Studies On Sucrose And Starch

[Wagner83]

Replacement of dietary fat by sucrose or starch: effects on 14 d ad libitum energy intake, energy expenditure and body weight in formerly obese and... - PubMed - NCBI

Average 14 d ad libitum energy intake was 13% and 12% lower on the starch diet compared with the sucrose and fat diets, respectively (P < 0.05). In both post-obese and normal-weight subjects, body weight and fat mass decreased significantly on the starch diet (by 0.7 +/- 0.2 kg and 0.4 +/- 0.1 kg, respectively, P < 0.05). No changes were observed on the fat or sucrose diets. After 14 d on the sucrose diet, 24 h energy expenditure as well as postprandial plasma adrenaline and noradrenaline concentrations, were significantly increased compared with the other two diets. Overall satisfy and palatability ratings were also highest on the sucrose diet.

CONCLUSION:
Intake of a 14-d ad libitum high-starch diet decreased energy intake and body weight compared with a high-fat or high-sucrose diet. The increased energy expenditure observed on the sucrose-rich diet can probably be explained both by the increased intake of energy and fructose (mainly from sucrose) on this diet.

Liquid versus solid carbohydrate: effects on food intake and body weight. - PubMed - NCBI

DESIGN AND METHODS:
Thirty two overweight/obese adults consumed glucose- or fructose-sweetened beverages (25% energy requirement) with their ad libitum diets for 8 weeks, followed by sweetened beverage consumption for 2 weeks with a standardized, energy-balanced diet. Plasma variables were measured at baseline, 2, 8, and 10 weeks, and body adiposity and insulin sensitivity at baseline and 10 weeks.
Fasting and postprandial ASP concentrations increased at 2 and/or 8 weeks. ASP increases correlated with changes in late-evening triglyceride concentrations. At 10 weeks, fasting adiponectin levels decreased in both groups, and decreases were inversely associated with baseline intra-abdominal fat volume. Sugar consumption increased fasting leptin concentrations; increases were associated with body weight changes. The 24-h leptin profiles increased during glucose consumption and decreased during fructose consumption. These changes correlated with changes of 24-h insulin levels.

Isocaloric exchange of dietary starch and sucrose in humans. II. Effect on fasting blood insulin, glucose, and glucagon and on insulin and glucose ... - PubMed - NCBI

Ten men and nine women ages 35 to 55 consumed two diets for 6 weeks each in a cross-over design. The diets were composed of identical natural foods and 30% of the calories as either sucrose or wheat starch. Carbohydrate, fat, and protein supplied 43, 42, and 15% of the calories, respectively. Of the calories 10% was eaten at breakfast (7:00 to 8:30 AM) and 90% at dinner (4:30 to 6:30 PM). Inital body weights were essentially maintained. Fasting serum insulin and glucose levels were significantly higher with the sucrose than with the starch diet. The insulin response and the insulin:glucose ratios after a sucrose load (2 g/kg body weight) were greater after the subjects consumed the sucrose diet. Sucrose feeding produced increases in fasting serum insulin, the insulin:glucose ratio and the insulin response to a sucrose load that were of greater magnitude in a subgroup of nine subjects classified as potentially carbohydrate-sensitive than in normal subjects. Glucose response to a sucrose load and fasting serum glucagon did not differ significantly with diet. Fasting insulin and glucose showed significant increases as a function of time on diet. These results indicate that sucrose feeding produces undersirable changes in several of the parameters associated with glucose tolerance.

This is interesting (but they're eating high fat), as there's a study on rats showing something similar:
Effects of sucrose vs starch diets on in vivo insulin action, thermogenesis, and obesity in rats. - PubMed - NCBI

High intake of simple sugars is generally seen as a detrimental factor in the etiology of both obesity and insulin resistance. To examine possible deleterious effects of sucrose, independent of changes in energy intake, rats were fed equal amounts of high-sucrose or high-starch diets over 4 wk. Energy expenditure was assessed by open-circuit respirometry and carcass analysis. In vivo insulin action in individual tissues was assessed with the hyperinsulinemic (1 nmol/L), euglycemic clamp combined with tracer glucose and 2-deoxyglucose administration. Whole-body glucose disposal was impaired by sucrose feeding (clamp glucose infusion rate of 77 +/- 4 vs 124 +/- 6 mumol/[kg.min], p less than 0.001, for sucrose and starch, respectively) because of a major impairment of insulin action at the liver with a smaller contribution from peripheral tissues. Sucrose feeding affected neither basal or stimulated energy expenditure nor accumulation of body fat. In conclusion, sucrose feeding produces a major impairment of insulin action, predominantly because of an effect at the liver.

