3D结构图
Mol
相似结构
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美国有毒物质控制法案(TSCA)目录
名称和标识我要纠错
中文别名
结晶果糖 (D-果糖)果糖(果哌喃糖,左旋糖)D-果糖(结晶果糖)D(-)-果糖D-果糖,PH. EUR.,BP,USP高纤无糖糖浆
英文别名
Β-d-FructoseKrystarFructose Standard, 100000ppmD-arabino-2-HexuloseFructose, furanose formFructose Standard, 20000ppmketo D-fructoseketo-D-fructoseFructose Standard, 200ppmD-fructofuranoseFructose Standard, 18000ppmMFCD00148910FructooligosaccharidesFujifructo L 95Hi-Fructo FFrutabsΒ-LevuloseNF 55Hi-Fructo M 75(3S,4R,5R)-1,3,4,5,6-Pentahydroxy-2-hexanoneHFD 951,3,4,5,6-pentahydroxyl-2-hexanonefructose powderDSSTox_CID_3081b-D-FructoseFructose (JP15/USP)Δ-FructoseΒ-D-arabino-HexuloseD-(-)-Fructose 〔Levulose〕Fructose Standard, 3000ppmbeta-D-fructofuranoseFructose Standard, 1800ppmFructose Standard, 1500ppmΒ-Fruit sugar(3S,4R,5R)-1,3,4,5,6-Pentahydroxy-2-hexanonΒ-Δ-fructoseUNII:02T79V874PLevuloseD-Fructose(2R,3S,4S,5R)-2,5-bis(hydroxymethyl)oxolane-2,3,4-triol
展开∨
CAS
Inchi
InChI=1S/C6H12O6/c7-1-3(9)5(11)6(12)4(10)2-8/h3,5-9,11-12H,1-2H2/t3-,5-,6-/m1/s1
InChIkey
BJHIKXHVCXFQLS-UYFOZJQFSA-N
Canonical Smiles
C([C@H]([C@H]([C@@H](C(=O)CO)O)O)O)O
国际化联命名
(2R,3S,4R,5R)-2-(hydroxymethyl)oxane-2,3,4,5-tetrol
物化属性我要纠错
密度：1.758
熔点：100 - 110oC
沸点：401.1 °C at 760 mmHg
折射率：1.5101 (108 C)
闪光点：196.4 °C
蒸汽压：0.0±3.4 mmHg at 25°C
PSA：110.38000
logP：-3.21980
溶解度：3750 g/L (20 oC)
最大Λ：λ: 260 nm Amax: 0.04λ: 280 nm Amax: 0.04
外观：白色水晶般的固体
存储：
天然品存在于蜂蜜、水果等中。 酸度系数（pka）：pKa (18°): 12.06 溶解性：易溶于水、热丙酮，1g产品可溶于15ml乙醇、14ml甲醇，溶于吡啶、乙胺和甲胺，微溶于冷丙酮。 稳定性：Stable. Incompatible with strong oxidizing agents. 存储温度：2-8°C
本品应密封于阴凉干燥处保存。
