Monday, February 27, 2017

High fructose corn syrup

High fructose corn syrup

From Wikipedia, the free encyclopedia
You must add a |reason= parameter to this Cleanup template - replace it with {{Cleanup|August 2006|reason=}}, or remove the Cleanup template.
High fructose corn syrup (HFCS) is a newer and sweeter form of corn syrup. Like ordinary corn syrup, the high fructose variety is made from corn starch using enzymes. The production process of HFCS was developed by Japanese researchers in the 1970s. HFCS was rapidly introduced in many processed foods and soda drinks in the US over the period of about 1975–1985, and usage continues to increase as sugar use decreases at a nearly one to one level (Bray, 2004 & U.S. Department of Agriculture, Economic Research Service, Sugar and Sweetener Yearbook series, Tables 50–52.). There are three main reasons for this switch; first is cost, as HFCS is a bit cheaper due to corn subsidies and import sugar tariffs. The second reason is that it is a liquid which is easier to blend and transport. The third is that a product made with HFCS has a much longer shelf life. (White JS. 1992. Fructose syrup: production, properties and applications, in FW Schenck & RE Hebeda, eds, Starch Hydrolysis Products – Worldwide Technology, Production, and Applications. VCH Publishers, Inc. 177-200)
By increasing the fructose content of corn syrup (primarily glucose) through enzymatic processing, the syrup is more comparable to table sugar (sucrose) in sweetness. This makes it useful to manufacturers as a possible substitute for sugar in soft drinks and other processed foods. Common commercial grades of high fructose corn syrup include fructose contents of 42%, 55%, or 90%. The 55% grade is most commonly used in soft drinks.
Unlike sucrose, HFCS consists of a mixture of glucose and fructose, which doesn't require an enzymatic step to break it down before absorption in the intestine.
Some people suspect that over-consumption of HFCS may be a main contributor to the epidemic of diabetes in the US. [1] Fructose is probably less cariogenic (cavity-causing) than sucrose.

Comparison to other sugars

Cane sugar is relatively pure sucrose. Sucrose is a disaccharide, as opposed to glucose and fructose, which are monosaccharides. Each molecule of sucrose is composed of one unit each of fructose and glucose linked together. A molecule of sucrose (with a chemical formula of C12H22O11) can be broken down into a molecule of glucose (C6H12O6) plus a molecule of fructose (C6H12O6). Sucrose is broken down during digestion into fructose and glucose through hydrolysis by the enzyme sucrase.
Because sucrose can be broken down into fructose and glucose, some people say that sucrose is "50% glucose and 50% fructose." This may easily be misunderstood. Pure sucrose contains only sucrose molecules. It contains no free fructose molecules and no free glucose molecules. It contains fructose moieties and sucrose moieties, but these moieties are bound together into sucrose molecules and thus are not free. When talking about chemistry, a "mixture" is defined as a blend of two or more different molecules. Thus, strictly speaking, it would be incorrect to say that sucrose is a mixture of 50% fructose and 50% glucose. On the other hand, because sucrose is broken down in the small intestine to fructose and glucose, one could argue that after ingested sucrose enters the small intestine and is broken down, it is metabolized by the body like a mixture of 50% glucose and 50% fructose.
HFCS can have a high or low fructose content, with a corresponding difference in sweetness. Honey is a mixture of different types of sugars, water, and small amounts of other compounds. Honey typically has a fructose/glucose ratio similar to HFCS, as well as containing some sucrose and other sugars.

Production

High-fructose corn syrup (HFCS) is produced by processing corn starch to yield glucose, and then processing the glucose to produce a syrup that contains fructose. First, cornstarch is treated with alpha-amylase to produce shorter chains of sugars called oligosaccharides. Then, an enzyme called glucoamylase breaks the sugar chains down even further to yield the simple sugar glucose. The third enzyme, glucose isomerase, converts glucose to a mixture of about 42% fructose and 50–52% glucose with some other sugars mixed in. While alpha-amylase and glucoamylase are added directly to the slurry, glucose-isomerase is packed into columns and the sugar mixture is then passed over it. This 42–43% fructose glucose mixture is then subjected to a liquid chromatography step where the fructose is enriched to approximately 90%. The 90% fructose is then back-blended with 42% fructose to achieve a 55% fructose final product. Numerous ion-exchange and evaporation steps are also part of the overall process.

