Comparison of the findings between rats and humans when studying the metabolic effect of sugar and HFCS

I have watched a video which summarized the findings in examining the sugar addiction in rats. The presenter talked about how they conditioned the rats to binge on sugar. One slide, however, reported GLUCOSE consumption patterns at 13:25 minute of the video: 

So the principle of attractive sweetness of fructose, which Dr Lustig has repeatedly highlighted, could not be applied here. In fact, rodents such as mice and rats naturally crave starches or sugars such as grains and fruits they find in nature, not the cheese as the cartoons notoriously portray them. Scroll down to point 3 in this article to find out yourself. 

Further in the video you will see how both groups of rats: 1. having short availability of large amounts of sugar and 2. having sugar available over 24-hours have increased their sugar consumption, but the first group had overall much higher sugar intake than those in the second group. Bingeing rats therefore compensated for the periods of no sugar availability and consumed overall more sugar. Interesting to see. But this was not to contrast with humans, it was just an interesting input from the curiosity.

What I found appealing was the slide (22:24) and the presenter mentioned it as well, was that high-fructose corn syrup (HFCS) had different metabolic effect from sucrose. 

That it is different from glucose is obvious. But from sucrose? I wonder where they got this information when my research and also Dr Lustig consistently report that there is no significant difference between the absorption and metabolism of HFCS and sucrose. This was not discussed in the video.

The two possible explanations would be that some people do not have sucrase - an enzyme cleaving sucrose into free glucose and fructose, which the HFCS actually is and in these people/animals the sucrose is not absorbed. But this is unlikely the case here. More probable explanation is the different content of fructose in HFCS than is in sugar. Especially the beverages contain HFCS-55, which has 5% more fructose than sugar, but solid foods tend to contain HFCS-42, which has 8% LESS fructose than sugar. And as such, in the first case there might be less insulin produced than in the second case, due to the proportionally different content of glucose. But is it that much? Again, the experts have reached the consensus that there is no significant difference in metabolism between HFCS and sugar. 

Moreover, going back to another point of the slide above: HFCS releases triglycerides (like a fat), if you have read my previous articles about fructose metabolism, you now might be aware that fructose contributes only little to the formation of new fats. Most of the increased triglycerides in the blood stream were the re-esterified free fatty acids that were already present in the blood stream - as their concentration always decreased after fructose intake challenge. Did they measure the free fatty acids concentration in the rats, or were they only happy to see the triglycerides rise and make the conclusion above? This was not said and I do not see any legible details of the study itself to check these details. 

The further slide suggest possible addiction-like properties of HFCS, but you could see that the rats behaved the same when receiving sucrose or even glucose. 

These results correspond with the previous slide above - adverse metabolic effect of HFCS. But it also informs us about increased body weight after feeding rats with HFCS. The amount of HFCS was 8% supplementation of the standard chow diet: 

However, nothing was said whether these 8% of extra HFCS were within or on top of the balanced energy intake. By balanced energy intake I mean the amount of calories needed to maintain stable body weight. When doing my research the studies on humans also varied in this: some were in isocaloric settings, when fructose or sugar replaced some other calories, others were in hypercaloric setting, providing calories on top of the balanced state. Any wonder why people gained weight? 

But, to be on the neutral side, I should also refer to this: 

The slide and information presented by the speaker suggests that rats which were bingeing on sugar did not increase their body weight, because although they consumed more sugar than any other group of rats, they compensated for the excess energy intake by consuming less of their normal chow. 

HOWEVER: 

1. this latter case was the observation for only 27 days, not 6 months.

2. the whole study design is different between these two cases: the HFCS study was not binge eating, the rats had normal feeding pattern, just consumed probably excess 8% of calories in a form of HFCS. 

It is therefore not wise to compare these two studies as it was a single trial comparing the effect of sugar and HFCS in one. 

Moreover, from the following slide you can see that all rats gained weight, whether having ad libitum access to HFCS over 12 hours (top curve), bingeing on HFCS when having it available for only 12 hours (middle black curve),  and also when consuming a normal chow (bottom curve). Only the two former cases led to a higher weight gain and of these two the first led to even higher than the second one. But the same was reported for SUGAR, do you remember? Check again the third paragraph of this article above. 

What does that actually say? 

Note the title of this slide: it mentions 5 weeks, but the whole x-axis covers 24 weeks. That is fine, but when you look above the point of 5 weeks, the difference in gained weight between the three designs is not that big, is it?

