Ale czy rownie dobre jest nadmierne soków owocowych czy napojow z wysoką zawartością HFCS (Syrop skrobiowy o wysokiej zawartości fruktozy)?
Fruktoza, czyli cukier owocowy (z łac. fructus - owoc) - monosacharyd występujący w owocach i miodzie. Wchodzi tez w skład dwucukru sacharozy (glukoza + fruktoza).
Fruktoza jest znacznie wolniej przyswajana przez organizm niz glukoza.
Ma mniejsze IG wiec z tego powodu jest polecana przed dietetykow dla diabetykow.
Ale czy mozna pozwolic sobie na dowolna ilosc fruktozy bez zadnych skutkow ubocznych?
Czy nadmiar fruktozy jest zdrowy dla czlowieka?
Czy jest 'bezpieczna' dawka?!
Hypothesis: Could Excessive Fructose Intake and Uric Acid Cause Type 2 Diabetes?
We propose that excessive fructose intake (>50 g/d) may be one of the underlying etiologies of metabolic syndrome and type 2 diabetes. The primary sources of fructose are sugar (sucrose) and high fructose corn syrup. First, fructose intake correlates closely with the rate of diabetes worldwide. Second, unlike other sugars, the ingestion of excessive fructose induces features of metabolic syndrome in both laboratory animals and humans. Third, fructose appears to mediate the metabolic syndrome in part by raising uric acid, and there are now extensive experimental and clinical data supporting uric acid in the pathogenesis of metabolic syndrome. Fourth, environmental and genetic considerations provide a potential explanation of why certain groups might be more susceptible to developing diabetes. Finally, we discuss the counterarguments associated with the hypothesis and a potential explanation for these findings. If diabetes might result from excessive intake of fructose, then simple public health measures could have a major impact on improving the overall health of our populace.
wysnuto hipoteze - ze dzienne spozycie frutozy powinno oscylowac ponziej 50g
nagminne spozywanie powyzej 50g frutozy dziennie moze prowadzic do powstania zespołu metabolicznego czy cukrzycu typu II.
zespół metaboliczny - wg definicji Światowej Organizacji Zdrowia (WHO) z 1998r. oznacza występowanie otyłości, nieprawidłowego metabolizmu glukozy, podwyższonego ciśnienia tętniczego, oporności na insulinę, zaburzeń lipidowych, mikroalbuminurii. Ze względu na małą użyteczność tej definicji w codziennej praktyce (2 spośród 6 kryteriów wymaga badań specjalistycznych) znacznie uproszczono charakterystykę zespołu metabolicznego.
Obecnie obowiązuje definicja International Diabetes Federation (IDF) z kwietnia 2005r. Zgodnie z tą definicją warunkiem niezbędnym dla rozpoznania zespołu metabolicznego jest obecność otyłości brzusznej (obwód w talii u Europejek równy lub powyżej 80 cm i równy lub powyżej 94 cm u Europejczyków), dodatkowo należy stwierdzić występowanie 2 spośród 4 następujących czynników:
1. zwiększenie stężenia triglicerydów powyżej 1,7 mmol/l (150mg/dl) lub leczenie hipertriglicerydemii,
2. ciśnienie tętnicze powyżej 130 / powyżej 85 mmHg lub leczenie wcześniej rozpoznanego nadciśnienia tętniczego,
3. zwiększone stężenie glukozy na czczo równe lub powyżej 5,6 mmol/l (100mg/dl) lub rozpoznana wcześniej cukrzyca typu 2,
4. zmniejszone stężenie HDL-C poniżej 1,0 mmol/l (40mg/dl) u mężczyzn i poniżej 1,3 mmol/l (50 mg/dl) u kobiet lub leczenie tego zaburzenia lipidowego.
Dlaczego postawiono taka hipoteze?
Dietary data from a nationally representative sample from 1977 to 1978 showed that mean estimated fructose intake was 37 g/day, or 8% of total intake. However, little is known about more recent patterns of fructose consumption.
The goal of the study by Dr. Vos and colleagues was to determine the amount and sources (natural fruit vs fructose added to beverages and other foods) of dietary fructose in 21,483 US adults and children. With a single 24-hour dietary recall administered as part of the third National Health and Examination Survey (NHANES III), patterns of fructose consumption were analyzed by sex, age group, race or ethnicity, socioeconomic status, and body mass index for children and adults. Weighted estimates of fructose intake were tested for significant between-group differences.
