We’ve been talking about very low calorie diets in type 2 diabetes for a couple of weeks now. If you haven’t already, check out the links below to get up to speed and get the crucial context for what follows:
Click to read Can Type 2 Diabetes be Reversed
Click to read Very Low Calorie Diets & Type 2 Diabetes Reversal Part 1: Blood Glucose
Click to read Very Low Calorie Diets & Type 2 Diabetes Reversal Part 2: Insulin
To quickly recap, very low calorie diets, generally 300-1000 kcal/day, can cause dramatic improvements in blood glucose, insulin sensitivity, and insulin production.
That may be good enough for you to give it a go, but actually understanding what's going on will give you more options to achieve your health goals. So let’s look a little closer at type 2 diabetes generally and the effects of very low calorie diets specifically.
Your Liver as Your Blood Glucose Regulator
The liver is a key player in blood glucose regulation because it can store, make, convert, and release glucose. In other words, it can take up excess glucose from the blood to bring blood glucose down, or release glucose into the blood to bring the glucose concentration up.
The liver is pretty special in that it can do a number of things with regards to glucose (1):
Hopefully you’re getting the picture that these things work in overlapping cycles, much of it isn’t a one way street. Below you can see a very simplified diagram of what’s going on.
Click to read Can Type 2 Diabetes be Reversed
Click to read Very Low Calorie Diets & Type 2 Diabetes Reversal Part 1: Blood Glucose
Click to read Very Low Calorie Diets & Type 2 Diabetes Reversal Part 2: Insulin
To quickly recap, very low calorie diets, generally 300-1000 kcal/day, can cause dramatic improvements in blood glucose, insulin sensitivity, and insulin production.
That may be good enough for you to give it a go, but actually understanding what's going on will give you more options to achieve your health goals. So let’s look a little closer at type 2 diabetes generally and the effects of very low calorie diets specifically.
Your Liver as Your Blood Glucose Regulator
The liver is a key player in blood glucose regulation because it can store, make, convert, and release glucose. In other words, it can take up excess glucose from the blood to bring blood glucose down, or release glucose into the blood to bring the glucose concentration up.
The liver is pretty special in that it can do a number of things with regards to glucose (1):
- It can convert fructose and galactose into glucose.
- It can convert certain components of proteins and fats, as well as lactate and some other things into glucose in a process called gluconeogenesis (gluco for glucose, neo for new, and genesis for making).
- The liver can store the glucose, whether it came from the diet as glucose, was made from the conversion of fructose or galactose, or made via gluconeogenesis. The storage form of glucose is glycogen (think animal version of starch). The process is called glycogenesis (glyco for glycogen and genesis for making).
- The liver can also break down the stored glycogen back to glucose in a process called glycogenolysis (glyco for glycogen and lysis for breaking up).
- The liver can convert excess glucose into fat by a process called de novo lipogenesis (lipid is the collective term for fats and oils, and de novo implies new).
Hopefully you’re getting the picture that these things work in overlapping cycles, much of it isn’t a one way street. Below you can see a very simplified diagram of what’s going on.
In a large part these processes in the liver are directed by insulin (made by the beta-cells of your pancreas), and glucagon (made by the alpha-cells of your pancreas) (1).
Insulin, providing the liver responds normally to it, tells the liver to store glucose by converting it to glycogen; that’s as opposed to releasing glucose into the blood (2).
At the same time, insulin tells the liver to reduce gluconeogenesis and glycogenolysis (1). Insulin also tells the liver to increase conversion of glucose to fat via de novo lipogenesis (3-5).
Glucagon, again assuming a normal response, tells the liver to release glucose, which we’ve now seen can come from a breakdown of glycogen via glycogenolysis (6). Contrary to what you may read elsewhere, the effect of glucagon on gluconeogenesis isn’t so clear cut (7), but that probably doesn’t matter to you.
Insulin and glucagon are always floating around in our blood streams, but the ratio changes. It’s not so much an on/off switch, as it is like a set of dials on your stereo to adjust left/right balance and base/treble output.
If this is new to you, I know the terms can be a little confusing at first. When you learn them, you’ll be better able to understand your condition, and better at spotting poor advice, so hang in there.
The Insulin Resistant Liver
One of the organs that can become insulin resistant is the liver, especially when it starts to store excess fat (8-10).
This insulin resistance is somewhat selective in that not all messages from insulin are ignored equally. Basically, the insulin resistant liver doesn’t respond to insulin’s message to store glucose, instead the liver keeps releasing glucose when it should be holding onto it (11).
Another problem is that the liver does respond to the signal to convert glucose to fat, above we called that de novo lipogenesis. Normally we only see any serious de novo lipogenesis going on for a few hours after a carbohydrate containing meal (12).
In people with type 2 diabetes, metabolic syndrome, and in people with the closely related condition non-alcoholic fatty liver disease, de novo lipogenesis is switched on 24/7 (4,13-16).