From the physiology point of view: deprivation of favorite substance (HFCS or sugar) causes an individual to overeat on it when it is available, especially after a fasting period. And that is typical for humans and rats. That also means that higher bulk of this substance is consumed in a shorter period of time - leading to increased insulin level and enhanced fat storage. So not only more calories are consumed at once when bingeing, but the physiological response to the excess of glucose mediates fat storage via insulin. Moreover, the excessive amount of fructose leads to increased fat synthesis, especially in rodents which are more effective in de-novo lipogenesis than humans are, do you remember? So these results cannot be directly applied to humans. 

I would like to finally explain the difference between just supplementation of diet with HFCS and bingeing on a substance, separately from consuming the usual and rather boring rat chow. The Summary slide I posted here did not specify, how the HFCS was supplemented: whether it was in a sweetened drink or mixed with the chow. Since rats like sweet taste, if their chow was sweetened, they were likely to consume more of it and finally gain weight, especially if those 8% were on top of their energy needs. In contrast, having sugar to binge on and then consuming the chow which did not taste as appealing in comparison to sugar, might have been a factor in a self-limiting intake of calories, leading to a stable body weight over time in those rats. The Summary slide also did not inform us about bingeing, so the rats probably only had their diet spiked with 8% of HFCS. This amount of sugar would represent extra 200 kcal, if consumed on top of the energy needs in a person requiring 2500 kcal per day. Overeating 200 kcal on daily basis for 6 months would definitely lead to increased body weight and also perhaps altered biochemistry in the body. One tin of sugary soft drink contains about 150 kcal, just for the comparison. 

And the persisting discrepancy between the body weight on sugar and HFCS bingeing rats over 5 weeks? This would require a closer look into the actual designs of the studies. But maybe rats really have different absorption or metabolism of sucrose from HFCS than humans. It would be interesting to find out what was behind these different results. For now I can tell you, if you have not watched the video to the very end, Dr Lustig was in the audience and questioned this discrepancy as well. But the speedy answer of Ms Avene, the presenter, did not sound convincing to me and I can only guess that Dr Lustig was not completely happy with her reasoning either. 

Exercise for weight loss does not work?

At 14:12 of Dr Lustig's lecture you can see the diagram of one meta-analysis which assessed whether there is the body of evidence that physical exercise helps to lose weight. Dr Lustig presented it in a very simple manner - not saying how long the exercise lasted, what the exercise actually was, how many calories equivalent it was to balance a daily energy intake, and so on. All these factors are important in evaluating why something like this works and why not. 

And that is exactly my point here. WHY exercise does not work to curb down the obesity levels? They say there was a small weight loss overall but it was presented as a negligible effect. Nothing was said about whether the people had also their diet altered or not and what their diet consisted of, in general.

Let me put it this way: when you are obese because you consume over 1000 kcal more per day than are your actual requirements for that body size and lifestyle, how long you have to exercise to burn this extra energy plus some more to achieve the weight-loss? 

Here is a brief overview where you can find that if a 68 kg weighing person performs light aerobics, within a half an hour they burn mere 120 kcal. That is not even half of a regular Mars bar in the UK! With the higher body weight the energy expenditure is higher, true, but is it that much? 120 kg heavy person burns around 200 kcal. Still not a regular Mars bar, which contains 260 kcal. How much was that burger? Over 1400 kcal.

How long DAILY can you expect an obese person to perform even light exercise? Not for 3.5 hours to burn off that extra burger calories, would you? And this is every day because they tend to overeat every day, some even double or triple the average energy requirements (extra 2000-4000 kcal) as I have seen in my favorite series Supersize vs. Superskinny. Watch it, it is eye-opening. Available on Youtube.

Any wonder why the exercise showed such a small result? And this is also why the first law of thermodynamics seems not to work here - because in such a high energy intake you cannot expect weight loss if the energy output is not exceeding it. Moreover, it needs a substantial amount of time to achieve significant results, which most of such studies do not have. They usually assess the participants over several weeks or a few months at their best. 

Therefore, the things have to be looked at from the whole perspective, not just looking at the data and dismiss this or that saying it is inefficient. The little success (half point of BMI as Dr Lustig said) actually has proven that the exercise works, but it has to be accompanied with dietary changes as well. It is generally easy to overeat when the food is so cheap, processed and palatable. Cheap processed food is very energy dense, which means that per 100 grams you can get more calories from the processed food than from the unprocessed, such as fruits and vegetables. And these calories are not always only sugar. Most of the time there is more fat calories than sugar calories. Add little salt and you have got a deadly trio that has the potential to make people addicted to this particular diet. 