Sweetener consumption patterns

In the United States

File:Usda sweeteners.jpg
US sweetener consumption, 1966-2004 (cane and beet sugar are both pure sucrose)
The accompanying graph shows the consumption of sweeteners per capita in the United States since 1966. Since HFCS and sucrose (cane and beet sugars) provide almost identical proportions of fructose and glucose, no metabolic changes would be expected from substituting one for the other. However, it is apparent from this graph that overall sweetener consumption, and in particular glucose-fructose mixtures, has increased since the introduction of HFCS. Thus, the proportion of fructose as a component of overall sweetener intake in the United States has increased since the early 1980s. This would be true whether the added sweetener was HFCS, table sugar, or any other glucose-fructose mixture.

International markets

HFCS is produced in the industrialized countries.The production of HFCS is dependent on the agricultural, especially sugar, policy.
In Europe, due to the fact that HFCS (isoglucose) is under the adjustment of production, the greater availability of cane sugar over maize would make its production there uneconomical. Also Europe does not allow genetically modifed foods (GMOs) and therefore does not allow HFCS.
In Japan, HFCS consumption accounts for one quarter of total sweetener consumption.

Health effect controversy

Overview

The average American consumed approximately 19.2 kg of HFCS versus 20 kg of sugar in 2004.[citation needed] Where HFCS is not used or rarely used, the sugar consumption per person can be higher than the USA; for example, the 2002 figures for some countries are: USA 32.4 kg, EU 40.1 kg, Brazil 59.7 kg, and Australia 56.2 kg.[2]
One study concluded that fructose "produced significantly higher fasting plasma triacylglycerol values than did the glucose diet in men" and "if plasma triacylglycerols are a risk factor for cardiovascular disease, then diets high in fructose may be undesirable"[3]. A study in mice suggests that fructose increases adiposity.[4] However, these studies looked at the effects of fructose alone. As noted by the U.S. Food and Drug Administration in 1996, the saccharide composition (glucose to fructose ratio) of HFCS is approximately the same as that of honey, invert sugar and the disaccharide sucrose (or table sugar).
A more recent study found a link exists between obesity and high HFCS consumption, especially from soft drinks.[5]
However, the obesity epidemic has many contributing factors. University of California, Davis nutrition researcher Peter Havel has pointed out that while there are likely differences between sweeteners, "the increased consumption of fat, the increased consumption of all sugars, and inactivity are all to blame for the obesity epidemic."[6]

Labeling restrictions

In May 2006, the Center for Science in the Public Interest (CSPI) threatened to file a lawsuit against Cadbury Schweppes for labeling 7 Up as "All Natural" despite containing high fructose corn syrup. While the FDA has no definition of "Natural", CSPI claims that HFCS is not a “natural” ingredient due to the high level of processing and the use of at least one genetically modifed (GMO) enzyme required to produce it.[7]
Posted by at No comments:

Fructose

Fructose

Previous (Frog)
Next (Fruit)
Fructose (or levulose) is a simple sugar (monosaccharide) with the same chemical formula as glucose (C6H12O6) but a different atomic arrangement. Along with glucose and galactose, fructose is one of the three most important blood sugars in animals.
Sources of fructose include honey, fruits, and some root vegetables. Fructose is often found in combination with glucose as the disaccharide sucrose (table sugar), a readily transportable and mobilizable sugar that is stored in the cells of many plants, such as sugar beets and sugarcane. In animals, fructose may also be utilized as an energy source, and phosphate derivatives of fructose participate in carbohydrate metabolism.
In addition to natural sources, fructose may be found in commercially produced high fructose corn syrup (HFCS). Like regular corn syrup, HFCS is derived from the hydrolysis of corn starch to yield glucose; however, further enzymatic processing occurs to increase the fructose content. Until recently, fructose has not been present in large amounts in the human diet; thus, the increasing consumption of HFCS as a sweetener in soft drinks and processed foods has been linked to concerns over the rise in obesity and type II diabetes in the United States.
Fructose’s Glycemic Index (an expression of the relative ability of various carbohydrates to raise blood glucose level) is relatively low compared to other simple sugars. Thus, fructose may be recommended for persons with diabetes mellitus or hypoglycemia (low blood sugar), because intake does not trigger high levels of insulin secretion. This benefit is tempered by a concern that fructose may have an adverse effect on plasma lipid and uric acid levels, and that higher blood levels of fructose can be damaging to proteins.

