How does sucrose provide energy




















They then travel to the liver to be metabolised. In other words, they are released into the blood for immediate energy, or stored as glycogen or fatty acids for later use. Bees produce honey, which is also a natural form of inverted sugar. They produce invertase and regurgitate it to add it to the nectar.

This enzyme transforms the nectar, essentially made up of water and sucrose, into glucose and fructose. Dictionnaire historique de la Suisse. Sugar World markets and trade.

Home Sucrose. Sucrose Table sugar is sucrose, synthesised by plants such as sugar cane and sugar beet. Overall this study suggests that normal sucrose intake may increase post-prandial TG levels, possibly due to reduced clearance, while it does not alter basal lipid profiles. Two studies in the review Grande et al.

Only the vegetable diet resulted in lower lipid levels. Similarly, Fraser et al. There were also 2 other conditions involving partial substitution of sucrose with root vegetables or leafy vegetables. However, higher fibre intakes in these conditions may have confounded the association. Taken together, these studies fail to provide good evidence of a significant detrimental effect of sucrose on lipid metabolism, at least over 2—3 weeks, although they do raise the possibility of small post-prandial changes of uncertain significance.

The diets were identical in protein, fat, and total carbohydrate content Using data given in the paper Reiser et al. Two other factors may have contributed to the magnitude of the sucrose effect on metabolism. Together with the heterogeneous responses between healthy and less healthy individuals identified above this may limit the extent to which these studies are generalizable to normal dietary patterns and healthy people.

More recently, another 6 week randomized controlled study using levels of sucrose consistent with modern European diets, Black et al. The high sucrose diet resulted in no significant differences in HDL or TG, or measures of vascular compliance blood pressure, arterial stiffness. IR, as measured by the gold standard method, was also unaffected see the next section.

Nor can it be assumed to be the same in ad libitum conditions, or in the context of underfeeding or overfeeding, discussed later. For example, in a study primarily designed to look at glycaemic effects, Anderson et al.

The unphysiological level of sucrose at which effects were observed means that results from this study are of limited value to the research question.

Weight loss occurred due to a significantly reduced energy intake and was correlated with the reduction in lipids, begging the question as to whether the negative energy balance or sucrose reduction caused improvement in fasting lipids. The authors took the view that negative calorie balance was the likely cause and speculated that weight loss from restriction of other constituents may have a similar effect. However, 24 hr plasma TG concentrations measured by continuous blood withdrawal were significantly higher on both sucrose diets Hayford et al.

In a longer study among young men in the British Antarctic survey team, Roberts examined the effect of substituting virtually all dietary sucrose with glucose for 14 weeks and then restoring sucrose for another 24 weeks Roberts, Weight did not change throughout the study and there was no change in TC overall. The author interpreted this as evidence for increased sucrose sensitivity although it might be attributable to regression to the mean Mann and Truswell, During the sucrose-restored period, TG initially rose but then slowly subsided toward normal preintervention levels.

Bearing in mind the small effects observed, this study does not suggest that sucrose produced lipid changes that were either harmful or beneficial. However, the longest study by far included in this review was a 2-year study of the effect on plasma lipids of replacing table sugar with dried glucose syrup each diet followed for 1 year; Lock et al. Fasting blood samples were taken every 4 weeks and dietary questionnaires administered every 3 months to monitor compliance in macronutrient composition.

However, there was no change in fasting TG except in those who gained weight. This study suggests that the elevated fasting TG levels seen in shorter studies may be a transient phenomenon. It also raises the possibility that carbohydrate type may modify some aspects of lipid metabolism e.

In a study comparing sucrose with fructose, Bosetti et al. Similarly, in a crossover study using fructose, sucrose, and glucose drinks for 3 weeks, lipoprotein concentrations were unchanged on all conditions, and sucrose and fructose results were similar with regard to LDL subclass distribution Aeberli et al.

Elevated fasting plasma insulin is regarded as an early sign of IR and results of this basic measurement correlate moderately well with the euglycaemic clamp technique. Homeostatic model assessment HOMA , derived from the ratio of fasting insulin and glucose concentrations, is better than fasting insulin per se, but this too reflects the basal state.

Most of insulin action occurs in the post-prandial state Daly, , therefore studies that provide evidence on response to a glucose or sucrose load after habituation to high sucrose diets are also valuable. In comparison to blood lipids, relatively few studies examined the effect of sucrose substitution on blood glucose or insulin.

