself, it if is high enough, turn it down, you’re not diabetic anymore, it’s really that central to the disease.
People also look at the other type of islet cells, the beta cells, and there is some dysfunction that is present there too, from lipotoxicity primarily, as well as glucotoxicity, and things like excessive inflammation, but for practical purposes, this is not our problem at all as far as being type 2 diabetics is concerned. Rather, we still tend to secrete too much insulin even with our beta cell dysfunction.
So restoring beta cell function, in itself, isn’t really going to solve the problem, and actually may even make things worse, as if your insulin levels are already too high, and high insulin causes lipotoxicity, and lipotoxicy causes high glucagon, and high glucagon causes diabetes, all of which is true, then you’re just fueling the fire by worrying about that, and are on the wrong track entirely as well.
So now, they are looking at pancreatic fat, for instance in this particular study they found that, basically, type 2 diabetic men have more pancreatic fat than similarly obese non diabetic men. I guess that’s good info to have, but we do want to keep this in perspective, as this doesn’t mean that the pancreatic fat is in itself causing or even contributing to the disease.
Rather, it makes more sense to say that this is probably just a proxy, and in other words, if the pancreas is exposed to more fat, this is indicative of it being exposed to more toxicity from fat. However, it’s not a great idea to have excess pancreatic fat either, but it’s not necessarily quite as simple as people like Dr. Roy Taylor of the Newcastle Diet fame would have us believe, that we need to lose one gram of fat, the gram in our pancreas, and then we’ll be OK.
It’s certainly true though that losing this one gram of fat will be indicative of things improving, but not necessarily due to the loss of that gram, that’s the important thing. What we need to do is look closely at what is behind this, we know that for instance high insulin causes such things, as does excessive carb intake, and there are other things to look at as well.
So the Newcastle diet does indeed address some of these metabolic markers, as it’s basically a starvation diet, but it’s not just a matter of getting rid of that pancreatic fat and then going back to whatever you were doing before, because the problem will just come back. I do think that fasting does have its place for sure, intermittent fasting in particular, which is another topic for another day really, but one that I need to speak more about for sure.
I really like this study though and it’s not because they showed that diabetics have more pancreatic fat, that’s no real surprise really, but what stands out for me is seeing the much higher triglyceride levels with the diabetics with the pancreatic fat than the non diabetic obese controls.
The controls had a triglyceride level of 1.2, very normal, where those with the pancreatic fat averaged 2.4, which is quite high, and the normal range here is 0.6 to 1.7, and outside of 1.7 you are now in the top 5%, meaning that 95% of people have lower levels. So to be at 2.4, you are in the top couple of percent of people, at the head of the class where high triglyceride levels are concerned.
Now we know that this causes fatty organs for sure, so there you have it, we’re on to something now. We can very reasonably expect that if these folks reduced their triglyceride levels down to where the controls were, then we may not be seeing this extra pancreatic fat at all.
So now let’s look at their fasting insulin levels. The controls actually had pretty high fasting insulin, which isn’t too surprising given that these people were overweight, with both groups coming in at around 30 BMI. Given that their triglyceride levels were well in the normal range, right around the mean actually, then given that we know that excess insulin puts this up, a fasting level of 56 wouldn’t be high enough presumably, and the diabetics must have fasting insulin a lot higher.
This is indeed the case, as their fasting insulin levels averaged a crazy 100 pmol/l. To give you an idea of how high this is, a normal person will only peak at around 60 after a high carb meal, and only stays that high for a brief period, and a healthy fasting insulin range is below 10, and some say even below 5. So these people are at 100 even without eating.
The non diabetics, with their fasting levels of 56, are hyperinsulinemic for sure, but as you can see, this is by degree, and more is worse, and more likely is driving up triglycerides to the roof and this is what is poisoning our pancreatic cells as well as making them fat.
Of course, there are the people who would say, nah, we don’t make too much insulin, we need more, and they would shoot up these people with more, hoping that this is going to fix things for them, and one of the things that this does is elevates triglyceride levels even higher, and in turn, causes more lipotoxicity and pancreatic fat.
It’s also worth noting that both total cholesterol and LDL cholesterol was lower in the diabetic patients, this is about triglycerides, not LDL. It’s also worth noting that the capacity for insulin secretion was reduced in the diabetic patients, not surprisingly, but the need for it is what the problem is here, too much insulin resistance in other words, which was, not surprisingly, notably higher. So the problem is, in a nutshell, too much insulin resistance in the diabetics.
By the way, the diabetic patients had twice as much pancreatic fat, corresponding almost exactly to their twice as high insulin levels and twice as high triglycerides.
We need to pay a lot more attention to all of this, but at the clinical level, we worry about our blood sugar of the moment instead, and worry about that exclusively, and don’t worry about making our pancreas fatter, and that’s the real problem here.