De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women

McDevitt, R. M.; Bott, S.; Harding, Michael C; Coward, W. A.; Bluck, Leslie J. C.; Prentice, Andrew M.

doi:10.1093/ajcn/74.6.737

Cited by 147 publications

(110 citation statements)

References 18 publications

Supporting

Mentioning

103

Contrasting

Unclassified

Order By: Relevance

“…In normal weight and obese women overfed for 4 d with 50% glucose or fructose above their energy requirement, de novo lipogenesis was found to be identical under both conditions. There was also no significant difference in plasma glucose, triacylglycerol, or insulin concentrations [45]. In healthy young normal weight subjects, a 6-d overfeeding with 3.5 g/kg fat-free mass/d (corresponding roughly to 30% energy requirements) fructose or glucose increased both VLDL-triacylglycerol concentrations and intrahepatic fat, with large interindividual variations, however [46].…”

Section: Are the Effects Of Fructose Different From Those Of Glucose?mentioning

confidence: 79%

Fructose and metabolic diseases: New findings, new questions

et al. 2010

View full text Add to dashboard Cite

There has been much concern regarding the role of dietary fructose in the development of metabolic diseases. This concern arises from the continuous increase in fructose (and total added caloric sweeteners consumption) in recent decades, and from the increased use of high-fructose corn syrup (HFCS) as a sweetener. A large body of evidence shows that a high-fructose diet leads to the development of obesity, diabetes, and dyslipidemia in rodents. In humans, fructose has long been known to increase plasma triglyceride concentrations. In addition, when ingested in large amounts as part of a hypercaloric diet, it can cause hepatic insulin resistance, increased total and visceral fat mass, and accumulation of ectopic fat in the liver and skeletal muscle. These early effects may be instrumental in causing, in the long run, the development of the metabolic syndrome. There is however only limited evidence that fructose per se, when consumed in moderate amounts, has deleterious effects. Several effects of a high-fructose diet in humans can be observed with high-fat or high-glucose diets as well, suggesting that an excess caloric intake may be the main factor involved in the development of the metabolic syndrome. The major source of fructose in our diet is with sweetened beverages (and with other products in which caloric sweeteners have been added). The progressive replacement of sucrose by HFCS is however unlikely to be directly involved in the epidemy of metabolic disease, because HFCS appears to have basically the same metabolic effects as sucrose. Consumption of sweetened beverages is however clearly associated with excess calorie intake, and an increased risk of diabetes and cardiovascular diseases through an increase in body weight. This has led to the recommendation to limit the daily intake of sugar calories.Pure, white, and deadly: the dark side of sugar was suspected many years ago, when an association between sugar consumption and coronary heart diseases was recognized and emphasized by John Yudkin [1]. Sugar, a natural sweetener obtained from either sugar cane or beets, is a disaccharide composed of one glucose molecule linked through an α1-4 glycoside bond to a fructose molecule. Fructose, besides contributing to half the total content of sugar, can also be found as a hexose in fruits and honey. More recently, sweeteners started to be produced from corn through starch isolation and hydrolysis to glucose, followed by enzymatic isomerization of part of the glucose into fructose [2,3]. The resulting mixture, known as high-fructose corn syrup (HFCS), has several industrial advantages over sugar, the most important being its low price, and has progressively replaced sugar consumption in North America over the past 30 years.Fructose metabolism has been reviewed extensively elsewhere [4][5][6] and will be only briefly outlined here. In the gut, fructose is transported by specific transporters, GLUT5 [7,8]. In some subjects, fructose absorption is quantitatively limited, and some malabsorption occurs when lar...

show abstract

Section: Are the Effects Of Fructose Different From Those Of Glucose?mentioning

confidence: 79%

Fructose and metabolic diseases: New findings, new questions

et al. 2010

View full text Add to dashboard Cite

show abstract

“…The absolute value of DNL in this study can be judged as low. Technical factors are unlikely to explain the low rates of DNL reported by McDevitt et al, 20 since their method may overestimate DNL because the deuterium method, if anything, will result in an artifactual overestimation of a few percent of DNL, and elongation of fatty acids might add a further slight overestimation of DNL.…”

Section: Do Obese Women Convert More Cho To Fat Than Lean Women?mentioning

confidence: 85%

“…20 For example, it can be assumed that food (or meals) with low glycemic index may be more favorable in moderating DNL since the pattern of CHO oxidation and storage will be delayed as compared to food with high glycemic index. 21 As a result, a large positive excursion is prevented in respiratory quotient in the postprandial phase, a time at which DNL is stimulated.…”