Some of this is likely also not helped by glucagon being chronically high (17). Recent research shows that metformin, the most commonly used diabetes medication, actually works to counter the effects of glucagon (18).
For more on this, check out my video series on reversing type 2 diabetes here.
The Pancreas in Type 2 Diabetes
If insulin resistance is one side of the type 2 diabetes coin, insulin under-production is the other.
Although people with type 2 diabetes often have chronically high blood insulin concentrations, research shows us that the peak capacity for insulin production by the pancreas often starts to decline well before the problem is bad enough to result in a diagnosis of diabetes (19-21).
It’s the beta-cells of the pancreas that produce insulin, so we talk about this reduced capacity as a loss of beta-cell function. That loss of function is on average 50% by the time type 2 diabetes is diagnosed (19). This decline usually continues despite medication (22).
Recent work shows that the pancreases of people with type 2 diabetes don’t just loose function, but also shrink, change shape, and become fatty (23-26). Bare that in mind when we look at what happens to the pancreas after a very low calorie diet.
What happens to the liver during a very low calorie diet in someone with type 2 diabetes?
The wording of this question is important, because not everyone’s liver will respond the same way to calorie restriction. This caused a lot of concern in the past as it was known that starvation made the liver store more fat (27). In a liver that already has excess fat stores, like we see in type 2 diabetes and other conditions, things work a little differently as we’re about to see.
Only a few studies discussed in part 1 and part 2 have looked at the liver specifically, but the results are striking. The findings of Lim and colleagues are summarised nicely in the graphs below (23).
Insulin, providing the liver responds normally to it, tells the liver to store glucose by converting it to glycogen; that’s as opposed to releasing glucose into the blood (2).
At the same time, insulin tells the liver to reduce gluconeogenesis and glycogenolysis (1). Insulin also tells the liver to increase conversion of glucose to fat via de novo lipogenesis (3-5).
Glucagon, again assuming a normal response, tells the liver to release glucose, which we’ve now seen can come from a breakdown of glycogen via glycogenolysis (6). Contrary to what you may read elsewhere, the effect of glucagon on gluconeogenesis isn’t so clear cut (7), but that probably doesn’t matter to you.
Insulin and glucagon are always floating around in our blood streams, but the ratio changes. It’s not so much an on/off switch, as it is like a set of dials on your stereo to adjust left/right balance and base/treble output.
If this is new to you, I know the terms can be a little confusing at first. When you learn them, you’ll be better able to understand your condition, and better at spotting poor advice, so hang in there.
The Insulin Resistant Liver
One of the organs that can become insulin resistant is the liver, especially when it starts to store excess fat (8-10).
This insulin resistance is somewhat selective in that not all messages from insulin are ignored equally. Basically, the insulin resistant liver doesn’t respond to insulin’s message to store glucose, instead the liver keeps releasing glucose when it should be holding onto it (11).
Another problem is that the liver does respond to the signal to convert glucose to fat, above we called that de novo lipogenesis. Normally we only see any serious de novo lipogenesis going on for a few hours after a carbohydrate containing meal (12).
In people with type 2 diabetes, metabolic syndrome, and in people with the closely related condition non-alcoholic fatty liver disease, de novo lipogenesis is switched on 24/7 (4,13-16).
Some of this is likely also not helped by glucagon being chronically high (17). Recent research shows that metformin, the most commonly used diabetes medication, actually works to counter the effects of glucagon (18).
For more on this, check out my video series on reversing type 2 diabetes here.
The Pancreas in Type 2 Diabetes
If insulin resistance is one side of the type 2 diabetes coin, insulin under-production is the other.
Although people with type 2 diabetes often have chronically high blood insulin concentrations, research shows us that the peak capacity for insulin production by the pancreas often starts to decline well before the problem is bad enough to result in a diagnosis of diabetes (19-21).
It’s the beta-cells of the pancreas that produce insulin, so we talk about this reduced capacity as a loss of beta-cell function. That loss of function is on average 50% by the time type 2 diabetes is diagnosed (19). This decline usually continues despite medication (22).
Recent work shows that the pancreases of people with type 2 diabetes don’t just loose function, but also shrink, change shape, and become fatty (23-26). Bare that in mind when we look at what happens to the pancreas after a very low calorie diet.
What happens to the liver during a very low calorie diet in someone with type 2 diabetes?
The wording of this question is important, because not everyone’s liver will respond the same way to calorie restriction. This caused a lot of concern in the past as it was known that starvation made the liver store more fat (27). In a liver that already has excess fat stores, like we see in type 2 diabetes and other conditions, things work a little differently as we’re about to see.
Only a few studies discussed in part 1 and part 2 have looked at the liver specifically, but the results are striking. The findings of Lim and colleagues are summarised nicely in the graphs below (23).
Basically what these graphs show is a rapid – within one week – reduction in blood glucose (graph a), an equally rapid reduction in glucose release by the liver (graph b), and a more gradual reduction in liver fat (graph c).