Differential effects of fructose versus glucose on brain and appetitive responses to food cues and decisions for food rewards. - PubMed - NCBI

Ingestion of fructose relative to glucose resulted in smaller increases in plasma insulin levels and greater brain reactivity to food cues in the visual cortex (in whole-brain analysis) and left orbital frontal cortex (in region-of-interest analysis). Parallel to the neuroimaging findings, fructose versus glucose led to greater hunger and desire for food and a greater willingness to give up long-term monetary rewards to obtain immediate high-calorie foods. These findings suggest that ingestion of fructose relative to glucose results in greater activation of brain regions involved in attention and reward processing and may promote feeding behavior.

 

[ecstatichamster]

Thank you @Wagner83

 

[Wagner83]

My pleasure. Some of those are really interesting, among other things I'm curious about the effects of sucrose on glucose tolerance (and if stimulating insulin is actually a bad thing) . I know you posted a thread on Ray being unclear on the topic of mixing simple sugars and starch, maybe he had this in mind as well?

 

[ecstatichamster]

I used to think insulin was THE problem.

Ray doesn't think so.

Glycemia, starch, and sugar in context

Insulin is important in the regulation of blood sugar, but its importance has been exaggerated because of the diabetes/insulin industry. Insulin itself has been found to account for only about 8% of the "insulin-like activity" of the blood, with potassium being probably the largest factor. There probably isn't any process in the body that doesn't potentially affect blood sugar.

 

[Wagner83]

Thanks for that quote.
By the way when it comes to starches, it seems to me that feeding time, how much I need carbs (after sports or really hungry I can eat a lot of it with less issues), ratio with other macro nutrients are important regarding how I'll react to the starches, I can sometimes eat plenty of rice with no issues, other times food coma is lurking in the shadows.
Dinner seems to be an easy time for me to eat starch , morning may be an other one and lunch much less so.
Too much fructose (e.g. apple juice) seems to be giving me a weird unpleasant sensation in the middle of the back, at the time I ditched most starches and used 1% milk, chocolate mousse , creme brulee etc.. (yet not crazy high in fat) I started having really worrysome problems . They resolved when I went back to starches.

 

[nikkmm]

I used to think insulin was THE problem.

Ray doesn't think so.

Glycemia, starch, and sugar in context

Do you have any details or links to more information about the relationship of potassium and blood sugar?

 

[Wagner83]

The glucose intolerance would make sense in that a lot of members who consume copious amounts of white sugar do not do well on starch and would maybe need quite some time before adapting to starch and glucose only (has Ray mentioned that humans stomach can adapt over a a period of few months? ). If you look at starch eaters they rarely eat more than some sucrose or fruit juices.
An other of the interesting point is the rise in adrenaline and noradrenaline (faster pulse, more "energy" ?) on the sucrose diet:
"After 14 d on the sucrose diet, 24 h energy expenditure as well as postprandial plasma adrenaline and noradrenaline concentrations, were significantly increased compared with the other two diets. "

An other point is that if one wants to lose weight, a starch-full low fat diet seems like a good option, better than high sucrose .

 

[Wagner83]

I have to dig a bit for them. But as far as the study you referred to in the other post on sucrose/starch - these were formerly obese people, which due to dieting are usually all profoundly hypothyroid as we discussed in the threads on lowering RMR with dieting/fasting. So, I would not take them as solid evidence. What is needed are studies on non-obese humans consuming the different diets and those have been done but are older. Here are some of the ones I have seen with focus on fructose.
http://www.tandfonline.com/doi/abs/10.1080/10408390903461426?journalCode=bfsn20
"...The purpose of this review was to critically evaluate the existing database for a causal relationship between the ingestion of fructose in a normal, dietary manner and the development of hyperlipidemia or increased body weight in healthy, normal weight humans, using an evidence-based approach. The results of the analysis indicate that fructose does not cause biologically relevant changes in TG or body weight when consumed at levels approaching 95th percentile estimates of intake."

http://www.tandfonline.com/doi/full/10.3109/10408363.2015.1084990?src=recsys
"...However, un-confounded studies conducted in healthy humans under a controlled, energy-balanced diet protocol that enables determination of the effects of sugar with diets that do not allow for body weight gain are lacking. Furthermore, recent reports conclude that there are no adverse effects of consuming beverages containing up to 30% Ereq sucrose or HFCS, and the conclusions from several meta-analyses suggest that fructose has no specific adverse effects relative to any other carbohydrate."