天然品存在于蜂蜜、水果等中。 酸度系数（pka）：pKa (18°): 12.06 溶解性：易溶于水、热丙酮，1g产品可溶于15ml乙醇、14ml甲醇，溶于吡啶、乙胺和甲胺，微溶于冷丙酮。 稳定性：Stable. Incompatible with strong oxidizing agents. 存储温度：2-8°C
安全信息我要纠错
危险品标志：C
危险类别码：34
安全说明编码 ：S24/25
危险品运输编号：White Cyrstalline Solid
WGK Germany：3
RTECS号：LS7120000
生产方法及用途我要纠错
制造方法
1.工业上规模生产采用淀粉水解制葡萄糖，经固定化葡萄糖异构酶转化为转化糖，其中含有42%的果糖和58%的葡萄糖，将其分离后即得到果糖。
用途
营养型甜味剂；加工助剂；赋形剂。甜味强而纯的优良甜味剂，适用于各种食品。由于有良好的吸湿性，故特别适用于需要保湿的食品和用于糖果，以防止结晶发砂。主要用于高级糖果和婴儿饮料。;
果糖有直接供给热能，补充体液及营养全身的功效，比葡萄糖容易吸收利用，用作供给能量补充体液比葡萄糖更佳。除作为药物外，也用于高级糖果，婴儿饮料中。果糖也用作生化试剂。;
生化和微生物研究用。硼酸的测定。;
用途 1、营养型甜味剂；加工助剂；赋形剂。甜味强而纯的优良甜味剂，适用于各种食品。由于有良好的吸湿性，故特别适用于需要保湿的食品和用于糖果，以防止结晶发砂。主要用于高级糖果和婴儿饮料。
2、果糖有直接供给热能，补充体液及营养全身的功效，比葡萄糖容易吸收利用，用作供给能量补充体液比葡萄糖更佳。除作为药物外，也用于高级糖果，婴儿饮料中。果糖也用作生化试剂。
3、营养性甜味剂；加工助剂；赋形剂。甜味强而纯的优良甜味剂，适用于各种食品。由于有良好的吸湿性，故特别适用于需要保湿的食品和用于糖果，以防止结晶法砂。主要用于高级糖果和婴儿饮料。是葡萄糖的同分异构体,易被机体吸收利用,且不依赖胰岛素,对血糖影响小,适用于葡萄糖代谢及肝功能不全的患者补充能量。主要制备成果糖注射液、果糖氯化钠注射液、甘油果糖注射液等。
4、生化和微生物研究用，硼酸的测定，细胞和昆虫细胞培养。
用途 D-果糖可用作营养型甜味剂；食品添加剂。加工助剂；赋形剂。甜味强而纯的优良甜味剂，适用于各种食品。由于有良好的吸湿性，故特别适用于需要保温的食品和用于糖果，以防止结晶发砂。D-果糖主要用于高级糖果和婴儿饮料。果糖有直接供给热能，补充体液及营养全身的功效，比葡萄糖容易吸收利用，用作供给能量补充体液比葡萄糖更佳。除作为药物外，也用于高级糖果，婴儿饮料中。果糖也用作生化试剂 。 用途 生化和微生物研究用，硼酸的测定，细胞和昆虫细胞培养。 用途
D-Fructose (D(-)-Fructose) 是存在于许多植物中的一种天然单糖。 生产方法 果糖以游离的形态大量存在于水果的浆汁和糖蜜中，由菊芋水解可得到果糖。将含有果糖的多糖体菊粉（Inulin，在秋季，土木香，蒲公英，大丽花等根中菊粉含量可达40%之多）进行水解，生成果糖，经分离而得成品，这是生产果糖的方法之一。蔗糖是工业生产果糖最丰富的原料，用稀酸或转化酶水解蔗糖，从混杂有D-葡萄糖的溶液中析离果糖，果糖不易结晶，但它与氢氧化钙形成不溶性的复合物，分离后，通入二氧化碳，即可得到果糖结晶。利用蔗糖发酵制葡聚糖的发酵糖液，经毡袋过滤器过滤，送入乙醇蒸馏塔回收乙醇，蒸馏后的废糖液加0.25%（重量/体积）活性炭搅拌，待液温降至40℃以下进行离子交换，分离得到果糖。目前工业上大规模生产采用淀粉水解制备葡萄糖，经固定化葡萄糖异构酶转化为转化糖，其中含有42%果糖和58%葡萄糖，商业上称果葡萄糖浆或高果糖浆。它的甜度与蔗糖相当，但具有天然蜂蜜香味和生产成本低等特点，已广泛用于饮料和糖果糕点等食品工业。 生产方法 由含菊糖量高的菊科植物(如菊芋、菊苣等)加水分解而得。
由玉米糖浆经葡萄糖异构酶转化而成。
由葡萄糖经酸、碱或酶处理后异构化而成。