However, studies using less extreme intakes have not shown the same results. For example, Dunnigan et al. However, no significant differences were found for fasting plasma insulin or area under curve AUC for blood glucose or insulin using the glucose tolerance test.

Overall, this study suggests that except for small changes in fasting blood glucose, carbohydrate tolerance was not altered. However, post-prandial differences were studied in 5 out of the 9 subjects. On the sucrose diet, there was a significantly lower glycaemic and insulin response compared with the starch diet provided by rice and potatoes , so this well-controlled study suggests that ingestion of sucrose at a normal physiological level may reduce post-prandial insulin secretion compared with starch.

This may be a consequence of the lower glycaemic index GI of sucrose compared with the starches used in the intervention. More recent studies have tended to confirm that diets high in sucrose do not cause greater insulinemia than starch, which is not unexpected given that the fructose component of sucrose is a poor insulin stimulator.

In fact on the basis of GI, the effect of sucrose would be predicted to be intermediate between low GI and high GI diets. By the end of the day period, fasting blood glucose and plasma insulin were not significantly higher on the high sucrose diet. However, there was also some evidence of adaptation resulting in a more rapid and larger insulin response over time. In agreement with these general findings are the Danish studies of Raben, Marckmann, and colleagues who examined diurnal metabolic profiles on day 15, after 2 weeks of ad libitum diets high in sucrose or starch.

Possibly due to the lower GI of sucrose relative to starch, the sucrose-rich diet appeared to improve glucose metabolism glucose AUCs were lower and there was no significant difference in insulin AUCs; Raben et al. These findings are in agreement with other work by Daly et al. Lastly, in the controlled study by Black et al. However, variation between studies may be partly explained by the form of starch and by total dietary GI, fibre, and fat content. Subjects required more insulin to achieve equivalent levels of blood glucose when they consumed sucrose than when they consumed starch, suggesting that they were less insulin-sensitive on the sucrose diet.

However, data presented show that this was only apparent among the 9 subjects who were hypertriglyceridaemic or potentially carbohydrate-sensitive, while the normal subjects showed no significant effect of diet on their insulin response to the sucrose load.

A subsequent paper Reiser et al. However, as the paper did not distinguish between carbohydrate-sensitive and normal subjects, it is not clear to what extent this applied to the latter. As noted in the previous section on lipid outcomes, the gorging pattern of sucrose delivery in this study may have exaggerated the metabolic effects.

Only 3 studies in the review include data on the glycaemic responses of sucrose compared with other sugars and none indicated significant differences in metabolic response. In an early study of sucrose versus glucose among men living on an Antarctic Base camp Fry, , the AUC for blood glucose was the same for both diets although the pattern of response was slightly different; blood glucose levels were slightly higher at 30 min for sucrose but declined more rapidly. Bosetti et al. One metabolic ward study in healthy young men aged 18—22 years found that a supra-physiologic level of sucrose over a relatively short time period resulted in an improvement of glucose tolerance.

The authors suggested that high CHO diets may increase insulin sensitivity in these normal individuals, possibly by enhancing activity of the important glycolytic and pentose phosphate pathway enzymes in various tissues. They contrasted their results in normal men with those in HTG patients, in whom abnormalities of lipid and glucose metabolism frequently occur together, suggesting that these may not be causally related but rather separate manifestations of a more basic underlying abnormality Anderson et al.

The third study Brynes et al. Overall, the studies included in our review do not provide evidence of any consistent difference between sucrose and starch or other carbohydrates in respect of the basic markers of insulin sensitivity. Short-term studies of post-prandial and diurnal metabolism offer a more precise means of assessing metabolic effects using more sophisticated assessment methods such as the hyperinsulinaemic, euglycaemic clamp.

These also suggest that 24 hr AUC for insulin may be comparable but patterns of response may differ Daly et al. As yet there is no evidence to determine which feature post-prandial elevation or 24 hr AUC has more influence on metabolic health over the longer term Daly, One of the questions raised by ad libitum and noneucaloric studies is whether the outcomes observed are attributable to altered energy intake.

In a series of papers from the same Danish study of 20 women, Raben et al. Energy intake was lower —1. However, the difference in fasting TG levels was found to be nonsignificant after correction for the unintended differences in body weight and energy and nutrient intake between the groups Raben et al. The authors commented that a high sucrose diet may lead to an undesirable lipid profile possibly due to fructose effects on TG production in the liver, on VLDL production and clearance.