The chemical structure of fructose


The open-chain structure of fructose
Fructose is a levorotatory monosaccharide (counterclockwise rotation of plane polarized light) with the same empirical formula as glucose but with a different structural arrangement of atoms (i.e., it is an isomer of glucose). Like glucose, fructose is a hexose (six-carbon) sugar, but it contains a keto group instead of an aldehyde group, making it a ketohexose.
Like glucose, fructose can also exist in ring form. Its open-chain structure is able to cyclize (form a ring structure) because a ketone can react with an alcohol to form a hemiketal. Specifically, the C-2 keto group of a fructose molecule can react with its C-5 hydroxyl group to form an intramolecular hemiketal. Thus, although fructose is a hexose, it may form a five-membered ring called a furanose, which is the structure that predominates in solution.
Fructose's specific conformation (or structure) is responsible for its unique physical and chemical properties relative to glucose. For example, although the perception of sweetness depends on a variety of factors, such as concentration, pH, temperature, and individual taste buds, fructose is estimated to be approximately 1.2-1.8 times sweeter than glucose.

Fructose as an energy source

Fructose absorption

Fructose is absorbed more slowly than glucose and galactose, through a process of facilitated diffusion (in which transport across biological membranes is assisted by transport proteins). Large amounts of fructose may overload the absorption capacity of the small intestine, resulting in diarrhea. For example, young children who drink a lot of fruit juice that is composed mainly of fructose may suffer from “toddlers’ diarrhea.” Fructose is absorbed more successfully when ingested with glucose, either separately or as sucrose.
Most dietary fructose is then metabolized by the liver, a control point for the circulation of blood sugar.

The breakdown of fructose

Energy from carbohydrates is obtained by nearly all organisms via glycolysis. It is only the initial stage of carbohydrate catabolism for aerobic organisms such as humans. The end-products of glycolysis typically enter into the citric acid cycle and the electron transport chain for further oxidation, producing considerably more energy per glucose molecule.
Fructose may enter the glycolytic pathway by two major routes: one predominant in liver, the other in adipose tissue (a specialized fat-storage tissue) and skeletal muscle. In the latter, the degradation of fructose closely resembles the catabolism of glucose: the enzyme hexokinase phosphorylates (adds a phosphate) to form fructose-6-phosphate, an intermediate of glycolysis.
The liver, in contrast, handles glucose and fructose differently. There are three steps involved in the fructose-1-phosphate pathway, which is preferred by liver due to its high concentration of fructokinase relative to hexokinase:
  1. Fructose is phosphorylated by the enzyme fructokinase to fructose-1-phosphate.
  2. The six-carbon fructose is split into two three-carbon molecules, glyceraldehyde and dihydroxyacetone phosphate.
  3. Glyceraldehyde is then phosphorylated by another enzyme so that it too can enter the glycolytic pathway.

Potential health effects of high fructose consumption

Because the liver metabolizes fructose differently than glucose, its breakdown also has different biochemical and physiological effects. Fructose metabolism provides the liver with an abundance of pyruvate and lactate for further degradation, so that metabolites of the citric acid cycle, such as citrate and malate, also build up. Citrate can be converted to acetyl CoA, which serves as a precursor for fatty acid synthesis or cholesterol synthesis. Thus, a long-term increase in fructose or sucrose consumption can lead to increased plasma levels of triglyceride and lactate, as well as increased lipid storage in adipose tissue.

Disorders involving fructose metabolism

Fructose intolerance (Hereditary Fructose Intolerance or HFI) is caused by an inherited deficiency of the enzyme Fructose-1-phosphate aldolase-B. The absence of this enzyme prevents the breakdown of fructose beyond its intermediate fructose-1-phosphate. The resulting accumulation of fructose-1-phosphate and depletion of phosphates for ATP production in the liver blocks both the synthesis of glucose (gluconeogenesis) and the release of glucose through the breakdown of glycogen (glycogenolysis). If fructose is ingested, vomiting and hypoglycemia will result; long-term effects include a decline in liver function and possible kidney failure.
Fructosuria, in contrast, is caused by a genetic defect in the enzyme fructokinase. This benign disorder results in the excretion of fructose in the urine.
Fructose malabsorption (Dietary Fructose Intolerance or DFI) stems from a deficiency of a fructose transporter enzyme in the enterocytes (specialized cells found on the surface of the intestines). In fructose malabsorption, the small intestine fails to absorb fructose properly. In the large intestine, the unabsorbed fructose is metabolized by normal colonic bacteria to short-chain fatty acids and the gases hydrogen, carbon dioxide, and methane, which leads to symptoms of abdominal bloating, diarrhea, or constipation. Foods with high glucose content help sufferers to absorb fructose.

