Study showing what fructose does after you eat it



By popular demand @Karim_Wassef:joy:

Results: Glucose homeostasis and incretin response to sucrose and Palatinose Oral challenge with the experimental sugars revealed that exposure to sucrose solutions induced a remarkable acute increase in glucose, insulin and GIP levels, without effects on GLP-1 secretion, which were avoided with Palatinose (ESM Fig. 1a–h).

This is going to need a little explaining.

Sucrose (table sugar) is made up of glucose and fructose. Palatinose a brand name of isomaltulose. It is also made up of glucose and fructose, but the fructose is hidden away by way of some tricky science voodoo in the construction of the molecule. So… what happens when you compare the effects of ingesting these two things? It should show you the fructose effects sepatrate from the glucose effects.

Take a look at the figure from the study below:

  1. The two sugars have simialar glucose response curves. This is because fructose by itself does not do much to blood glucose.

  2. The sugar with an active fructose component raises insulin more. Fructose by itself does not raise insulin levels. So why the increase? …

  3. Fructose acts upon the GIP sensors in your stomach to potentiate a higher insulin response to the same amount of glucose in the sugar. Remember, regular starches are broken down into glucose too by amylase in the saliva. GIP acts directly on the pancreas beta cells (including insulin and glucagon), bone, fat, gastrointestinal (GI) tract and brain.

That’s not to say that fructose in isolation doesn’t cause other problems, like increased triglycerides.

Glucose and fructose from both disaccharides are completely digested and absorbed, just not at the same zone of the small intestines. This difference has completely opposite effects on metabolism kick responses. Fructose still has a small effect on the pancreas in the bloodstream. (Thx @erdoke )

What did you learn today?
Studies showing Sweeteners that Raise Insulin Levels?

[This topic was created following a discussion starting in ‘What did you learn today?’, merged below]

I learned that Robert Lustig only has it half right about fructose. It’s the combination of fructose with glucose or starches that potentiates the glycemic and insulinogenic effects through sweet sensors in the gut and, to a lesser extent, pancreas. 100% fructose and a zero carb meal - not so bad.

What did you learn today?
(Karim Wassef) #3

??? Please share sources


I thought you’d never ask. :wink:

Fructose and the pancreas

Fructose and GIP

Fructose and diabetics

Note the caveat about increasing trigs in that last one. I assume liver health makes a big difference too.

(Karim Wassef) #5

So this is saying that small amounts of fructose without glucose doesn’t cause fatty liver?

Is it the insulin signaling due to glucose that causes it to be stored in the liver or will just excess fructose do it?

(bulkbiker) #6

Don’t forget this one too

Fructose and NAFLD


According to my source for such information (chat), the increase in DNL in the liver “… is a downstream effect of increased (visceral) adipose lipolysis.”
And " Isocaloric, isonutrient, same amount of fructose. The only difference is where glucose (!) is absorbed, and this differentiates between healthy and fatty liver."

My understanding is as long as the liver is producing trigs and exporting them the fat won’t build up there.


…for example in rodents submitted to a 60% high fructose diet for eight weeks [18] or to a western diet where fructose is provided as a 30%-fructose containing beverage for eight weeks [19].
Thus, as fructose is both substrate and activator of DNL, it appears as the most potent lipogenic carbohydrate contributing to the development of liver steatosis.

Eating fructose with glucose or starch makes the problem worse. Much like eating carbs AND high fat together. Pure fructose (if you can find any) would be malabsorbed by the gut at a certain point before you could eat a lot of it.

[dang, I have to go drive somewhere now]

(bulkbiker) #9

Yeah but pure fructose is not in our diet… only in a lab?

(Karim Wassef) #10

I think this deserves it own thread


Closest real food would be whole fiberous fruit. I’d stl separate that from a fatty meal.

Curiosly, some artifucial sweetners do the same thing.

(bulkbiker) #12

Isn’t fruit 50:50 fructose sucrose
I just avoid it altogether… the joy of carnivore.


I don’t understand all the mechanisms well enough to be coherent on it. I can dig up a FB link when i get home.

(KCKO, KCFO) #14

This convo on fruits lead me to learn this:


You are correct. For some reason I thought they would be mostly fructose. The slow digestion of a whole fruit will blunt the effect compared to a juice.

Table of types of sugars in fruit here :

It wouldn’t be too difficult to make a pure fructose sweetener from HFCS would it? I’m thinking they manipulate the content of different HFCS ratios already.

Found some!

(bulkbiker) #16

Depends where you are HFCS is banned in the UK I think…


Found an applicable FB link of you’re interested in mechanisms of DNL NAFLD

Another great mechanistic study looking into the development of non-alcoholic fatty liver disease (NAFLD) and its relationship with hepatic and systemic insulin resistance.

[I’m going to try to explain the two main methods of fatty liver formation described in this study in a future post.]

(bulkbiker) #18

Not quite banned but its use is restricted by quotas

(Wendy) #19

Are you sure? He did add starches to his kids meals, made them the same calories and saw very different results.


Merged topic ends here ^^