After 14 days on the high sucrose diet, 24 hr energy expenditure as well as post-prandial plasma adrenaline and noradrenaline concentrations were significantly increased compared with the other two diets, although with no untoward effect on blood pressure Raben et al. In this case, the subjects were in energy balance on the sucrose diet and the improved lipid profiles on the starch diet could be due at least in part to a spontaneous reduction in energy intake in that phase.

By contrast, the ad libitum crossover study of Brynes et al. The high sucrose diet had effects intermediate between that of the low GI and high GI diets but only the high GI diet appeared to increase post-prandial IR. Although instructed to maintain weight, men tended to lose weight on the low GI diet —0. Surwit et al. Both groups had similar fasting plasma glucose levels, achieved a similar weight loss, and showed a decrease in percentage body fat, blood pressure, resting energy expenditure, and plasma lipids.

The findings of this study and the ad libitum studies above would suggest that metabolic effects may be more strongly related to energy balance than carbohydrate type and in the eucaloric weight maintaining or hypocaloric situation there are few adverse effects of sucrose. Studies demonstrated a high degree of heterogeneity in design and quality.

Most were on small numbers of subjects only 7 studies used more than 20 adults and, given the variation in response between individuals, may have been underpowered. Thus, for example, most studies involving both men and women did not distinguish results by gender. Second, there were few studies 3 reporting specifically on women, and only one was both isocaloric between diet groups and eucaloric weight maintaining and this found no effect on plasma lipids Behall et al.

The ad libitum and hypocaloric studies have been included because they offer insights into the possible impact of changing dietary composition in the real world, although confounding effects have to be borne in mind in interpreting the findings. Lack of control over diet composition is also a more general issue for studies involving real foods. Thus in some cases, manipulation of sucrose content also allowed carbohydrate, protein, or fat content to differ between treatment groups, while in others diets were matched in regard to macronutrient composition fat:protein:carbohydrate but differed in regard to SFA, PUFA, or fibre content.

Thus, some of the observed effects could be due to confounding by other dietary constituents. In our view the evidence is too poorly defined and heterogeneous to derive reliable conclusions on any sucrose substitution except that with starch. By excluding studies lasting less than 3 days, the protocol omitted studies of post-prandial and 24 hr metabolism, except where these were investigated as part of a longer study i.

Nevertheless, results from included studies suggest that there may be subtle differences in the time course of post-prandial response to sucrose compared with other macronutrients. Studies specifically on fructose were also outside the scope of the search strategy, but it is apparent from the large number of recent reviews on fructose that these studies may have implications for sucrose, which is the major source of dietary fructose worldwide.

Some groups have hypothesized that high fructose consumption results in increased visceral adiposity, lipid dys-regulation, and also IR Stanhope and Havel, and that fructose has similar effects to sucrose Stanhope et al. By focusing on human intervention studies in adults without diagnosed CVD, diabetes, or NIDDM, we have tried to avoid what we consider a major threat to validity, that of drawing conclusions based on subjects with preexisting metabolic abnormality.

However, in a number of studies subjects had elevated blood lipids at the start of the study Dunnigan et al. Such factors and others such as genetics and lifestyle may modify the response to dietary change Hellerstein, Nevertheless, there appeared to be heterogeneity in subject response even among apparently healthy individuals. One of the most reproducible findings was that increases in plasma TGs tended to be correlated with baseline levels. This raises the question as to whether subjects with high baseline levels should be excluded from analysis in studies or whether they should be considered as part of the normal distribution.

It is our view that results for all subgroups should be reported separately where power permits. This was mostly followed, although in a few studies and also in some reviews there was evidence of possible reporting bias where conclusions were based on selected subgroups. A further cause of confounding that affects interpretation and generalizability is weight loss or gain and energy deficit or excess during the study.

Energy balance may be as or even more important than diet composition in promoting hyperlipidemia and IR, but whether diets high in sugar always result in higher energy intakes compared with diets high in starch or fat is not established; thus we have considered it legitimate to discuss ad libitum studies, with caveats. Probably the major consideration in evaluating the generalizability of findings is the realism of the sucrose levels used in interventions.

However, two studies in women showed no effect Behall et al. Those that did report adverse effects included a week study on men Mann et al. One study reported changes in components of the atherogenic lipoprotein profile, including LDL particle size, not accompanied by increases in other CVD risk factors Aeberli et al.

Confirmation of these findings and their significance is awaited as these proposed markers have yet to be shown to be associated with CVD risk by prospective studies in a general population cohort. However, intakes are higher among adolescents mean Gibson, unpublished.