High fructose corn syrup

Production


United States sweetener consumption, 1966-2004 (Sugarcane and beet sugar are both pure sucrose)
The production process of high fructose corn syrup (HFCS) was developed by Japanese researchers in the 1970s. HFCS was rapidly introduced in many processed foods and soft drinks in the United States over the period 1975–1985, and usage continues to increase (Bray et al. 2004).
The preference for fructose over glucose or sucrose in U.S. commercial food production can be explained in part by its cheaper cost, due to corn subsidies and import sugar tariffs. In addition, fructose does not form crystals at acid pH and has better freezing properties than sucrose, which leads to easier transport and a longer shelf life for food products.
Common commercial grades of high fructose corn syrup include fructose contents of 42 percent, 55 percent, or 90 percent. The 55 percent grade is most commonly used in soft drinks and is equivalent to caster sugar.

The potential impact on human health

One study concluded that fructose "produced significantly higher fasting plasma triacylglycerol values than did the glucose diet in men" and "if plasma triacylglycerols are a risk factor for cardiovascular disease, then diets high in fructose may be undesirable" (Bantle et al. 2000). A study in mice suggests that fructose increases adiposity (amount of body fat or adipose tissue) (Jurgens et al. 2005). However, these studies looked at the effects of fructose alone. As noted by the U.S. Food and Drug Administration (FDA) in 1996, the saccharide composition (glucose to fructose ratio) of HFCS is approximately the same as that of honey, invert sugar, and the disaccharide sucrose.
A more recent study found a link exists between obesity and high HFCS consumption, especially from soft drinks (Bray et al. 2004). While the over-consumption of HFCS may be a contributor to the epidemic of obesity and Type II diabetes in the United States, the obesity epidemic has many contributing factors. University of California, Davis nutrition researcher Peter Havel has pointed out that while there are likely differences between sweeteners, "the increased consumption of fat, the increased consumption of all sugars, and inactivity are all to blame for the obesity epidemic" (Warner 2006).
Posted by at No comments:

Fructolysis

Fructolysis

From Wikipedia, the free encyclopedia
Fructolysis refers to the metabolism of fructose from dietary sources. Though the metabolism of glucose through glycolysis uses many of the same enzymes and intermediate structures as those in fructolysis, the two sugars have very different metabolic fates in human metabolism. Unlike glucose, which is metabolized widely in the body, fructose is metabolized almost completely in the liver in humans, where it is directed toward replenishment of liver glycogen and triglyceride synthesis.[1]Under one percent of ingested fructose is directly converted to plasma triglyceride.[2] 29% - 54% of fructose is converted in liver to glucose, and about quarter of fructose is converted to lactate. 15% - 18% is converted to glycogen.[3] Glucose and lactate are then used normally as energy to fuel cells all over the body.[2]
Fructose is a dietary monosaccharide present naturally in fruits and vegetables, either as free fructose or as part of the disaccharide sucrose, and as free monosaccharides in honey. It is also present in the form of refined sugars including granulated sugars (white crystalline table sugar, brown sugar, confectioner's sugar, and turbinado sugar), refined crystalline fructose and as high fructose corn syrups. About 10% of the calories contained in the Western diet are supplied by fructose (approximately 55 g/day).[4]
Unlike glucose, fructose is not an insulin secretagogue, and can in fact lower circulating insulin.[5] In addition to liver, fructose is metabolized in intestine, testis, kidney, skeletal muscle, fat tissue and brain,[6][7] but it is not transported into cells via insulin-sensitive pathways (insulin regulated transporters GLUT1 and GLUT4). Instead fructose is taken in by GLUT5.