Even in obese people, fructose does not seem to worsen the condition.
http://www.tandfonline.com/doi/full/10.1080/10408398.2010.512990?src=recsys
"...The purpose of this review was to critically evaluate the existing database for a causal relationship between the ingestion of fructose in a normal, dietary manner and the development of hyperlipidemia or increased body weight in overweight or obese humans, using an evidence-based approach. The results of the analysis indicate that there is no evidence which shows that the consumption of fructose at normal levels of intake causes biologically relevant changes in triglycerides (TG) or body weight in overweight or obese individuals."

But I will find the intervention studies and post here as those contained information on specific dietary measures that may have influenced the findings. Speaking of which, did anybody verify that the "sucrose" diet in that study comparing with starch was not in fact a high-fat+high-sucrose diet as is commonly done in metabolic studies?

From the summary of the study Replacement of dietary fat by sucrose or starch: effects on 14 d ad libitum energy intake, energy expenditure and body weight in formerly obese and... - PubMed - NCBI:

In both post-obese and normal-weight subjects, body weight and fat mass decreased significantly on the starch diet (by 0.7 +/- 0.2 kg and 0.4 +/- 0.1 kg, respectively, P < 0.05). No changes were observed on the fat or sucrose diets.

So the study was done on 9 post obese subjects and 11 normal ones.
I have not checked the exact diet as I assumed comparing high fat diet to high starch or high sucrose would make no sense if high sucrose/starch were also high fat, so if someone has access to the text he's more than welcome.
Similarly, from the quote of the third study you mentioned, do you know what is the "normal level " of fructose intake they talk about?

Also I'm curious about this bit on adrenaline and noreadrenaline:

After 14 d on the sucrose diet, 24 h energy expenditure as well as postprandial plasma adrenaline and noradrenaline concentrations, were significantly increased compared with the other two diets. Overall satisfy and palatability ratings were also highest on the sucrose diet

For the record I'm not mainly concerned by the potential fattening effect of a sucrose diet, but as you know I ( and @EIRE24) experienced a lot of issues when I tried it for weeks.

----
From the second link you posted:

There are plausible mechanisms and research evidence that supports the suggestion that consumption of excess sugar promotes the development of cardiovascular disease (CVD) and type 2 diabetes (T2DM) both directly and indirectly.The direct pathway involves the unregulated hepatic uptake and metabolism of fructose, leading to liver lipid accumulation, dyslipidemia, decreased insulin sensitivity and increased uric acid levels. The epidemiological data suggest that these direct effects of fructose are pertinent to the consumption of the fructose-containing sugars, sucrose and high fructose corn syrup (HFCS), which are the predominant added sugars. Consumption of added sugar is associated with development and/or prevalence of fatty liver, dyslipidemia, insulin resistance, hyperuricemia, CVD and T2DM, often independent of body weight gain or total energy intake. There are diet intervention studies in which human subjects exhibited increased circulating lipids and decreased insulin sensitivity when consuming high sugar compared with control diets. Most recently, our group has reported that supplementing the ad libitum diets of young adults with beverages containing 0%, 10%, 17.5% or 25% of daily energy requirement (Ereq) as HFCS increased lipid/lipoprotein risk factors for CVD and uric acid in a dose–response manner.

 

[haidut]

From the summary of the study Replacement of dietary fat by sucrose or starch: effects on 14 d ad libitum energy intake, energy expenditure and body weight in formerly obese and... - PubMed - NCBI:


So the study was done on 9 post obese subjects and 11 normal ones.
I have not checked the exact diet as I assumed comparing high fat diet to high starch or high sucrose would make no sense if high sucrose/starch were also high fat, so if someone has access to the text he's more than welcome.
Similarly, from the quote of the third study you mentioned, do you know what is the "normal level " of fructose intake they talk about?