Section: Fat Balance and De Novo Lipogenesis Y Schutzmentioning

confidence: 99%

Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis

Schütz

2004

Int J Obes

View full text Add to dashboard Cite

The measurement of fat balance (fat input minus fat output) involves the accurate estimation of both metabolizable fat intake and total fat oxidation. This is possible mostly under laboratory conditions and not yet in free-living conditions. In the latter situation, net fat retention/mobilization can be estimated based on precise and accurate sequential body composition measurements. In case of positive balance, lipids stored in adipose tissue can originate from dietary (exogenous) lipids or from nonlipid precursors, mainly from carbohydrates (CHOs) but also from ethanol, through a process known as de novo lipogenesis (DNL). Basic equations are provided in this review to facilitate the interpretation of the different subcomponents of fat balance (endogenous vs exogenous) under different nutritional circumstances. One difficulty is methodological: total DNL is difficult to measure quantitatively in man; for example, indirect calorimetry only tracks net DNL, not total DNL. Although the numerous factors (mostly exogenous) influencing DNL have been studied, in particular the effect of CHO overfeeding, there is little information on the rate of DNL in habitual conditions of life, that is, large day-to-day fluctuations of CHO intakes, different types of CHO ingested with different glycemic indexes, alcohol combined with excess CHO intakes, etc. Three issues, which are still controversial today, will be addressed: (1) Is the increase of fat mass induced by CHO overfeeding explained by DNL only, or by decreased endogenous fat oxidation, or both? (2) Is DNL different in overweight and obese individuals as compared to their lean counterparts? (3) Does DNL occur both in the liver and in adipose tissue? Recent studies have demonstrated that acute CHO overfeeding influences adipose tissue lipogenic gene expression and that CHO may stimulate DNL in skeletal muscles, at least in vitro. The role of DNL and its importance in health and disease remain to be further clarified, in particular the putative effect of DNL on the control of energy intake and energy expenditure, as well as the occurrence of DNL in other tissues (such as in myocytes) in addition to hepatocytes and adipocytes.

show abstract

“…The extent to which excessive fructose, aspartame and caramel consumption might contribute to the high prevalence of liver disease in western societies and to the progression of NAFLD to NASH has not been investigated. One study of lean women found that four days of overfeeding with sucrose (glucose plus fructose) drink increased de novo lipogenesis by 200% to 300% (21). Another feeding study showed that two days of a high-fructose diet (30% of the total energy consumed per day, consumed as a sweetened beverage at every meal) resulted in decreased postprandial glucose concentration and insulin response, and prolonged alimentary lipemia in women (22).…”

Section: Discussionmentioning

confidence: 99%

Soft Drink Consumption Linked with Fatty Liver in the Absence of Traditional Risk Factors

Assy

Nasser

Kamayse

et al. 2008

Canadian Journal of Gastroenterology

290

194

View full text Add to dashboard Cite

BACKGROUND: Little is known about dietary habits and their relationships with liver disease in nonalcoholic fatty liver disease (NAFLD) patients, particularly in the absence of obesity, diabetes or hyperlipidemia. OBJECTIVE: To assess the association between soft drink consumption and the presence of fatty liver in NAFLD patients who do not have classic risk factors. METHODS: Three hundred ten patients with NAFLD diagnosed by ultrasound were assessed for 36 months in a cross-sectional manner. Thirty-one patients (10%) who had NAFLD without classic risk factors were compared with 30 healthy controls. Physical activity was assessed during the preceding week and year, and every six months for 36 months. Data on daily dietary intake of food and soft drink, and the source of added sugar were collected during two seven-day periods, at the beginning of the study, and within two weeks after the metabolic tests by using a validated food questionnaire given by a trained dietician. Insulin resistance and lipid peroxidation were assessed by homeostasis model assessment-insulin resistance index (HOMA-IRI) and malondialdehyde (MDA) levels, respectively. RESULTS: Eighty per cent of patients (25 of 31) consumed an excessive amount of soft drink beverages (more than 50 g/day of added sugar) for 36 months, compared with 20% in healthy controls (P<0.001). Twenty per cent of patients consumed one drink per day, 40% consumed two to three drinks per day, and 40% consumed more than four drinks per day for most days during 36 months. The most common soft drinks consumed were regular Coca-Cola (40% of patients), Diet Coke (40%) and flavoured fruit juices (20%). Ultrasound findings revealed mild fatty liver in 44% of cases (n=14), moderate fatty liver in 38% (n=12), and severe fatty liver in 18% (n=5). HOMA-IRI and MDA levels were significantly higher in patients with NAFLD than in healthy controls (HOMA-IRI, 3.7 versus 1.7, P<0.001; and MDA, 420±300 μmol/mL versus 200±100 μmol/mL; P<0.001). When controlled for other factors, including dietary composition and physical activity, soft drink beverage consumption was the only independent variable that was able to predict the presence of fatty liver in 82.5% of cases with a sensitivity of 100%, a specificity of 76%, a positive predictive value of 57% and a negative predictive value of 100%. CONCLUSION: The present study may add important insight into the role of sugar-sweetened beverage consumption as a cause of fatty liver in patients without risk factors. Patients are encouraged to change their long-standing drinking behaviour.

show abstract

De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women

Abstract: De novo lipogenesis increases after overfeeding with glucose and sucrose to the same extent in lean and obese women but does not contribute greatly to total fat balance.

Cited by 147 publications

References 18 publications

Fructose and metabolic diseases: New findings, new questions

Fructose and metabolic diseases: New findings, new questions

Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis

Soft Drink Consumption Linked with Fatty Liver in the Absence of Traditional Risk Factors

Contact Info

Product

Resources

About