Fructolysis and glycolysis are independent pathways[edit]

Although the metabolism of fructose and glucose share many of the same intermediate structures, they have very different metabolic fates in human metabolism. Fructose is metabolized almost completely in the liver in humans, and is directed toward replenishment of liver glycogen and triglyceride synthesis, while much of dietary glucose passes through the liver and goes to skeletal muscle, where it is metabolized to CO2, H2O and ATP, and to fat cells where it is metabolized primarily to glycerol phosphate for triglyceride synthesis as well as energy production.[1] The products of fructose metabolism are liver glycogen and de novo lipogenesis of fatty acids and eventual synthesis of endogenous triglyceride can be divided into two main phases: The first phase is the synthesis of the trioses, dihydroxyacetone(DHAP) and glyceraldehyde; the second phase is the subsequent metabolism of these trioses either in the gluconeogenic pathway for glycogen replenishment and/or the complete metabolism in the fructolytic pathway to pyruvate, which enters the Krebs cycle, is converted to citrate and subsequently directed toward de novo synthesis of the free fatty acid palmitate.[1]

The metabolism of fructose to DHAP and glyceraldehyde[edit]

The first step in the metabolism of fructose is the phosphorylation of fructose to fructose 1-phosphate by fructokinase (Km = 0.5 mM, ≈ 9 mg/100 ml), thus trapping fructose for metabolism in the liver.Hexokinase IV (Glucokinase), also occurs in the liver and would be capable of phosphorylating fructose to fructose 6-phosphate (an intermediate in the gluconeogenic pathway); however, it has a relatively high Km (12 mM) for fructose and, therefore, essentially all of the fructose is converted to fructose-1-phosphate in the human liver. Much of the glucose, on the other hand, is not phosphorylated (Km of hepatic glucokinase (hexokinase IV) = 10 mM), passes through the liver directed toward peripheral tissues, and is taken up by the insulin-dependent glucose transporter, GLUT 4, present on adipose tissue and skeletal muscle.
Fructose-1-phosphate then undergoes hydrolysis by fructose-1-phosphate aldolase (aldolase B) to form dihydroxyacetone phosphate (DHAP) and glyceraldehyde; DHAP can either be isomerized to glyceraldehyde 3-phosphate by triosephosphate isomerase or undergo reduction to glycerol 3-phosphate by glycerol 3-phosphate dehydrogenase. The glyceraldehyde produced may also be converted to glyceraldehyde 3-phosphate by glyceraldehyde kinase or converted to glycerol 3-phosphate by glyceraldehyde 3-phosphate dehydrogenase. The metabolism of fructose at this point yields intermediates in gluconeogenic pathway leading to glycogen synthesis, or can be oxidized to pyruvate and reduced to lactate, or be decarboxylated to acetyl CoA in the mitochondria and directed toward the synthesis of free fatty acid, resulting finally in TG synthesis.
Figure 1: The metabolic conversion of fructose to DHAP, glyceraldehyde and glyceraldehyde-3-Phosphate in the liver

Synthesis of glycogen from DHAP and glyceraldehyde-3-phosphate[edit]

The synthesis of glycogen in the liver following a fructose-containing meal proceeds from gluconeogenic precursors. Fructose is initially converted to DHAP and glyceraldehyde by fructokinase and aldolase B. The resultant glyceraldehyde then undergoes phosphorylation to glyceraldehyde-3-phosphate. Increased concentrations of DHAP and glyceraldehyde-3-phosphate in the liver drive the gluconeogenic pathway toward glucose-6-phosphate, glucose-1-phosphate and glycogen formation. It appears that fructose is a better substrate for glycogen synthesis than glucose and that glycogen replenishment takes precedence over triglyceride formation.[8] Once liver glycogen is replenished, the intermediates of fructose metabolism are primarily directed toward triglyceride synthesis.
Figure 2: The metabolic conversion of fructose to glycogen in the liver

Synthesis of triglyceride from DHAP and glyceraldehyde-3-phosphate[edit]

Carbons from dietary fructose are found in both the FFA and glycerol moieties of plasma TG. Excess dietary fructose can be converted to pyruvate, enter the Krebs cycle and emerges as citrate directed toward free fatty acid synthesis in the cytosol of hepatocytes. The DHAP formed during fructolysis can also be converted to glycerol and then glycerol 3-phosphate for TG synthesis. Thus, fructose can provide trioses for both the glycerol 3-phosphate backbone, as well as the free fatty acids in TG synthesis. Indeed, fructose may provide the bulk of the carbohydrate directed toward de novo TG synthesis in humans.[citation needed]
Figure 3: The metabolic conversion of fructose to triglyceride (TG) in the liver

Fructose induces hepatic lipogenic enzymes[edit]