Also I'm curious about this bit on adrenaline and noreadrenaline:



For the record I'm not mainly concerned by the potential fattening effect of a sucrose diet, but as you know I ( and @EIRE24) experienced a lot of issues when I tried it for weeks.

----
From the second link you posted:

Also I'm curious about this bit on adrenaline and noreadrenaline:

Could be increased dopamine turnover, which would normally lead to increased catecholamine turnover as well. If dopamine was also elevated, which they did not seem to measure, then the higher catecholamines would be OK. If only the catecholamines were elevated then it is an issue.

From the second link you posted:

Yes, but as you saw they also said proper large scale intervention studies have not been done. It may very well come down to things like liver function, and other dietary factors like mineral balance, etc. If fructose is indeed a chelator then it can potentially cause issues if mineral balance is suboptimal. Actually, even by increasing PDH actitivy and thus overall sugar metabolism and CO2 synthesis it would increase needs for calcium, and sodium. Not saying this alone explains negative effects but increased trigs in the blood are due usually due (in that order) to 1) increased fat intake; 2) increased lipolysis; 3) high estrogen; 4) excessive carb consumption. So, I would try to rule out the first 3 before assuming sucrose was the issue.

 

[Giraffe]

An other point is that if one wants to lose weight, a starch-full low fat diet seems like a good option, better than high sucrose .

In that first study (sucrose vs. starch vs. fat) the energy intake was reduced on the starch diet. The authors assume that reason must be "either an increased satiating power or reduced palatability compared with the sucrose and fat diets." The diet contained a lot more fiber than the other ones.

Look at the changed body compostion!

e

C = control, PO = post obese

 

[Wagner83]

Could be increased dopamine turnover, which would normally lead to increased catecholamine turnover as well. If dopamine was also elevated, which they did not seem to measure, then the higher catecholamines would be OK. If only the catecholamines were elevated then it is an issue.


Yes, but as you saw they also said proper large scale intervention studies have not been done. It may very well come down to things like liver function, and other dietary factors like mineral balance, etc. If fructose is indeed a chelator then it can potentially cause issues if mineral balance is suboptimal. Actually, even by increasing PDH actitivy and thus overall sugar metabolism and CO2 synthesis it would increase needs for calcium, and sodium. Not saying this alone explains negative effects but increased trigs in the blood are due usually due (in that order) to 1) increased fat intake; 2) increased lipolysis; 3) high estrogen; 4) excessive carb consumption. So, I would try to rule out the first 3 before assuming sucrose was the issue.

Ok.

I had done blood tests for many minerals except calcium which I consumed a lot of, there were all perfectly within range. If there's one mineral that is annoying to get it's magnesium, also other people have suggested the calcium:magnesium ratio is important so that's one possibility.

There could definitely be an other reason for elevated triglycerides than fructose:

Arterioscler Thromb 1991 Jul-Aug;11(4):1059-67
Will a high-carbohydrate, low-fat diet lower plasma lipids and lipoproteins without producing hypertriglyceridemia?
Ullmann D, Connor WE, Hatcher LF, Connor SL, Flavell DP. Department of Medicine, Oregon Health Sciences University, Portland 97201-3098.

A sudden increase in dietary carbohydrate invariably increases the plasma levels of very low density lipoprotein (VLDL) and triglyceride. The present studies were designed to test the hypothesis that dietary carbohydrate-induced hypertriglyceridemia need not occur. In the first study we fed gradually increasing amounts of carbohydrate and gradually decreasing amounts of fat to eight subjects. The usual American diet (40% fat, 45% carbohydrate, and 15% protein) was followed in sequence by four diets in a phased regimen, the carbohydrate increasing by 5% of total calories and the fat content decreasing by 5% for each dietary period. In the last dietary period (phase 4), 20% of the energy was in the form of fat and 65% in the form of carbohydrates; the cholesterol content was 100 mg/day. Throughout the study, plasma triglyceride and VLDL triglyceride levels did not change significantly. The plasma total and low density lipoprotein (LDL) cholesterol levels were greatly reduced, by 15% and 22%, respectively (p = 0.004). Plasma high density lipoprotein (HDL) cholesterol levels decreased concomitantly. In the second study, after a washout period six of the subjects were initially fed the phase 4 high-carbohydrate diet for a 10-day period. The plasma triglyceride concentration increased over baseline levels by 47%, and VLDL triglyceride levels increased by 73%. We conclude that although a sudden increase in dietary carbohydrate increases the plasma triglyceride level, patients gradually introduced to a high-carbohydrate, low-fat diet may achieve a significant reduction of plasma total and LDL cholesterol without developing carbohydrate-induced hypertriglyceridemia.