Moreover, the exercise has been found to be very effective in decreasing the risk of metabolic diseases such as type 2 diabetes. In fact, the exercise alone was found to be even more effective than the dietary changes alone. Surprised? I am not. It has its rationale based on our physiology. It is very simple: when you over consume, you store the energy not only in the fat, but also in the muscles and liver. Especially muscles are responsible for the most of the insulin mediated glucose uptake in the body. When you overeat and have a sedentary lifestyle or remain bed bound for several days, they are kept in the 'full of energy' state during the day and cannot take in any more. In excess, the glucose, instead of refueling the muscles, keeps circulating in the body and the body keeps producing more insulin to fit it somewhere as it should not stay in the blood in high concentrations. And humans have quite a low capacity for the de-novo lipogenesis (DNL) as you could see elsewhere. There are other processes that happen in such a hypercaloric state but this is the main mechanism. Once the person starts exercising, the muscles burn the energy they have and start taking in more again which results in the drop of a high blood glucose and also blood lipids. That's it!

We as a species have evolved being physically active and that is the need of our physiology today, too. Stop being active and the consequences come. Plug the hole in the sink and it will soon overflow. As long as one or two days of being bed bound with excessive eating can lead to the changes in our biochemistry indicating a pre-diabetic state. Keep doing the exercise while overeating and you will just keep gaining weight while you will most likely remain metabolically healthy for a pretty long time. Just please do not take this as my approval to overeat, OK? Healthy weight also matters. 

And finally: look at the diagram above again. The plot contains the results of different studies. Some worked, others did not, when examining the effectiveness of exercise on the weight management. It was only the overall figure of pooling all these together that Dr Lustig presented as the small and negligible difference. At least three studies (towards the left from the vertical line expressing that mean results) showed quite a success, did they not? I would have to look at each of them individually to give you a full report what made them show the effect and what not. But even from this you can see that it really depends on the circumstances whether the exercise does work or not. The first law of thermodynamics still applies here and the exercise DOES work when the energy output exceeds the energy input on a regular basis.  

One more thing I have noticed when listening the lecture further at the minute 18:55:

Look at the right column Activity. So, if the lowered level of activity has contributed to the obesity epidemics and associated metabolic diseases in children, why suddenly the physical activity does not seem to work, according to Dr Lustig? Yes, he did question this aspect and went for the usual toxic substance (fructose) in our diet after that but it is generally accepted in the scientific community that physical activity does play a role in the weight management and overall health of people and it is usually advised and promoted by the health authorities and implemented into the government policies, too. Dr Lustig provided no sufficient evidence that the physical activity is negligible or does not work in maintaining a healthy body weight, except of the meta-analysis study mentioned earlier. 

To be on a neutral side I must say that other studies also concluded that the exercise has little impact on weight loss and the change in the diet produces a higher effect, but this was only because of the insufficient balance of the calories I have discussed above. It is more effective not to eat that chocolate than trying to burn it off.

I know it from myself: I have been maintaining a lower body weight for some time now, with tiny fluctuations in one kilo up or down. And I know that when my physical activity suddenly increases for a couple of days while the diet remains the same and balanced, my body analyzing scales notice this and also estimate a lower percentage of body fat in my legs while increasing the percentage of water and muscles. I need no further evidence that the exercise works. I assess my body composition regularly. I maintain a record and do it at pretty constant conditions. The measurements were consistent, sometimes two or three days in a row produced identical results. 

And here I come to the last point of this article: there is a difference between maintaining a healthy body weight and reducing the body weight of obese people. These two premises are quite different, because when you are of a healthy weight, it requires less effort from you to exercise and you also need to exercise less to keep the energy in balance. For obese people this is particularly difficult to do on a regular basis and the drop-off rate is also very high, which contributes to the failure of such programs. What may be a light aerobic exercise for a fit person, for an obese person it can become quite a burden after 5 or 10 minutes. Now, imagine them doing this for an hour to merely burn the single Mars bar... 

