Fructose consumption did not significantly affect fasting glucose or insulin. Data were expressed as mean difference (MD) for fasting glucose and insulin, and .. Bayer Consumer Care; Oldways Preservation Trust; The International Tree Nut Council Nutrition . Moher D,; Liberati A,; Tetzlaff J,; Altman DG,; PRISMA Group. Sugar. Nutrition. Lipids and lipoprotein metabolism. Clinical trial. Systematic review at ≥g/d , a threshold roughly equivalent to the average fructose intake in the for triglycerides, and 2-h triglyceride difference post-meal) were extracted. .. Bayer Consumer Care, Oldways Preservation Trust, The International Tree. Mar 19, Identify the relationship between each pair of compounds: D-glucose and D- fructose are -- constitutional isomers. D-galactose and D-fructose.
Fructose has been claimed to be of concern due to several factors: First, in the 's, sucrose was replaced to a large extent, particularly in North America, by high fructose corn syrup HFCS in carbonated beverages. The intake of soft drinks containing HFCS has risen in parallel with the epidemic of obesity [ 3 ].
Second, dietary fructose has been implicated in risk factors for cardiovascular disease CVD: Fructose intake has been found to predict LDL particle size in overweight schoolchildren [ 4 ]; 3.
A positive relationship has been demonstrated between fructose intake and uric acid levels [ 5 ].
Health implications of fructose consumption: A review of recent data
Third, the use of fructose as a sweetener has increased. These studies suggest that the relationship between fructose and health needs re-evaluation. Fructose consumption and body weight Lipogenesis from fructose consumption may theoretically be greater than that induced after eating other types of sugars such as glucose and sucrose [ 7 ].
But could this be physiologically true?
Is high fructose corn syrup (HFCS) worse than sugar? | hair-restore.info
Evidence from experimental studies in animals The evidence of the action of dietary fructose, but not glucose, on increasing appetite and food intake in acute-term studies has been derived mainly from experimental studies in animals. Although glucose and fructose utilize the same signaling pathway to control food intake, they act in an inverse manner and have reciprocal effects on the level of the hypothalamic malonyl-CoA, a key intermediate in the hypothalamic signal cascade that regulates energy balance in animals [ 8 ].
When injected into the cerebroventricles of rats, fructose has been found to induce increase in food intake via a reduction of hypothalamic malonyl-CoA levels, whereas similar concentrations of injected glucose increased malonyl- CoA suppressing appetite-agonist and food intake [ 9 ]. The rapid initial steps of central fructose metabolism deplete hypothalamic ATP level, whereas the slower regulated steps of glucose metabolism elevate hypothalamic ATP level.
The question has been raised as to whether fructose may induce the same effects if presented in the systemic circulation and not injected directly in the brain. Consequently, Cha et al [ 10 ], demonstrated that when glucose was administered intra-peritoneally, hence entered the systemic circulation, it was rapidly metabolized by the brain, increasing the level of hypothalamic malonyl-Co-A.
Fructose administration, however, had the opposite effect on malonyl-Co-A and food intake. Such a finding might appear to set off another alarm bell about the problems of dietary fructose. While this paper demonstrated that high doses of fructose and glucose acted on different pathways, the physiological significance of these results remains unclear.
Fructose ingestion is unlikely to increase fructose levels in the cerebrospinal fluid, and plasma fructose levels will never exceed the micromolar range under physiological conditions.
Some authors suggested the uncertainty of these effects [ 11 ]. Therefore, no evidence of cause for health concern could be drawn from such acute studies in rodents. The effects of fructose on body weight were further questioned.
Thus, in rodents while excessively high fructose intake may increase appetite by different mechanisms, its' effect on body weight needs long term dietary periods. Acute studies in humans: More recently, the intensity of the debate was fuelled by the hypothesis that HFCS lead to obesity because fructose bypasses food intake regulatory system insulin and leptin and favors lipogenesis [ 17 ]. It was hypothesized that energy containing drinks, especially those sweetened with HFCS promotes energy imbalance and thereby play a role in the development of obesity.
What is the relationship between D-glucose and D-fructose?
As expected, glucose excursions and insulin secretion were lower after fructose meals than after glucose ones. This was associated to a decrease in leptin levels, which is an expected consequence of lowering insulin levels. It is important to notice that the reduction in leptin levels remained within physiological normal levels and fluctuated between: After this acute- term study, following only one meal, the authors rapidly suggested that because insulin and leptin the main regulatory factors of food intake were lower after fructose meals; they might increase caloric intake and ultimately contribute to weight gain and obesity.