Estimated mean consumption of fructose was 54.7 g/day (range, 38.4 - 72.8 g/day), accounting for 10.2% of total energy intake.
srednie spozycie fruktozy w USA w latach 1977-1978 wynosi 8% dziennego zapotzrebowania na kalorie - co dawalo 37g fruktozy/dzien
w 2004roku spzycie fruktozy wzroslo do 10,2% dziennego zapotzrebowanie - co daje (srednio) 54,7g fruktozy na dzien .
wynik jest sredni - maksymalne spozycie fruktozy podczas testow wynosilo az ~73g/dzien!
Metabolic effects of fructose and the worldwide increase in obesity.
While virtually absent in our diet a few hundred years ago, fructose has now become a major constituent of our modern diet. Our main sources of fructose are sucrose from beet or cane, high fructose corn syrup, fruits, and honey. Fructose has the same chemical formula as glucose (C(6)H(12)O(6)), but its metabolism differs markedly from that of glucose due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. Fructose was initially thought to be advisable for patients with diabetes due to its low glycemic index. However, chronically high consumption of fructose in rodents leads to hepatic and extrahepatic insulin resistance, obesity, type 2 diabetes mellitus, and high blood pressure. The evidence is less compelling in humans, but high fructose intake has indeed been shown to cause dyslipidemia and to impair hepatic insulin sensitivity. Hepatic de novo lipogenesis and lipotoxicity, oxidative stress, and hyperuricemia have all been proposed as mechanisms responsible for these adverse metabolic effects of fructose. Although there is compelling evidence that very high fructose intake can have deleterious metabolic effects in humans as in rodents, the role of fructose in the development of the current epidemic of metabolic disorders remains controversial. Epidemiological studies show growing evidence that consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose) is associated with a high energy intake, increased body weight, and the occurrence of metabolic and cardiovascular disorders. There is, however, no unequivocal evidence that fructose intake at moderate doses is directly related with adverse metabolic effects. There has also been much concern that consumption of free fructose, as provided in high fructose corn syrup, may cause more adverse effects than consumption of fructose consumed with sucrose. There is, however, no direct evidence for more serious metabolic consequences of high fructose corn syrup versus sucrose consumption.
chroniczne zbyt wysokie spozycie fruktozy u gryzoni prowadzi do insulinoopornosci,do otylosci do cukrzycy typu 2,wysokiego cisnienia
u ludzi przyjmownie fruktozy w duzych dawkach powoduje podobne efekty
coraz wiecej badan pokazuje ze spozywanie coraz to wiekszych ilosci napojow z duza zawartosci fruktozy czy sacharozy - powoduje epidemie otylosci,z metabolzimem czy problemy z cisnieniem
Effects of dietary fructose on plasma lipids in healthy subjects
Background: About 9% of average dietary energy intake in the United States comes from fructose. Such a high consumption raises concern about the metabolic effects of this sugar.
Objective: The objective of this study was to determine the effect of dietary fructose on plasma lipids.
Design: The study was conducted in the General Clinical Research Center at Fairview-University of Minnesota Medical Center. The participants were 24 healthy adult volunteers (12 men and 12 women; 6 of each sex were aged <40 y and 6 of each sex were aged ?40 y). All subjects received 2 isoenergetic study diets assigned by using a randomized, balanced crossover design. One diet provided 17% of energy as fructose. The other diet was sweetened with glucose and was nearly devoid of fructose. Each diet was fed for 6 wk. Both diets were composed of common foods and contained nearly identical amounts of carbohydrate, protein, fat, fiber, cholesterol, and saturated, monounsaturated, and polyunsaturated fatty acids. All meals were prepared in the metabolic kitchen of the General Clinical Research Center.
Results: The responses to the study diets differed by sex. In men, the fructose diet produced significantly higher fasting, postprandial, and daylong plasma triacylglycerol concentrations than did the glucose diet. The daylong plasma triacylglycerol concentration after 6 wk of the fructose diet was 32% greater in men than the corresponding concentration during the glucose diet (P < 0.001). The fructose diet had no significant effect on fasting or postprandial plasma triacylglycerol concentrations in women. The fructose diet also had no persistent effect on fasting plasma cholesterol, HDL cholesterol, or LDL cholesterol in either men or women.
Conclusions: Dietary fructose was associated with increased fasting and postprandial plasma triacylglycerol concentrations in men. Diets high in added fructose may be undesirable, particularly for men. Glucose may be a suitable replacement sugar.
