Et for høyt fruktoseinntak i kombinasjon med kalorioverskudd gjør deg insulinresistent og feit, samt gir deg fettlever.
Fruktose tas opp i leveren og lagres der som glykogen, men leverens kapasitet for å håndtere fruktose er begrenset. Når leveren er "full" (leveren kan lagre 75-100 g) så går fruktosen ut i blodet, men ettersom musklene savner de enzymene som kreves for å omdanne fruktose til glykogen så er den eneste gjenværende muligheten for det å omdannes til fettsyrer.
Det finnes imidlertid ikke noe som helst grunn til å unngå frukt og grønnsaker. Man må f.eks. spise over ti epler for å få i seg den samme mengden fruktose som man får fra en liten pose sukkergodteri på 150 g. Det er vanlig raffinert hvitt sukker (sukrose) som er det sorte fåret her, da sukrose er halvparten fruktose (sukrosemolekylet består av en fruktosemolekyl og en glukosemolekyl).
Altså:
Kroppen (leveren) er tilpasset til å håndtere den mengden fruktose du får i deg fra frukt og grønnsaker. Men hvis du tilfører fruktose som tilskudd, og fremfor alt får i deg mye sukker (sukrose) så får du fort i deg mye mer fruktose enn hva leveren din takler, og da omdannes det lett til fett, ved kalorioverskudd. Prøv å holde ditt samlede inntak av fruktose under 75-100 g om dagen. Husk at sukker er 50% fruktose.
Dog viktigere å tenke på dette hvis man er overvektig og spiser for mye. Ved underskudd har det mindre betydning da det vil bli brukt som energi uansett.
"The alarming increase in fructose consumption may be an important contributor to the epidemic of obesity and insulin resistant diabetes in both pediatric and adult populations. For thousands of years, the human diet contained a relatively small amount of naturally occurring fructose from fruits and other complex foods. Adaptation of humans to a high glucose/low fructose diet has meant that hepatic carbohydrate metabolism is designed to actively metabolize glucose with a limited capacity for metabolizing a small daily intake of fructose. The increasing application of high fructose sweeteners over the past few decades has resulted in a considerable rise in the dietary intake of fructose. A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, disturbs normal hepatic carbohydrate metabolism leading to two major consequences: perturbations in glucose metabolism and glucose uptake pathways, and a significantly enhanced rate of de novo lipogenesis and TG synthesis, driven by the high flux of glycerol and acyl portions of TG molecules coming from fructose catabolism."
Nutr Metab (Lond). 2005; 2: 5.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=552336
"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."
American Journal of Clinical Nutrition, Vol. 72, No. 5, 1128-1134, November 2000
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=11063439&dopt=Abstract
"Peak postprandial serum triglycerides were significantly higher only at day 1 of the fructose diet. Day-28 fasting serum total and LDL cholesterol for the fructose diet were 9.0% and 11.0% higher, respectively, than the corresponding values for the starch diet. A high-fructose diet compared with a high-starch diet resulted in significantly higher fasting serum total and LDL cholesterol and also caused transient changes in postprandial serum lactate and triglycerides."
American Journal of Clinical Nutrition, Vol 55, 851-856, April 1992
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=1550068&dopt=Abstract
"To determine if hypertension could be produced in normal rats by feeding them a fructose-enriched diet, Sprague-Dawley rats were fed either normal chow or a diet containing 66% fructose as a percentage of total calories for approximately 2 weeks. At the end of this period systolic blood pressure had increased from 124 +/- 2 to 145 +/- 2 (SEM) mm Hg in the fructose-fed rats, whereas no change occurred in the control group. In addition, hyperinsulinemia and hypertriglyceridemia were associated with hypertension in fructose-fed rats. The addition of clonidine to the drinking water inhibited fructose-induced hypertension, but not the increase in plasma insulin or triglyceride concentration seen in fructose-fed rats. Thus, the metabolic changes associated with fructose-induced hypertension are unlikely to be secondary to an increase in sympathetic activity. Whether or not this is also true of the hypertension remains to be clarified."
Hypertension. 1987 Nov;10(5):512-6.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=3311990&dopt=Abstract
"Most of the metabolic effects of fructose are due to its rapid utilization by the liver and it by-passing the phosphofructokinase regulatory step in glycolysis, leading to far reaching consequences to carbohydrate and lipid metabolism. These consequences include immediate hepatic increases in pyruvate and lactate production, activation of pyruvate dehydrogenase, and a shift in balance from oxidation to esterification of nonesterified fatty acids, resulting in increased secretion of very-low-density-lipoprotein (VLDL). These effects are augmented by long-term absorption of fructose, which causes enzyme adaptations that increase lipogenesis and VLDL secretion, leading to triglyceridemia, decreased glucose tolerance, and hyperinsulinemia. Acute loading of the liver with fructose causes sequestration of inorganic phosphate in fructose-1-phosphate and diminished ATP synthesis. Consequently, the inhibition by ATP of the enzymes of adenine nucleotide degradation is removed and uric acid formation accelerates with consequent hyperuricemia. These effects are of particular significance to potentially hypertriglyceridemic or hyperuricemic individuals."
American Journal of Clinical Nutrition, Vol 58, 754S-765S, 1993
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=8213607&dopt=Abstract
"Hepatic and extrahepatic insulin sensitivity was assessed in six healthy humans from the insulin infusion required to maintain an 8 mmol/l glucose concentration during hyperglycemic pancreatic clamp with or without infusion of 16.7 micromol. kg(-1). min(-1) fructose. Glucose rate of disappearance (GR(d)), net endogenous glucose production (NEGP), total glucose output (TGO), and glucose cycling (GC) were measured with [6,6-(2)H(2)]- and [2-(2)H(1)]glucose. Hepatic glycogen synthesis was estimated from uridine diphosphoglucose (UDPG) kinetics as assessed with [1-(13)C]galactose and acetaminophen. Fructose infusion increased insulin requirements 2.3-fold to maintain blood glucose. Fructose infusion doubled UDPG turnover, but there was no effect on TGO, GC, NEGP, or GR(d) under hyperglycemic pancreatic clamp protocol conditions. When insulin concentrations were matched during a second hyperglycemic pancreatic clamp protocol, fructose administration was associated with an 11.1 micromol. kg(-1). min(-1) increase in TGO, a 7.8 micromol. kg(-1). min(-1) increase in NEGP, a 2.2 micromol. kg(-1). min(-1) increase in GC, and a 7.2 micromol. kg(-1). min(-1) decrease in GR(d) (P < 0. 05). These results indicate that fructose infusion induces hepatic and extrahepatic insulin resistance in humans."
Am J Physiol Endocrinology and Metabolism, Vol. 279, Issue 4, E907-E911, October 2000
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=11001775&dopt=Abstract
"Obesity is a major epidemic, but its causes are still unclear. In this article, we investigate the relation between the intake of high-fructose corn syrup (HFCS) and the development of obesity. We analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents > 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged > or = 2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/d. The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity."
American Journal of Clinical Nutrition, Vol. 79, No. 4, 537-543, April 2004
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=15051594&dopt=Abstract