But, as one large supermarket chains advertises: 'Every little helps'. The burned 120 or 200 kcal means they were not deposited in the fat stores and the muscles are now ready to take more glucose and more fat from the blood stream, reducing the risk of type 2 diabetes. Remember Dr Lustig saying that obesity is not a problem and that 20% of obese people are metabolically healthy? Well, 80% are not and physical activity has a huge potential in helping them out of this doom. He also admitted this in another video at 1:18:05 time that he has been struggling with his high body weight and the diet, but that the constant physical exercise helps him to reduce the abdominal fat deposits but his body weight does not change that much. He is simply replacing the fat with muscles. And if the studies do not examine the change in body composition of the participants but instead they only use BMI for the assessment, is it such a mystery they do not find significant changes? 

Fructose induced de-novo lipogenesis (DNL) - to what extent? Get ready for a surprise.

You have probably heard already that fructose is commonly portrayed as the fat sugar. Even Dr Lustig once said that 30% of fructose is converted to fat and the media keep repeating it. I would like to focus on this in this article because I believe the things are not so simple and we still do not exactly know enough about the lipogenic (fat forming) properties of fructose to make such statements. Make yourself comfortable, this will be long. 

Dr Lustig presented results of ONE study (Hudgins et al, 2011) that examined the de-novo lipogenesis (DNL) after fructose ingestion: 

I have done my own independent research on metabolic consequences of fructose intake given in various study settings for my final year project at the uni. And I know that the figures vary from study to study. Therefore - using only one study like this and demonstrate its results in figures that should be representative for everybody is not quite right. But there is far more to be criticized here. Get ready for an interesting surprise.

From my research I have learned that there are many methodologies of the assessment of DNL. All these have their strengths and limitations. I am not going to bore you with details, but I would like to say that most of these (including the one presented here) rely on isotope traced acetate and/or palmitate, as an indirect method when the effect of fructose intake on DNL is assessed. Other studies followed the metabolic pathway of the examined sugar as such: when examining the metabolic fate of fructose, they also labelled the fructose with an isotope and then assessed to which extent the fructose contributed to the DNL. The reason why I have brought these two examples to your attention was the comparison of the findings of two such studies of fructose effect on DNL within as similar conditions as possible. 

Dr Lustig presented the results of the study mentioned above (Hudgins et al) and said that in a fasting state fructose increased DNL by 5%. I have read that study myself. For achieving this result they fed their overweight to obese participants with 0.5 g of fructose per kg of body weight, corresponding to about 35 g of fructose for a 70 kg man. Heavier participants received proportionally more, of course. FIY: one 330 ml tin of Coca Cola has exactly 35 g of sugar, of which it is around half fructose, the other half is glucose. 

In comparison, Chong et al (2007) also performed similar assessment on fasting participants with similar amount of people, similar profile of people but tracing also the labelled fructose as such, which the previous study did not. They fed the participants with 0.75 g of fructose per kg of body weight, which would be 52.5 g of fructose for a 70 kg man, therefore more than the previous study. What they have found was that fructose contributed only with 0.4% to the DNL. The remaining increased appearance of lipoproteins and triglycerides above this amount was explained as re-esterification of free fatty acids already present in the system (their concentration is always reported to decrease in this kind of studies) and by reduced lipids clearance into the fat cells because fructose does not trigger such high insulin response as glucose does. Now, do you not think that the 33% higher dose of fructose resulting in 12.5 times lower DNL outcome is interesting? 

If you were shocked by the substantially increased effect of fructose in a fed state that Dr Lustig discussed later (those 25% increase), let me tell you what amounts of fructose/sugar it was based on. The team of Hudgins et al fed the participants with the following amounts of sugars:  

• 35/35 g of fructose and glucose = 70g of sugar = 280 kcal for a 70 kg heavy man (0.5/0.5 g of fructose and glucose per kg of body weight)
• 70/70 g fructose and glucose = 140g of sugar per 70 kg man = 560 kcal. If the overweight or obese person weighing 100 kg (they did not include people of healthy weight in this second protocol) consumed the adequate proportion of sugar for their weight, it would be 200g of sugar = 800 kcal, because this group received 1 g of fructose and 1 g of glucose per body weight.  

Any wonder why the results were so bad after all? Dr Lustig did not give you these numbers, he only shocked you with the results. 800 kcal of sugar given in the morning in a form of drink - do you think it is real for most of us? This amount would correspond to the consumption of mere 3% of the US population. 