果糖有直接供给热能，补充体液及营养全身的功效，比葡萄糖容易吸收利用，用作供给能量补充体液比葡萄糖更佳。除作为药物外，也用于高级糖果，婴儿饮料中。果糖也用作生化试剂。;
生化和微生物研究用。硼酸的测定。;
用途 1、营养型甜味剂；加工助剂；赋形剂。甜味强而纯的优良甜味剂，适用于各种食品。由于有良好的吸湿性，故特别适用于需要保湿的食品和用于糖果，以防止结晶发砂。主要用于高级糖果和婴儿饮料。
2、果糖有直接供给热能，补充体液及营养全身的功效，比葡萄糖容易吸收利用，用作供给能量补充体液比葡萄糖更佳。除作为药物外，也用于高级糖果，婴儿饮料中。果糖也用作生化试剂。
3、营养性甜味剂；加工助剂；赋形剂。甜味强而纯的优良甜味剂，适用于各种食品。由于有良好的吸湿性，故特别适用于需要保湿的食品和用于糖果，以防止结晶法砂。主要用于高级糖果和婴儿饮料。是葡萄糖的同分异构体,易被机体吸收利用,且不依赖胰岛素,对血糖影响小,适用于葡萄糖代谢及肝功能不全的患者补充能量。主要制备成果糖注射液、果糖氯化钠注射液、甘油果糖注射液等。
4、生化和微生物研究用，硼酸的测定，细胞和昆虫细胞培养。
用途 D-果糖可用作营养型甜味剂；食品添加剂。加工助剂；赋形剂。甜味强而纯的优良甜味剂，适用于各种食品。由于有良好的吸湿性，故特别适用于需要保温的食品和用于糖果，以防止结晶发砂。D-果糖主要用于高级糖果和婴儿饮料。果糖有直接供给热能，补充体液及营养全身的功效，比葡萄糖容易吸收利用，用作供给能量补充体液比葡萄糖更佳。除作为药物外，也用于高级糖果，婴儿饮料中。果糖也用作生化试剂 。 用途 生化和微生物研究用，硼酸的测定，细胞和昆虫细胞培养。 用途
D-Fructose (D(-)-Fructose) 是存在于许多植物中的一种天然单糖。 生产方法 果糖以游离的形态大量存在于水果的浆汁和糖蜜中，由菊芋水解可得到果糖。将含有果糖的多糖体菊粉（Inulin，在秋季，土木香，蒲公英，大丽花等根中菊粉含量可达40%之多）进行水解，生成果糖，经分离而得成品，这是生产果糖的方法之一。蔗糖是工业生产果糖最丰富的原料，用稀酸或转化酶水解蔗糖，从混杂有D-葡萄糖的溶液中析离果糖，果糖不易结晶，但它与氢氧化钙形成不溶性的复合物，分离后，通入二氧化碳，即可得到果糖结晶。利用蔗糖发酵制葡聚糖的发酵糖液，经毡袋过滤器过滤，送入乙醇蒸馏塔回收乙醇，蒸馏后的废糖液加0.25%（重量/体积）活性炭搅拌，待液温降至40℃以下进行离子交换，分离得到果糖。目前工业上大规模生产采用淀粉水解制备葡萄糖，经固定化葡萄糖异构酶转化为转化糖，其中含有42%果糖和58%葡萄糖，商业上称果葡萄糖浆或高果糖浆。它的甜度与蔗糖相当，但具有天然蜂蜜香味和生产成本低等特点，已广泛用于饮料和糖果糕点等食品工业。 生产方法 由含菊糖量高的菊科植物(如菊芋、菊苣等)加水分解而得。
由玉米糖浆经葡萄糖异构酶转化而成。
由葡萄糖经酸、碱或酶处理后异构化而成。
合成路线
CAS No.：57-48-7 D-果糖合成路线共计: 144条合成路线
上下游产品我要纠错
第2部分 危险性概述
- 紧急情况概述：
-
无资料
- GHS危险性类别：
-
无危害分类
- 标签要素：
-
- 象形图：
- 无危险图标
- 警示词：
-
无警示词。
- 危险性说明：
-
无
- 防范说明：
-
- 预防措施：
- 无
- 事故响应：
- 无
- 安全储存：
- 无
- 废弃处置：
- 无
- 预防措施：
- 物理和化学危险：
- 无资料
- 健康危害：
- 无资料
- 环境危害：
- 无资料
海关数据我要纠错
- 中国海关编码：17025000
- 概述：
- 申报要素：
- Summary：
图谱
核磁图谱：
红外图谱(IR)：
红外图谱(IR)：
质谱(MS/Mass)：
质谱(MS/Mass)：
13C NMR : in DMSO-d6收起↑
ppm Int. Assign.