Another study showed this reduction in glucose release from the liver was already substantial after just two days of a very low calorie diet (28). This was despite stopping volunteers’ medication.
These and other studies show that the liver rapidly becomes more insulin sensitive, and explains a lot of the rapid reduction in fasting glucose we discussed in part 1 (23,28,29).
Another study reported a liver fat reduction from 21% to 3% after 16 weeks of very low calorie diet (30). Similar diets also reduce liver fat in obese non-diabetic volunteers (31). Liver fat reduction is therefore a goal when it comes to reversing type 2 diabetes.
What happens to the pancreas during a very low calorie diet in someone with type 2 diabetes?
In part 2 of this series we saw that estimates of beta-cell function improved with very low calorie diets. More direct measures improve too, so we can conclude that the pancreas can, given the right circumstances, recover even in people on insulin (23,25).
Also, much as with the liver, the excess fat in the pancreas goes down (23,25). As fat goes down, function goes up. By function, I mean that the pancreas regains its responsiveness to rising blood glucose, and becomes more capable of releasing insulin (23,32).
This process in the pancreas is slower though, probably because the pancreas, unlike the liver, isn’t well equipped to shift fat.
What about glucagon?
One study that provided 1000 kcal/day for an average 10 kg weight reduction over an average of 8 weeks found glucagon reductions across the board (33). By that I mean fasting, peak, and during an oral glucose tolerance test. The other studies didn’t look specifically at glucagon.
Take home message
Very low calorie diets reduce fat in the liver and in the pancreas. The result is that the liver becomes more responsive to insulin, and the pancreas recovers in terms of both insulin production and appropriate response to glucose.
Warning!
I said it in an earlier blog, but this bares repeating – if you are planning on trying to reverse your type 2 diabetes, partly or fully, with diet and/or exercise, let your medical care team know so they can monitor you and adjust your medication to keep you safe.
That brings us to the end of part 3. In part 4 we’ll look at how all the changes discussed so far actually translate into glucose tolerance, in other words, how the body copes with carbohydrates.
This is really the big question because it’s all fine and good for things to look great while on a low calorie diet, but you can’t keep it up forever, so what matters is what happens afterwards.
Click here to read part 4.
References: click here for a full list of references
To learn more about type 2 diabetes and what you can do to better manage, and often reverse it, watch my free video education series. If you want one-on-one help dealing with your type 2 diabetes, contact me here to book a consultation.
Another study showed this reduction in glucose release from the liver was already substantial after just two days of a very low calorie diet (28). This was despite stopping volunteers’ medication.
These and other studies show that the liver rapidly becomes more insulin sensitive, and explains a lot of the rapid reduction in fasting glucose we discussed in part 1 (23,28,29).
Another study reported a liver fat reduction from 21% to 3% after 16 weeks of very low calorie diet (30). Similar diets also reduce liver fat in obese non-diabetic volunteers (31). Liver fat reduction is therefore a goal when it comes to reversing type 2 diabetes.
What happens to the pancreas during a very low calorie diet in someone with type 2 diabetes?
In part 2 of this series we saw that estimates of beta-cell function improved with very low calorie diets. More direct measures improve too, so we can conclude that the pancreas can, given the right circumstances, recover even in people on insulin (23,25).
Also, much as with the liver, the excess fat in the pancreas goes down (23,25). As fat goes down, function goes up. By function, I mean that the pancreas regains its responsiveness to rising blood glucose, and becomes more capable of releasing insulin (23,32).
This process in the pancreas is slower though, probably because the pancreas, unlike the liver, isn’t well equipped to shift fat.
What about glucagon?
One study that provided 1000 kcal/day for an average 10 kg weight reduction over an average of 8 weeks found glucagon reductions across the board (33). By that I mean fasting, peak, and during an oral glucose tolerance test. The other studies didn’t look specifically at glucagon.
Take home message
Very low calorie diets reduce fat in the liver and in the pancreas. The result is that the liver becomes more responsive to insulin, and the pancreas recovers in terms of both insulin production and appropriate response to glucose.
Warning!
I said it in an earlier blog, but this bares repeating – if you are planning on trying to reverse your type 2 diabetes, partly or fully, with diet and/or exercise, let your medical care team know so they can monitor you and adjust your medication to keep you safe.
That brings us to the end of part 3. In part 4 we’ll look at how all the changes discussed so far actually translate into glucose tolerance, in other words, how the body copes with carbohydrates.
This is really the big question because it’s all fine and good for things to look great while on a low calorie diet, but you can’t keep it up forever, so what matters is what happens afterwards.
Click here to read part 4.
References: click here for a full list of references
To learn more about type 2 diabetes and what you can do to better manage, and often reverse it, watch my free video education series. If you want one-on-one help dealing with your type 2 diabetes, contact me here to book a consultation.
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