Putting this in numbers, Mariott et al 2010 reported that the 97th centile of the U.S. population consumed 35% of total energy intake in a form of sugar between years 2003-2006. I have calculated that this corresponds to about 14% of daily calories from fructose or 350 kcal for a person consuming 2500 kcal. In normal diet the approximate ratio of fructose to glucose is 0.8, not half on half as it is for sucrose. Even the top 10% of highest sugar consumers (90th centile) had 25% of total calories from sugars (10% from fructose), meaning that 90% of the U.S. population had lower sugar intake. And these amounts are consumed during the whole day in a liquid and solid form, not only in a drink within 15 minutes on an empty stomach as the study participants had to. This is the reality check. And remember that since year 2000 the sugar consumption has been decreasing.

If this study had examined the effect of sugar on DNL using the method of Chong et al (isotope labelled fructose as well) are we sure we would achieve the same results? You could already see how different the results were when compared the two similar settings with different methodology earlier. 

Moreover, the high sugar effect (those 25% increase from the diagram) was found in people already overweight and obese, suggesting they already might have had their metabolism affected, not only by the high sugar feeding but also by their body weight. This was not told to you either.

Even more: while our bodies can vary enormously in their size due to the fat or muscle content, our liver size does not. And since you know that fructose is primarily metabolized by the liver, do you not think that such immense overload of sugar will show up with negative consequences after all? Whether the person is 70 kg or 120 kg, their liver capacity for metabolism of fructose does not vary that much, but the second person receives almost double the dose of the first one. Bear this in mind. 

Something I found fascinating in the study (among few other things). Look at the bit I copied for you: 

Have you noticed something? Fifteen mild to moderately overweight participants, of which the BMI ranged from 25.8 to 35.6. For those who are familiar with the grades of BMI this must be a bad dream. Those moderately overweight were not only obese, but beyond BMI 34.9 it is even Class II or severe obesity. Even the mean BMI was in the range of obesity (31.0). It took me a while to realize that their term 'overweight' was probably just a politically correct one since I remember a suggestion by someone to avoid using a word 'obese' because it could traumatize the obese person. Take it as a curiosity.

The truth is that no person had a weight below 80 kg in the second protocol, including women, so my reference man weighing 70 kg (once a true reference man for the Europe, 60 kg for women) was a different league. They intentionally tested these high doses of sugars on people with already altered energy metabolism. Moreover, while consuming the mega doses of sugars they were only allowed to remain passive, such as reading or watching the TV. In contrast, most of us move around daily. We take care of ourselves, we go to work, chase the bus, some walk the dog regularly or pick up children from school and do not normally consume such amounts of sugar anyway.

I have also found one part of the study discussion a bit manipulating. They compared the highest dose of sugars they gave to the obese participants (if weighing 100 kg -> 200g = 800 kcal) to the "amount of sugar in a commercial "supersize" soft drink consumed by 60 kg person". I tried to find out how big this supersize soft drink was but I could not find a specific figure for this term. Instead I calculated the amount of sugar the 60 kg person would consume in this study and it came out that it would be 120g of sugar or 480 kcal. That is far more than a 500 ml coke (53 g sugar, 210 kcal) or 16 ounces, above which the sale of soft drink volume was banned by the major of New York. While I agree that some extra large people may gulp down the 1300 ml of mega size soft drink in one sitting, I have doubts that an average 60 kg person would manage it.  

To make you more amazed, I will continue with debunking the blame put on fructose when combined sugars were consumed. To make the diagram from above more legible, I will copy it from the actual study:

I want you to focus on the two bars in the middle, the F and F:G ones. From the description you see that the first group received 0.5 g of fructose per kg of body weight and the second one received the same plus the same amount of glucose. The figures above them (0.49 and 1.50) refer to the magnitude of change from the baseline. The rationale of added glucose to he fructose was to mimic the consumption of sugar or HFCS because we rarely consume fructose alone and also that the fructose has poor absorption rate on its own whereas it has the highest absorption rate when accompanied with the same amount of glucose. 

How much more fructose do you think we absorb in the presence of glucose so it could increase the DNL three times as much? Do you guess it TRIPLED? WRONG. The same study reported the increased blood concentration of fructose in the presence of glucose from the mean 57 micrograms per mililitre (fructose alone) to only 72 micrograms (when fructose and glucose consumed together in the same amounts). The difference was not 2x57, but only mere 15. Even if one would argue that this was the systemic blood circulation level, whereas the liver captures most of the ingested fructose and may not release the extra in the proportional manner to the influx, this high jump is unlikely to be only due to the fructose alone. So the two-fold rise from the first test you can see above could have been largely accountable to the glucose, not fructose, since the dose of fructose has not changed and even at its highest absorption rate it is not 100% absorbed. 