104.01 456 1
101.86 1000 7
82.79 334 2
81.76 825 8
80.76 326 3
75.67 315 4
75.56 745 9 *
75.19 790 10 *
63.60 296 5
62.81 867 11 #
62.79 841 12 #
60.94 275 6
IR : nujol mull展开↓
IR : KBr disc展开↓
Mass spectrum (electron ionization)展开↓
Mass展开↓
Source Temperature: 210 °C
Sample Temperature: 160 °C
DIRECT, 75 eV
计算化学数据
- 分子量：180.156g/mol
- 化合物是否规范：True
- 疏水参数计算参考值（XLogP3-AA）：-3.2
- 准确质量：180.06338810
- 同位素质量：180.06338810
- 复杂度：147
- 可旋转化学键数量：5
- 氢键供体数量：5
- 氢键受体计数：6
- 拓扑极表面积：118
- 重原子数量：12
- 确定原子立构中心数量：3
- 不确定原子立构中心数量：0
- 确定化学键立构中心数量：0
- 不确定化学键立构中心数量：0
- 同位素原子计数：0
- 共价键单元数量：1
- CACTVS Substructure Key Fingerprint：AAADccBgOAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAGgAACAAACBSggAIAAAAAAgAIAIAQAAIAAAAAAAAAAAFAAAABEBYAAAAAQAAFIAABAAHKZAQAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA==
其他
化学性质
吸湿性极强的白色无臭结晶或结晶性粉末。味甜，甜度约为蔗糖的1.6倍，为糖类中最甜者。熔点(分解)103～105℃(β型)。密度约1.6g/cm3有α-和β-两种型式，前者旋光度[α]D20为-63.6°，后者旋光度[α]D20为-135.5°，水溶液平衡后的旋光度[α]D20为-92.3°。易溶于水，溶于甲醇(1g/14m1)和乙醇(1g/15m1)，不溶于乙醚。
天然品存在于蜂蜜、水果等中。 General Description D-Fructose is present as a monosaccharide in fruits and vegetables[1], as a disaccharide in sucrose (with D-glucose), and as oligoand polysaccharides (fructans) in many plants. It is also used as an added sweetener for food and drink, and as an excipient in pharmaceutical preparations, syrups, and solutions[2].
In equal amounts, it is sweeter than glucose or sucrose and is therefore commonly used as a bulk sweetener. An increase in high fructose corn syrup, as well as total fructose, consumption over the past 10 to 20 years has been linked to a rise in obesity and metabolic disorders[3]. This raises concerns regarding the short and long-term effects of fructose in humans.
Fructose is present more or less frequently than glucose in the juices of plants, fruits, and especially the honey, which is about half the solid matters[4]. It leads to an equal amount of glucose by the hydrolysis of sugar cane and a smaller proportion than some other less common sugars. It is used, such as glucose, in the production of glycogen. It enters the body through either be eaten as such or as the result of digestion of sugar cane. It is mainly changed into glycogen or triglycerides after reaching the liver, so do not enter largely in the blood circulation. Glucose and fructose are partially inter-convertible under the influence of very dilute alkali. It is not surprising; therefore, that fructose must be converted to glycogen in the liver, which on hydrolysis yields of glucose[5]. Dubois et al. reported that regular consumption of sugary drinks between meals increases risk of overweight among preschool children[6].
Fructose has been claimed to be of concern due to several factors: First, in the 1980’s, sucrose was replaced to a large extent, particularly in North America, by high fructose corn syrup (HFCS) in carbonated beverages. The intake of soft drinks containing HFCS has risen in parallel with the epidemic of obesity[7]. Second, dietary fructose has been implicated in risk factors for cardiovascular disease (CVD): 1. Plasma triglycerides (TG) and VLDL-TG increased following the ingestion of large quantities of fructose; 2. Fructose intake has been found to predict LDL particle size in overweight schoolchildren[8]. 3. A positive relationship has been demonstrated between fructose intake and uric acid levels[9]. Third, the use of fructose as a sweetener has increased. The third National Health Examination Survey (NHANES) demonstrated that over 10% of Americans’ daily calories were from fructose[10]. These studies suggest that the relationship between fructose and health needs re-evaluation. Rise of fructose consumption Fructose consumption has been escalating over the past several decades and is believed to play a role in the rising epidemic of metabolic disorders[14]. Fructose is a simple monosaccharide that occurs naturally in fruit, though the two main sources of dietary fructose in the Western diet are sucrose (table sugar) and high-fructose corn syrup (HFCS)[14]. Sucrose is cleaved enzymatically during digestion to produce one fructose molecule and one glucose molecule. HFCS, on the contrary, contains free fructose and glucose in varying ratios. A popular type of HFCS that is used to sweeten beverages in the United States – HFCS-55 – contains 55% fructose, 42% glucose and 3% oligosaccharides[15]. The 1999–2004 data from the National Health and Nutrition Examination Survey (NHANES) show that the average daily intake of fructose in the United States is now approximately 49 g, which equates to 9.1% of total energy intake[16]. In comparison, the average daily intake of fructose during 1977–1978 was 37 g[16]. The highest consumers of fructose are 19–22-year-olds, largely due to excess consumption of sugar-sweetened beverages. Fructose consumption as a percentage of total energy intakes amongst male and female 19–22-year-olds in the 95th percentile is 17.5 and 17.9%, respectively[16]. Fructose and diseases Fructose and hyperuricemia
Increased intake of fructose is associated with hyperuricemia. Various studies indicate that that increased intake of sugar sweetened soft drinks and fructose is associated with risk of hyperuricemia in men[24].