Fructose consumption results in the insulin-independent induction of several important hepatic lipogenic enzymes including pyruvate kinase, NADP+-dependent malate dehydrogenase, citrate lyase, acetyl CoA carboxylase, fatty acid synthase, as well as pyruvate dehydrogenase. Although not a consistent finding among metabolic feeding studies, high refined fructose diets have been shown to lead to hypertriglyceridemia in a wide range of populations including individuals with normal glucose metabolism as well as individuals with impaired glucose tolerance, diabetes, hypertriglyceridemia, and hypertension. The hypertriglyceridemic effects observed are a hallmark of increased dietary carbohydrate, and fructose appears to be dependent on a number of factors including the amount of dietary fructose consumed and degree of insulin resistance.
Table 1: Hepatic lipogenic enzyme activity ‡ in control and streptozotocin-induced diabetic rats§ follow a 14-day period with or without 25% fructose diet
GroupPyruvate KinaseNADPH-Malate
Dehydrogenase		Citrate LyaseAcetyl CoA
Carboxylase		Fatty Acid Synthase
Control Animals
Control Diet495 ± 2335 ± 521 ± 36.5 ± 1.03.6 ± 0.5
Fructose Diet1380 ± 110*126 ± 9*69 ± 7*22.5 ± 2.7*10.8 ± 1.4*
Diabetic Animals
Control Diet196 ± 2114 ± 39 ± 23.1 ± 0.81.4 ± 0.6
Fructose Diet648 ± 105*70 ± 9*37 ± 6*10.3 ± 2.0*3.9 ± 0.9*
‡ = Mean ± SEM activity in nmol/min per mg protein
§ = 12 rats/group
* = Significantly different from control at p < 0.05
Shafrir, E. Fructose/Sucrose metabolism, its physiological and pathological implications. In Kretchmer, N. & Hollenbeck, CB. Sugars and Sweeteners, CRC Press, Boca Raton:FL, 1991.

Abnormalities in fructose metabolism[edit]

The lack of two important enzymes in fructose metabolism results in the development of two inborn errors in carbohydrate metabolism – essential fructosuria and hereditary fructose intolerance. In addition, reduced phosphorylation potential within hepatocytes can occur with intravenous infusion of fructose.

Inborn errors in fructose metabolism[edit]

Essential fructosuria[edit]

The absence of fructokinase results in the inability to phosphorylate fructose to fructose-1-phosphate within the cell. As a result, fructose is neither trapped within the cell nor directed toward its metabolism. Free fructose concentrations in the liver increase and fructose is free to leave the cell and enter plasma. This results in an increase in plasma concentration of fructose, eventually exceeding the renal threshold for fructose reabsorption resulting in the appearance of fructose in the urine. Essential fructosuria is a benign asymptomatic condition.

Hereditary fructose intolerance[edit]

The absence of fructose-1-phosphate aldolase (aldolase B) results in the accumulation of fructose 1 phosphate in hepatocytes, kidney and small intestines. An accumulation of fructose-1-phosphate following fructose ingestion inhibits glycogenolysis (breakdown of glycogen) and gluconeogenesis, resulting in severe hypoglycemia. It is very symptomatic resulting in severe hypoglycemia, abdominal pain, vomiting, hemorrhage, jaundice, hepatomegaly, and hyperuricemia eventually leading to liver and/or renal failure and death. The incidence varies throughout the world, but is it estimated at about 1/20,000 (range 1/12,000 to 1/58,000) live births.[citation needed]

Reduced phosphorylation potential[edit]

Intravenous (i.v.) infusion of fructose has been shown to lower phosphorylation potential in liver cells by trapping Pi as fructose 1-phosphate.[9] The fructokinase reaction occurs quite rapidly in hepatocytes trapping fructose in cells by phosphorylation. On the other hand, the splitting of fructose 1 phosphate to DHAP and glyceraldehyde by Aldolase B is relatively slow. Therefore, fructose-1-phosphate accumulates with the corresponding reduction of intracellular Pi available for phosphorylation reactions in the cell. This is why fructose is contraindicated for total parenteral nutrition (TPN) solutions and is never given intravenously as a source of carbohydrate. It has been suggested that excessive dietary intake of fructose may also result in reduced phosphorylation potential. However, this is still a contentious issue. Dietary fructose is not well absorbed and increased dietary intake often results in malabsorption. Whether or not sufficient amounts of dietary fructose could be absorbed to cause a significant reduction in phosphorylating potential in liver cells remains questionable and there are no clear examples of this in the literature.
Posted by at No comments:
Subscribe to: Posts (Atom)