Look at the changed body compostion!

Rofl .
The study should have lasted longer .

 

[Giraffe]

Rofl .
The study should have lasted longer .

I had the impression that it was this very same study that made you think that for weight loss "a starch-full low fat diet" was better than a high-sucrose diet.

I do agree that it takes more than two weeks to see what the long-term effect of a diet is.

 

[Wagner83]

I had the impression that it was this very same study that made you think that for weight loss "a starch-full low fat diet" was better than a high-sucrose diet.

I do agree that it takes more than two weeks to see what the long-term effect of a diet is.

Lol yeah I guess I should not rely on the summary of studies, not sure how they come to such poor conclusions from such poor studies.

Here is an other one:
https://www.ncbi.nlm.nih.gov/pubmed/11756055

BACKGROUND:
Overweight individuals with metabolic syndrome are at increased risk of type 2 diabetes and coronary vascular disease. Weight gain and features of the syndrome may be ameliorated by dietary intervention.

OBJECTIVE:
We investigated the effects of replacing one-quarter of daily fat intake by complex or simple carbohydrate on body weight and intermediary metabolism.

DESIGN:
Forty-six subjects with > or =3 metabolic syndrome risk factors were randomly assigned to receive a control diet; a low-fat, complex carbohydrate diet (LF-CC); or a low-fat, simple carbohydrate diet (LF-SC) for 6 mo. Thirty-nine subjects completed the trial. About 60% of daily dietary intake was provided free of charge through a grocery store. Energy intake was ad libitum. Body weight, body mass index (BMI), blood pressure, and blood lipids were measured at months 0, 2, 4, and 6.

RESULTS:
There was a significant diet x time interaction on body weight and BMI (P < 0.001). Weight loss was greatest with the LF-CC diet [change in body weight: control diet, 1.03 kg (NS); LF-CC diet, -4.25 kg (P < 0.01); LF-SC diet, -0.28 kg (NS)]. Total cholesterol decreased by 0.33 mmol/L, 0.63 mmol/L, and 0.06 mmol/L in subjects consuming the control, LF-CC, and LF-SC diets, respectively (difference between the LF-CC and LF-SC groups: P < 0.05). There were no significant changes in LDL cholesterol, whereas HDL cholesterol decreased over time in all 3 groups (P < 0.0001). Triacylglycerol concentrations were higher in the LF-SC group than in the other 2 groups (P < 0.05).

CONCLUSIONS:
A low-fat, high-polysaccharide diet in overweight individuals with abnormal intermediary metabolism led to moderate weight loss and some improvement in serum cholesterol. Increasing simple carbohydrates did not promote weight gain, but nor was there improvement in body weight or lipid profile.

 

[Giraffe]

Lol yeah I guess I should not rely on the summary of studies, not sure how they come to such poor conclusions from such poor studies.

Actually the design of that one study (first link in OP) wasn't that bad (realistic diets, rating palatability etc), and as far as I can see, their conclusions were not hyperbolic.

Here is an other one:
Long-term effects of ad libitum low-fat, high-carbohydrate diets on body weight and serum lipids in overweight subjects with metabolic syndrome. - PubMed - NCBI

" Triacylglycerol concentrations were higher in the LF-SC group than in the other 2 groups (P < 0.05)."

Peat said in one interview that triglycerides made from sugar or other carbs are "evidence that you are under stress and eating more than you need", and that they aren't harmful.

Dr. Ray Peat: Glycemia, Starch and SUGAR in context!

.....

There is some information missing in that study, for example fiber content of the diets, percentage male participants. It's a pity that they did not measure body composition, the only hint is the waist circumference (figure 2), but some of their data are interesting.

Data from the weighed-food records in our trial showed total energy intake to be 8022, 8108, and 9578 kJ/d in the control, LF-CC, and LF-SC groups, respectively. Because diet records are reliable only as a tool by which to rank intake and not as an absolute measure (23), it is necessary to be cautious when interpreting these results.