Fructose meals should be compared to sucrose the usual sugar and not to glucose which gives extreme levels. The question was then raised whether HFCS has different effect on satiety than other isoenergetic drinks as sucrose or milk; again this question was investigated in an acute study. In order to have a simple response Soenen and Westerterp [ 18 ] compared the satiating effects of ml of HFCS, sucrose and milk containing each 1.
Health implications of fructose consumption: A review of recent data
They measured satiety by a visual analogue scale and by determining the satiety hormones leptin and ghrelin concentrations. They concluded that energy balance consequences were the same between the three isoenergetic drinks evaluated.
Therefore, fructose in term of satiety is not different from that of usually consumed sugar and even that of another isocaloric drink milk.
In another study Akhavan et al [ 19 ] aimed to evaluate whether HFCS in soft drinks is different from sucrose solutions. F50 on food intake, average appetite and on plasma concentrations of glucose, insulin and ghrelin.
Measurements were taken from base line to 80 minutes only. The authors of the latter paper concluded that all the solutions tested do not have significantly different effects on subjective and physiologic measures of satiety at a subsequent meal.
Therefore, there is no solid evidence that sucrose, when consumed in its intact form, would confer any benefits over HFCS, which contains the 2 unbound monosaccharides. Similarly, in a 24 hour study Stanhope [ 20 ] and Melanson [ 21 ] did not find substantially different effects between meals with either sucrose or HFCS on 24 hour plasma glucose, insulin, leptin and ghrelin levels.
Even TG profiles were found to be similar between the two tests. These responses were found to be intermediate between the lower responses after the pure fructose syrup consumption and the higher responses after glucose solution ingestion.
There was no difference in food intake during a meal consumed 50 min later or in the components of food intake regulatory mechanisms.
Chronic studies in humans Although acute fructose consumption could not stimulate leptin secretion, an increase in fasting leptin levels was detected after chronic high fructose intake 1 to 4 weeks in healthy individuals, which may suggest that high fructose feeding may suppress food intake in the long term [ 22 ].
In a cluster randomized controlled study [ 24 ], the effect of a focused educational intervention program on carbohydrate sweetened beverage consumption and overweight was studied using children years old. Children participated in a program designed to emphasize the consumption of a balanced diet and to discourage the consumption of sweetened drinks mainly by sucrose: Sweetened drink consumption decreased in the intervention group and increased in the control one. Parallel changes in BMI occurred in each group, but without any difference between the two groups.
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Therefore, no conclusion could be given on appetite or body weight even if fructose is present as a part of sucrose. Epidemiological studies The recent epidemiological study of Vos et al [ 6 ] created new concern in regards to fructose consumption. Investigators found that fructose consumption had increased to The consumption was highest among adolescents years at Bray et al [ 25 ] suggested that the increase in obesity in the last 35 years has paralleled the increasing use of high-fructose corn syrup HFCSwhich first appeared just before Current soft drinks and many other foods are sweetened with this product because it is inexpensive and has useful manufacturing properties.
The fructose in HFCS and sugar makes beverages very sweet, and this sweetness may underlie the relationship between obesity and soft drink consumption. Indeed in the United States, HFCS has increasingly replaced sucrose in many foods and sweetened beverages, a fact that might appear to strengthen the hypothesis that there is a relationship between fructose and obesity.
The search was restricted to human studies without language restrictions. Manual searches of the reference lists of included studies supplemented electronic searches. Study selection We included prospective cohort studies that assessed intake of fructose-containing sugars total sugars, fructose, sucrose, high-fructose corn syrup or added sugars and incident type 2 diabetes in participants who did not have diabetes.
Data extraction Two reviewers C.
Authors were contacted for missing data. Risk of bias The Newcastle-Ottawa Scale NOS was used to assess the risk of bias in included studies, where up to 9 points were awarded based on cohort selection, comparability adjustments and ascertainment of the outcome.
Statistical analysis To obtain summary estimates, we natural log-transformed and pooled the RRs using the generic inverse variance method with random-effects models. To assess whether any single study exerted an undue influence on the summary estimates, we performed sensitivity analyses by systematically removing each study with recalculation of the summary estimates. We performed additional sensitivity analyses by restricting pooled analyses to studies using validated measures of sugars intake to assess any influence of how the exposures were assessed.
Prespecified subgroup analyses were done by sex, follow-up, NOS and individual domains of NOS using meta-regression analyses. If 10 or more cohort comparisons were available, we investigated publication bias by visual inspection of funnel plots and using the Begg and Egger tests. Data were analyzed using Review Manager RevMan version 5. Results Figure 1 shows the flow of the literature search. Out of reports, we included 9 reports of 15 cohort studies involving unique participants and 16 cases of type 2 diabetes: There were no cohort comparisons available for high-fructose corn syrup or added sugars.