Yet the scientists still focused on fructose as the main villain, similarly as Dr Lustig has been all the time. And nobody should now have doubts about the flawed argument that when the glucose tolerance test alone caused the reduction of the blood lipids (the very first column marked OGTT) that the enormous rise of new palmitate after added glucose to fructose was only due to the fructose alone. The truth is that glucose not only enhances absorption of fructose, but the body also alters the metabolism of both sugars when they are in the system both at once. Unless the labelled fructose AND glucose are traced and only fructose detected in the newly formed palmitate while the glucose is not, we cannot be 100% confident about the findings. The metabolism of glucose and fructose is very much inter-connected and that is why these specific tracer studies came into place: to distinguish between the resultant effects of these two sugars.

The best for the last. Look at some information from the slide once more: 

What Dr Lustig said was that at fasted state the DNL after fructose was only 5% higher from the baseline whereas in fed, obese and insulin resistant state it was 25%. WRONG again. All these results from the diagram above were on the same people under the same conditions, only the composition and amounts of sugar changed. So all of them received the fructose in fasting state, just in different amounts and the diagram presents the effect of different doses of fructose, not the difference between fasting and fed state. All of these participants were overweight or obese (Protocol 2) and all of them were tested for the response to those three different doses of either fructose or fructose and glucose in the mentioned amounts. Do you understand? That 5% was of 0.5 g per kg of body weight of fructose alone, those 25% was of 1 g of fructose and 1 g of glucose together, for the same participants under the same conditions, just spaced in time because it was the cross-over study. I have found nothing in the study saying that this amount was given before eating and this was after eating or that they would come up with these different responses before or after eating.

The Protocol 1 was slightly different. Instead of giving the whole volume of drink at once to be consumed within 15 minutes, it gave the participants regular doses of fructose sweetened drink, which made total 1.4 g per kg of body weight within 6 hours. To give you an idea, this amount would represent 98 g of fructose for a 70 kg  man. 100kg person would receive 140g of fructose only. Too much of fructose, hardly representative of the general population. To match this amount of fructose with the glucose (as we normally consume them together), it would have to be mind blowing 280g of sugar = 1120 kcal consumed just within 6 hours and on empty stomach (if taking 50/50, not 0.8 fructose to glucose ratio). Luckily for the participants, the scientists did not bring this idea into practice. Note, this last protocol was not pictured in the diagrams above. 

Instead, the link illustrates how the measured concentrations of lipids shot up during the first 8 hours in the Protocol 1 and then steadily dropped towards the end of the 24-hour monitoring period when the participants consumed food, therefore were in a fed state. And when you look at the bottom picture, you will see that at the beginning of the curve the concentration of palmitate started to rise even before time zero, which means even before fructose was given! This is just normal because after the 12-h fasting there was not enough insulin secreted, which was a signal to the fat cells to release fat for energy metabolism because even the glycogen stores were at their minimum after so many hours without a food intake. The participants simply switched to the keto-metabolism. Once you eat carbohydrates again, insulin rises and opens the gates for the glucose to enter into the cells (and for fat into the fat cells, too) and the fat burning mode is reduced again. And because it was a 'fructose challenge', the same applies what was discussed in case of Chong et al: lower level of insulin secreted after fructose then after glucose, hence lower clearance of lipids into the adipose tissue and although fructose is converted to fats in high doses, it may not be as high as we think, especially in the fasting state as both Protocols administered it. 

Once again: nothing was mentioned in that study about fasted and fed state in terms of assessed biochemistry for the Protocol 2 and from the Protocol 1 you can see that the DNL steadily decreased after the participants no more received fructose and started receiving food (containing glucose and some fructose).

This slide presented by Dr Lustig was just a nonsense as were the claims related to it. 

However, I am not saying that consumed fats along sugars (as per fed state) do not worsen the situation when it is overdone. I am saying that this video was full of crap. 

Remember all these flaws and selectively presented information when you will listen to other Dr Lustig's horror conclusions about the sugar again. The studies like those two introduced here aim to assess the actual mechanism of the metabolism of the examined substrates. They usually do not aim to assess the real life situation of you or me. In fact, I consume very little added sugar, so I am not a good representative for this. Therefore I have no reason for trying to deny these results to curb the guilt or something. And I am definitely not sponsored by the sugar industry. These are the scientific findings that contradict each other to some extent, followed with my critical evaluation of how inappropriately these materials have been presented to you. And that was the point of this article, not to deny that fructose or sugar can be dangerous when consumed in excess.