-przyjmujaca 17% zapotrzebowania z fruktozy
-druga grupa unikala fruktozy
efekt po 6 tygodniach:(dosc ciekawy)
-u grupy spozywajacej fruktoze zanotowano wzrost poziomu trojglicerydow o 32% ale tylko u mezczyzn!
u kobiet nie wykazano zdnych zmian!
Dietary sugars stimulate fatty acid synthesis in adults.
The goal of this study was to determine the magnitude by which acute consumption of fructose in a morning bolus would stimulate lipogenesis (measured by infusion of 13C1-acetate and analysis by GC-MS) immediately and after a subsequent meal. Six healthy subjects [4 men and 2 women; aged (mean +/- SD) 28 +/- 8 y; BMI, 24.3 +/- 2.8 kg/m(2); and serum triacylglycerols (TG), 1.03 +/- 0.32 mmol/L] consumed carbohydrate boluses of sugars (85 g each) in a random and blinded order, followed by a standardized lunch 4 h later. Subjects completed a control test of glucose (100:0) and a mixture of 50:50 glucose:fructose and one of 25:75 (wt:wt). Following the morning boluses, serum glucose and insulin after 100:0 were greater than both other treatments (P < 0.05) and this pattern occurred again after lunch. In the morning, fractional lipogenesis was stimulated when subjects ingested fructose and peaked at 15.9 +/- 5.4% after the 50:50 treatment and at 16.9 +/- 5.2% after the 25:75 treatment, values that were greater than after the 100:0 treatment (7.8 +/- 5.7%; P < 0.02). When fructose was consumed, absolute lipogenesis was 2-fold greater than when it was absent (100:0). Postlunch, serum TG were 11-29% greater than 100:0 and TG-rich lipoprotein-TG concentrations were 76-200% greater after 50:50 and 25:75 were consumed (P < 0.05). The data demonstrate that an early stimulation of lipogenesis after fructose, consumed in a mixture of sugars, augments subsequent postprandial lipemia. The postlunch blood TG elevation was only partially due to carry-over from the morning. Acute intake of fructose stimulates lipogenesis and may create a metabolic milieu that enhances subsequent esterification of fatty acids flowing to the liver to elevate TG synthesis postprandially.
-spozywajaca 100g glukozy
-spozywajaca 50g glukozy + 50g fruktozy
-spozywajaca 25g glukozy + 75g fruktozy
-poziom glukozu i insuliny byl najwyzszy po spozyciu samej glukozy (co bylo do przewidzenie)
-lipogeneza w grupy spozywajacej glukoze wynosila 7,8%,u grupy 50:50 wynosila 15,9 a u grupy 75:25 wynosila 16,9
Metabolic effects of dietary fructose.
Fructose, a naturally occurring hexose, is a component of many fruits, vegetables, and sweeteners. Because of the introduction of high fructose corn sweeteners in 1967, the amount of free fructose in the diet of Americans has increased substantially in the last 20 years. Fructose is sweeter, more soluble, and less glucogenic than glucose or sucrose, so it has been recommended as a replacement for these sugars in the diets of diabetic and obese people. Although an acute dose of fructose causes smaller increases in glucose and insulin than a comparable dose of glucose, there are a number of changes after dietary adaptation that may reduce its desirability as a sugar replacement in certain segments of the population. Fructose is absorbed primarily in the jejunum and metabolized in the liver. When consumed in excess of dietary glucose, it may be malabsorbed. Fructose is more lipogenic than glucose or starches, and usually causes greater elevations in triglycerides and sometimes in cholesterol than other carbohydrates. Dietary fructose has resulted in increases in blood pressure, uric acid, and lactic acid. People who are hypertensive, hyperinsulinemic, hypertriglyceridemic, non-insulin-dependent diabetic, or postmenopausal are more susceptible to these adverse effects of dietary fructose than healthy young subjects. Although consumption of fructose as a component of fruits and vegetables is an unavoidable consequence of eating a healthy diet, added fructose seems to provide little advantage over other caloric sweetners and compares unfavorably to complex carbohydrates in susceptible segments of the population.
fructoza dlatego ze nie podnosi tak poziomu glukozy i poziomu insuliny jest polecana dla cukrzykow i osob otylych
ale badania wykazaly ze jest wiele powiklan zostapienia glukozy nadmiernymi dawkami fruktozy
nadmierne spozycie powodowac moze wzrost cianienia krwi,kwasu moczowego czy mlekowego,powoduje wzrost poziomu trojglicerydow i cholesterolu
osoby cierpiece na nadcisnienie,hiperinsulinizm,czy opornych na insuline (cukrzyca typu 2) powinni unikac duzych ilosci fruktozy
Metabolic effects of fructose.