Subjects in the high-sugar group found it difficult to incorporate the very high sugar component into their diet, and encouragement by the dietitians resulted in supplementation of, rather than substitution for, both fat and complex carbohydrates. A high sugar intake has been proposed as a causal factor in the etiology of obesity. The results of epidemiologic studies, however, oppose this view (29) and are supported by our current trial. Despite a considerable increase in sugar intake, there was no evidence of weight gain in the LF-SC group.

 

[Braveheart]

"Peat said in one interview that triglycerides made from sugar or other carbs are "evidence that you are under stress and eating more than you need", and that they aren't harmful."

I find this to be the case.....

 

[Wagner83]

@Giraffe, thanks for digging those.

 

[schultz]

In that first study (sucrose vs. starch vs. fat) the energy intake was reduced on the starch diet. The authors assume that reason must be "either an increased satiating power or reduced palatability compared with the sucrose and fat diets." The diet contained a lot more fiber than the other ones.

Look at the changed body compostion!

View attachment 5202e

C = control, PO = post obese

Where did you get the full text? I wasn't able to get any because I couldn't find the DOI's.

It's hard to critique any of these abstracts without the full text.

The first study posted didn't control for calorie intake. Also it says this...

"Overall satisfy and palatability ratings were also highest on the sucrose diet."

Yep sugar is yummy.

"Average 14 d ad libitum energy intake was 13% and 12% lower on the starch diet compared with the sucrose and fat diets"

The adrenaline and noradrenaline is odd. I would love to go over the full text.

The third study is a bit strange. 90% of calories for dinner, with 42% of those calories coming from fat? Again, I would love to read the full paper as I am a little unsure what they mean by "undersirable changes in several of the parameters associated with glucose tolerance."

 

[Wagner83]

THE EFFECT OF GLUCOSE AND FRUCTOSE INGESTION ON THE ADRENALINE AND NORADRENALINE LEVELS IN HUMAN PLASMA

Failure of adrenaline to induce hyperglycaemia after fructose injection in young mice.

 

[SOMO]

THE EFFECT OF GLUCOSE AND FRUCTOSE INGESTION ON THE ADRENALINE AND NORADRENALINE LEVELS IN HUMAN PLASMA

Failure of adrenaline to induce hyperglycaemia after fructose injection in young mice.

Does adrenaline normally cause hyperglycemia?

 

[Wagner83]

Chronic high-sucrose diet increases fibroblast growth factor 21 production and energy expenditure in mice. - PubMed - NCBI

J Nutr Biochem. 2017 Nov;49:71-79. doi: 10.1016/j.jnutbio.2017.07.010. Epub 2017 Jul 25.
Chronic high-sucrose diet increases fibroblast growth factor 21 production and energy expenditure in mice.
Maekawa R1, Seino Y2, Ogata H1, Murase M1, Iida A1, Hosokawa K1, Joo E3, Harada N3, Tsunekawa S1, Hamada Y1, Oiso Y1, Inagaki N3, Hayashi Y4, Arima H1.
Author information
Abstract
Excess carbohydrate intake causes obesity in humans. On the other hand, acute administration of fructose, glucose or sucrose in experimental animals has been shown to increase the plasma concentration of anti-obesity hormones such as glucagon-like peptide 1 (GLP-1) and Fibroblast growth factor 21 (FGF21), which contribute to reducing body weight. However, the secretion and action of GLP-1 and FGF21 in mice chronically fed a high-sucrose diet has not been investigated. To address the role of anti-obesity hormones in response to increased sucrose intake, we analyzed mice fed a high-sucrose diet, a high-starch diet or a normal diet for 15 weeks. Mice fed a high-sucrose diet showed resistance to body weight gain, in comparison with mice fed a high-starch diet or control diet, due to increased energy expenditure. Plasma FGF21 levels were highest among the three groups in mice fed a high-sucrose diet, whereas no significant difference in GLP-1 levels was observed. Expression levels of uncoupling protein 1 (UCP-1), FGF receptor 1c (FGFR1c) and β-klotho (KLB) mRNA in brown adipose tissue were significantly increased in high sucrose-fed mice, suggesting increases in FGF21 sensitivity and energy expenditure. Expression of carbohydrate responsive element binding protein (ChREBP) mRNA in liver and brown adipose tissue was also increased in high sucrose-fed mice. These results indicate that FGF21 production in liver and brown adipose tissue is increased in high-sucrose diet and participates in resistance to weight gain.