Thus, current mean intakes are well below the level at which adverse effects on metabolic health were observed in this review. However, it would be unwise, on the basis of current evidence, to place more emphasis on dietary sugars intake than on physical fitness, weight control, and a healthy balanced diet, which have well-established benefits on cardiometabolic risk factors.

Although relatively few studies examined the effects on blood glucose and insulin, there was little evidence of adverse effects on plasma glucose and some evidence of improved glucose tolerance on diets high in sucrose compared with starch Kiens and Richter, ; Raben et al. Fasting insulin, which is a better risk indicator than plasma glucose for impaired insulin action or reduced insulin sensitivity, was only found to be higher with the sucrose diet in one study whose subjects were potentially carbohydrate-sensitive Reiser et al.

It is important to distinguish between statistical significance and clinical significance. This is similar to normal day-to-day variation but the increment indicative of increased risk remains a matter of debate Parks and Hellerstein, Insufficient data are available to draw reliable conclusions on the effect of substitution of sucrose for other macronutrients, although evidence of any detrimental effect is limited.

On our estimates, less than 0. New research appears to be focusing on the metabolic effects of fructose as the component purported to be responsible for adverse effects of sucrose.

More studies are needed that directly address possible effects of moderately high intake of sucrose on atherogenic lipoprotein phenotype and other indicators of risk of CVD and metabolic syndrome, including inflammatory markers and endothelial function.

Longer-term interventions are needed to establish whether any changes attenuate, persist, or worsen over time and how they are related to IR and visceral adiposity. There is a need to differentiate between subjects at high and low risk and to use healthy adults rather than those in whom metabolism already shows evidence of dysregulation. Studies are especially needed among women of different ages, hormonal status, and body fat distribution. The physical form of sucrose consumed liquid beverages vs.

Finally, intervention studies are desirable to compare the relative impact on CVD risk factors of dietary change with that of changes in body weight and exercise, as these are the two modifiable physiological factors that appear to have greatest impact on response to dietary carbohydrate Hellerstein, This study followed ILSI guidelines relating to financial conflicts and scientific integrity Rowe, It was funded by the World Sugar Research Organisation.

National Center for Biotechnology Information , U. Critical Reviews in Food Science and Nutrition. Crit Rev Food Sci Nutr. Published online Apr 5. Sigrid Gibson 1 Sig-Nurture Ltd. Pippa Gunn 1 Sig-Nurture Ltd. Author information Copyright and License information Disclaimer. E-mail: moc. This article has been cited by other articles in PMC. Abstract We systematically reviewed interventions substituting sucrose for other macronutrients in apparently healthy adults to assess impact on cardiometabolic risk indicators.

Keywords: Sugar, glucose metabolism, lipid metabolism, macronutrient, diet recommendation. Open in a separate window. Figure 1. Table 1 Inclusion and exclusion criteria.

Inclusion criteria Exclusion criteria A Intervention studies or experimental studies involving 2 or moreconditions where subjects are asked to increase or decrease intake of sucrose in exchange for other caloric sources Observational studies, recommendations, guidelines.

E English language Not in English language F Published since Published before G Experimental period lasting 3 days or more Single meal studies, studies shorter than 3 days. Table 2 Studies on the metabolic effects of isocaloric substitution of sucrose for starch ordered by sucrose dose. Starch fed as wheat flour or leguminous seeds. Marckmann et al. Sucrose diet higher in saturated fat.

Raben et al. TG differences were not significant once corrected for differences between groups e. TC and LDL increased but remained within normal range.

Sucrose included in high GI diet. Fraser et al. Comparison with starches from 3 different vegetable types, leafs, grains, and roots. It naturally occurs in many fruits and vegetables, although sugar cane and beets are the sources most used for its commercial production.

Sucrose is readily metabolized by your body and used for energy, although too much at a time spikes blood sugar levels and insulin release while promoting fat storage. Sucrose is a type of carbohydrate called a disaccharide, which is a variety of sugar. It's composed of two simpler sugars, or monosaccharides, called glucose and fructose.

Glucose is the end-product of carbohydrate metabolism and used by virtually all cells, especially your brain, to produce energy and do work. Fruits and vegetables contain a variety of complex and simple sugars, which all have different levels of sweetness. Compared to milk sugar, or lactose, sucrose is five times sweeter. Once there, the intestinal lining releases an enzyme called sucrase, which cleaves sucrose into one molecule of glucose and one molecule of fructose.



0コメント

  • 1000 / 1000