Fructose metabolism in humans – what isotopic tracer studies tell us

Sun, Sam Z.; Empie, Mark W.

doi:10.1186/1743-7075-9-89

Cited by 265 publications

(241 citation statements)

References 81 publications

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“…E. Energy expenditure and net substrate oxidation were calculated using the equations of Livesey and Elia (18), assuming that total nitrogen excretion was equal to (urinary urea nitrogen excretion)/ 0.85 (19).…”

Section: Obesitymentioning

confidence: 99%

Effects of roux‐en‐Y gastric bypass surgery on postprandial fructose metabolism

Surowska

Giorgi

Theytaz

et al. 2016

Obesity

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Objective: Fructose is partly metabolized in small bowel enterocytes, where it can be converted into glucose or fatty acids. It was therefore hypothesized that Roux-en-Y gastric bypass (RYGB) may significantly alter fructose metabolism. Methods: We performed a randomized clinical study in eight patients 12-17 months after RYGB and eight control (Ctrl) subjects. Each participant was studied after ingestion of a protein and lipid meal (PL) and after ingestion of a protein1lipid1fructose1glucose meal labeled with 13 C-fructose (PLFG). Postprandial blood glucose, fructose, lactate, apolipoprotein B48 (apoB48), and triglyceride (TG) concentrations, 13 C-palmitate concentrations in chylomicron-TG and VLDL-TG, fructose oxidation ( 13 CO 2 production), and gluconeogenesis from fructose (GNGf) were measured over 6 hours. Results: After ingestion of PLFG, postprandial plasma fructose, glucose, insulin, and lactate concentrations increased earlier and reached higher peak values in RYGB than in Ctrl. GNGf was 33% lower in RYGB than Ctrl (P 5 0.041), while fructose oxidation was unchanged. Postprandial incremental areas under the curves for total TG and chylomicrons-TG were 72% and 91% lower in RYGB than Ctrl (P 5 0.064 and P 5 0.024, respectively). ApoB48 and 13 C-palmitate concentrations were not significantly different. Conclusions: Postprandial fructose metabolism was not grossly altered, but postprandial lipid concentrations were markedly decreased in subjects having had RYGB surgery.

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Section: Obesitymentioning

confidence: 99%

Effects of roux‐en‐Y gastric bypass surgery on postprandial fructose metabolism

Surowska

Giorgi

Theytaz

et al. 2016

Obesity

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“…In addition, it has little effect on blood glucose levels as it is digested primarily in the liver (Tappy and Le, 2010). The liver metabolizes fructose much like a lipid, and the energy is either converted to glucose or lactate (a process that takes hours, not minutes) or it is converted into glycogen (for a review see Sun and Empie, 2012). The stored glycogen then can be converted to glucose if necessary through glycogenolysis (Tappy and Le, 2010).…”

Section: Fructose and Persistencementioning

confidence: 99%

Self-regulatory depletion in dogs: Insulin release is not necessary for the replenishment of persistence

Miller

Pattison

Laude

et al. 2015

Behavioural Processes

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It has been hypothesized that self-control is constrained by a limited energy resource that can be depleted through exertion. Once depleted, this resource can be replenished by the consumption or even the taste of glucose. For example, the need to inhibit reduces subsequent persistence at problem solving by humans and dogs, an effect that is not observed when a glucose drink (but not placebo) is administered following initial inhibition. The mechanism for replenishment by glucose is currently unknown. Energy transfer is not necessary, though insulin secretion may be involved. This possibility was investigated in the current study by having dogs exert self-control (sit-stay) and subsequently giving them (1) glucose that causes the release of insulin, (2) fructose that does not result in the release of insulin nor does it affect glucose levels (but is a carbohydrate), or (3) a calorie-free drink. Persistence measures indicated that both glucose and fructose replenished canine persistence, whereas the calorie-free drink did not. These results indicate that insulin release is probably not necessary for the replenishment that is presumed to be responsible for the increase in persistence.(182 words)

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“…Some investigators have focused on the fructose component of sucrose/HFCS as the "evildoer" of sugar consumption as glucose and fructose are absorbed and metabolized differently (2). The impact of fructose on body weight was reviewed above and the evidence suggests no difference between fructose and any other monosaccharide (12,38).…”

Section: What About Fructose or Hfcs?mentioning

confidence: 99%

“…Finally, whereas glucose and fructose are metabolized differently, the belief that sucrose is metabolized differently than HFCS is a myth. No study has shown any difference between the two when each is given isocalorically, nor is there any difference in sweetness or caloric value (1)(2)(3).…”

mentioning

confidence: 99%

Dietary Sugar and Body Weight: Have We Reached a Crisis in the Epidemic of Obesity and Diabetes?

Kahn

Sievenpiper

2014

Diabetes Care

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In the preceding point narrative, Drs. Bray and Popkin provide their opinion and review data that suggest to them that we need to reconsider the consumption of dietary sugar based on the growing concern of obesity and type 2 diabetes. In the counterpoint narrative below, we argue that there is no clear or convincing evidence that any dietary or added sugar has a unique or detrimental impact relative to any other source of calories on the development of obesity or diabetes. Sugar is purely a highly palatable source of energy; because it has no other property that appears to contribute to our nutritional well-being, it is not an essential food for most of us. For those who wish to reduce energy consumption, ingesting less sugar is a good place to start. However, doing so does not automatically portend any clinical benefit.In this counterpoint discussion, we use the phrase "dietary sugar" or "added sugar" to mean sucrose or high-fructose corn syrup (HFCS). Almost all dietary or added sugar used as an ingredient in either solid (e.g., desserts, snacks) or liquid (e.g., sugar-sweetened beverages [SSB]) foods is in the form of these two disaccharides. Although we will discuss evidence from feeding studies in which fructose itself was used as the sole added sweetener, it should be noted that fructose rarely occurs alone in foods commonly consumed by humans. Also of importance is the fact that sucrose and HFCS are both composed of glucose and fructose. Whereas the ratio of glucose to fructose is equal in sucrose, in HFCS the ratio is usually 55% fructose, 42% glucose, and 3% glucose polymers; other forms of HFCS have a lower proportion of fructose. In addition, the glucose and fructose in HFCS are free in solution; in sucrose they are initially bound together. But when sucrose is used in processed or prepared foods/beverages an appreciable amount is broken down to free fructose and glucose prior to consumption. Finally, whereas glucose and fructose are metabolized differently, the belief that sucrose is metabolized differently than HFCS is a myth. No study has shown any difference between the two when each is given isocalorically, nor is there any difference in sweetness or caloric value (1-3).Much of the condemnation of sugar in the last few years owes its origin to an article by Bray et al. (4) showing an ecological relationship between sugar availability (a crude measure of intake) and obesity, which has now been expanded to explain a myriad of metabolic abnormalities (5-7). Table 1 shows that the rise in the prevalence of overweight/obesity in the early 1980s does indeed appear to be related to an increase in the availability of added sugars. However, starting around 2000, sugar

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Fructose metabolism in humans – what isotopic tracer studies tell us

Cited by 265 publications

References 81 publications

Effects of roux‐en‐Y gastric bypass surgery on postprandial fructose metabolism

Effects of roux‐en‐Y gastric bypass surgery on postprandial fructose metabolism

Self-regulatory depletion in dogs: Insulin release is not necessary for the replenishment of persistence

Dietary Sugar and Body Weight: Have We Reached a Crisis in the Epidemic of Obesity and Diabetes?

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