PURPOSE OF REVIEW: Fructose is consumed in significant amounts in Western diets. An increase in fructose consumption over the past 10-20 years has been linked with a rise in obesity and metabolic disorders. Fructose/sucrose produces deleterious metabolic effects in animal models. This raises concern regarding the short-term and long-term effects of fructose and its risk in humans.
RECENT FINDINGS: In rodents, fructose stimulates lipogenesis and leads to hepatic and extrahepatic insulin resistance, dyslipidaemia and high blood pressure. Insulin resistance appears to be related to ectopic lipid deposition. In humans, short-term fructose feeding increases de-novo lipogenesis and blood triglycerides and causes hepatic insulin resistance. There is presently no evidence for fructose-induced muscle insulin resistance in humans. The cellular mechanisms underlying the metabolic effects of fructose involve production of reactive oxygen species, activation of cellular stress pathways and possibly an increase in uric acid synthesis.
SUMMARY: Consuming large amounts of fructose can lead to the development of a complete metabolic syndrome in rodents. In humans, fructose consumed in moderate to high quantities in the diet increases plasma triglycerides and alters hepatic glucose homeostasis, but does not appear to cause muscle insulin resistance or high blood pressure in the short term. Further human studies are required to delineate the effects of fructose in humans
u ludzi krotkotrwale nadmierne spoozycie fruktozy nasila proces lipogenezy (syntezy tluszczu),podnosi poziom trojglicerydow we krwi i powoduje insulinoopornosc watrobowa
nie ma wplywu na wrazliwosc miesniowa!
Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.
Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.
badono wplyw spozywania glukozy i frutozy dostarczajacej 25% dziennego zapotrzebowania w osob z nadwaga i otylych przez 10tygodni
-spozycie fruktozy podnosi DNL (de novo lipogenesis)
-nasila/promuje powstanie dyslipidemii (zaburzenie gospodarki lipidowej)
-zwieksza poziom trojglicerydow
-zmniejsza wrazliwosc insulinowa
-zwieksza otylosc trzewna ( Otyłość brzuszna - zajmuje głównie górne partie ciała, takie jak ramiona, kark i brzuch)
Endocrine and metabolic effects of consuming beverages sweetened with fructose, glucose, sucrose, or high-fructose corn syrup.
Our laboratory has investigated 2 hypotheses regarding the effects of fructose consumption: 1) the endocrine effects of fructose consumption favor a positive energy balance, and 2) fructose consumption promotes the development of an atherogenic lipid profile. In previous short- and long-term studies, we showed that consumption of fructose-sweetened beverages with 3 meals results in lower 24-h plasma concentrations of glucose, insulin, and leptin in humans than does consumption of glucose-sweetened beverages. We have also tested whether prolonged consumption of high-fructose diets leads to increased caloric intake or decreased energy expenditure, thereby contributing to weight gain and obesity. Results from a study conducted in rhesus monkeys produced equivocal results. Carefully controlled and adequately powered long-term studies are needed to address these hypotheses. In both short- and long-term studies, we showed that consumption of fructose-sweetened beverages substantially increases postprandial triacylglycerol concentrations compared with glucose-sweetened beverages. In the long-term studies, apolipoprotein B concentrations were also increased in subjects consuming fructose, but not in those consuming glucose. Data from a short-term study comparing consumption of beverages sweetened with fructose, glucose, high-fructose corn syrup, and sucrose suggest that high-fructose corn syrup and sucrose increase postprandial triacylglycerol to an extent comparable with that induced by 100% fructose alone. Increased consumption of fructose-sweetened beverages along with increased prevalence of obesity, metabolic syndrome, and type 2 diabetes underscore the importance of investigating the metabolic consequences of fructose consumption in carefully controlled experiments.
badano wplyw napojow slodzonych
-HFCS (Syrop skrobiowy o wysokiej zawartości fruktozy)
-napoj z fuktoza,z sacharoza i z HFCS podnosi poziom trojglicerydow podobnie
nadmierne spozycie takich produktow/napojow moze prowadzic do otylosci,do powstanie zespolu metabolicznego,czy do powstanie cukrzycu typu 2
Zmieniony przez - solaros w dniu 2011-02-11 14:06:59