Metabolic Effects Of A Prolonged, Very-high-dose Dietary Fructose Challenge In Healthy Subjects

Mito

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ABSTRACT
Background
Increased fructose intake has been associated with metabolic consequences such as impaired hepatic lipid metabolism and development of nonalcoholic fatty liver disease (NAFLD).

Objectives
The aim of this study was to investigate the role of fructose in glucose and lipid metabolism in the liver, heart, skeletal muscle, and adipose tissue.

Methods
Ten healthy subjects (age: 28 ± 19 y; BMI: 22.2 ± 0.7 kg/m2) underwent comprehensive metabolic phenotyping prior to and 8 wk following a high-fructose diet (150 g daily). Eleven patients with NAFLD (age: 39.4 ± 3.95 y; BMI: 28.4 ± 1.25) were characterized as “positive controls.” Insulin sensitivity was analyzed by a 2-step hyperinsulinemic euglycemic clamp, and postprandial interorgan crosstalk of lipid and glucose metabolism was evaluated, by determining postprandial hepatic and intra-myocellular lipid and glycogen accumulation, employing magnetic resonance spectroscopy (MRS) at 7 T. Myocardial lipid content and myocardial function were assessed by 1H MRS imaging and MRI at 3 T.

Results
High fructose intake resulted in lower intake of other dietary sugars and did not increase total daily energy intake. Ectopic lipid deposition and postprandial glycogen storage in the liver and skeletal muscle were not altered. Postprandial changes in hepatic lipids were measured [Δhepatocellular lipid (HCL)_healthy_baseline: −15.9 ± 10.7 compared with ± ΔHCL_healthy_follow-up: −6.9 ± 4.6; P = 0.17] and hepatic glycogen (Δglycogen_baseline: 64.4 ± 14.1 compared with Δglycogen_follow-up: 51.1 ± 9.8; P = 0.42). Myocardial function and myocardial mass remained stable. As expected, impaired hepatic glycogen storage and increased ectopic lipid storage in the liver and skeletal muscle were observed in insulin-resistant patients with NAFLD.

Conclusions
Ingestion of a high dose of fructose for 8 wk was not associated with relevant metabolic consequences in the presence of a stable energy intake, slightly lower body weight, and potentially incomplete absorption of the orally administered fructose load. This indicated that young, metabolically healthy subjects can at least temporarily compensate for increased fructose intake. This trial was registered at www.clinicaltrials.gov as NCT02075164.

Metabolic effects of a prolonged, very-high-dose dietary fructose challenge in healthy subjects
 

haidut

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As expected, impaired hepatic glycogen storage and increased ectopic lipid storage in the liver and skeletal muscle were observed in insulin-resistant patients with NAFLD

Great find! I think it further corroborates that insulin resistance and NAFLD are endocrine issues that have little to do with sugar and are instead linked to PUFA, cortisol, serotonin, estrogen and growth hormone.
Cortisol And Fatty Liver: Researchers Find Cause Of Severe Metabolic Disorders
Liver Disease Is Caused By Low ATP Driven By Fat (PUFA) Oxidation
 

yerrag

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@Mito what does H and C MRS at 7T mean? I can't read the authors' minds.

What does AUC mean?
 
Last edited:

yerrag

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While the study posits that Table 3 there's no significant change in the healthy subjects after 8 weeks of heavy fructose consumption, in a mixed meal test, as far as hepatic lipids and hepatic glycogen, goes I'm not seeing it:

Before the hepatic lipids was 1.11 +- 1.2, and on followup, it was 1.6 +- 0.5.
And with hepatic glycogen, before it was 64.4 +- 14.1, and on followup, it was 51.1 +- 9.8 (in arbitrary units).

I also think that the study selection of healthy subjects - defined as those with no blood sugar regulation problems, and with no NAFLD problems, as well as no fructose malabsorption problems, pretty much disposes them to be young. In the study, they have an average age of 28 years, whereas the control subjects, with NAFLD, have an average age of 39.4 years.

Being relatively young, they have not accumulated enough insults typical of a Western lifestyle (study is in Vienna) and this makes them able to withstand the challenges posed by a high fructose diet.

How would they fare after they reach 40 I wonder. If they manage to not have NAFLD by then, they could probably still do well ingesting large amount of fructose. But even if they don't acquire NAFLD, what would their gut microbiome be like by then? Would the fructose be feeding more bacteria, and the endotoxins that translocate to blood, would they cause more inflammation in the whole body, and wouldn't this inflammation cause impairment in the sugar uptake by cells, and wouldn't this lead to hyperglycemia and subsequent hypoglycemia from the insulin response? With the insulin response that leads to de novo lipogenesis, wouldn't hepatic lipids increase? And will more fats taking up liver space, wouldn't there be less space for glycogen storage? And wouldn't this lead to the body running out of sugar from endogenous glycogen, and wouldn't this lead to more prevalent stress response?

I think the study is simply saying that when you're young, you could get away with high fructose consumption, generally.
 

S-VV

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I think the H refers to proton-MRS and the C to carbon-MRS
 

yerrag

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SOMO

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I also think that the study selection of healthy subjects - defined as those with no blood sugar regulation problems, and with no NAFLD problems, as well as no fructose malabsorption problems, pretty much disposes them to be young. In the study, they have an average age of 28 years, whereas the control subjects, with NAFLD, have an average age of 39.4 years.

Being relatively young, they have not accumulated enough insults typical of a Western lifestyle (study is in Vienna) and this makes them able to withstand the challenges posed by a high fructose diet.

I understand your point and I don't mean to nitpick, but there are many, many overweight and unhealthy people under 30. I was one myself
 

yerrag

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I understand your point and I don't mean to nitpick, but there are many, many overweight and unhealthy people under 30. I was one myself
And by your reasoning the exception makes the rule?
 

NathanK

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I can’t access the full study, but is this the study Chris Masterjohn referenced that showed they ate a high methionine diet that mediated the response by increasing choline?
 
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