Fructose and metabolic syndrome
It is hypothesized that fructose induces metabolic syndrome in health individuals. Study was carried out to investigate the role of uric acid in the hypertensive response. In this study, allopurinol was given to patients to lower the serum uric acid level. Ultimately it was found that excessive intake of fructose can increase the blood pressure and is responsible of metabolic syndrome but the lowering of serum uric acid level by allopurinol prevents the increase in mean arterial blood pressure[25].
Fructose and obesity
Fructose is almost similar to glucose because they are isomers to each other. Difference is in their metabolic pathway due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. In initial period when science was not so progressed, the diabetics patients were using fructose due to its low glycemic index. It has been observed now that obesity, diabetes mellitus, insulin resistance and hypertension are associated with chronic consumption of fructose. Dyslipidemia and impairment in hepatic insulin resistance are also due to increase intake of fructose in the diet. Adverse metabolic effects of fructose are responsible for hepatic de novo lipogenesis, hyperuricemia, oxidative stress and lipotoxicity. Epidemiological studies show that obesity, metabolic and cardiovascular disorders are also due to consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose). Adverse metabolic effects of fructose are usually on high consumption and there is lack of evidence of adverse effect on moderate consumption of fructose. Study shows that free fructose is more dangerous than consumption of fructose consumed with sucrose[26].
Fructose and hypertension
The rise in fructose intake has been paralleled by a rise in hypertension. A study of the US population during 2007–2008 found that 29% of adults were hypertensive, compared to 11–13% in 1939 and 24% during 1988–1994[27,28]. Epidemiological studies have hinted at a link between fructose consumption and hypertension. Jalal et al.[29] reported that excess dietary fructose (>74 g/day) in the form of added sugar was associated with higher blood pressure (BP) values in US adults who did not have a history of hypertension. Similarly, a study of 4867 adolescents found that SBP rose by 2mmHg from the lowest to the highest category of sugar-sweetened beverage intake[30]. In a prospective study of US adults, Chen et al.[31] found that drinking one less sugar-sweetened beverage per day was associated with a 1.8mmHg reduction in SBP and a 1.1mmHg reduction in DBP over 18 months. References
天然品存在于蜂蜜、水果等中。 General Description D-Fructose is present as a monosaccharide in fruits and vegetables[1], as a disaccharide in sucrose (with D-glucose), and as oligoand polysaccharides (fructans) in many plants. It is also used as an added sweetener for food and drink, and as an excipient in pharmaceutical preparations, syrups, and solutions[2].
In equal amounts, it is sweeter than glucose or sucrose and is therefore commonly used as a bulk sweetener. An increase in high fructose corn syrup, as well as total fructose, consumption over the past 10 to 20 years has been linked to a rise in obesity and metabolic disorders[3]. This raises concerns regarding the short and long-term effects of fructose in humans.
Fructose is present more or less frequently than glucose in the juices of plants, fruits, and especially the honey, which is about half the solid matters[4]. It leads to an equal amount of glucose by the hydrolysis of sugar cane and a smaller proportion than some other less common sugars. It is used, such as glucose, in the production of glycogen. It enters the body through either be eaten as such or as the result of digestion of sugar cane. It is mainly changed into glycogen or triglycerides after reaching the liver, so do not enter largely in the blood circulation. Glucose and fructose are partially inter-convertible under the influence of very dilute alkali. It is not surprising; therefore, that fructose must be converted to glycogen in the liver, which on hydrolysis yields of glucose[5]. Dubois et al. reported that regular consumption of sugary drinks between meals increases risk of overweight among preschool children[6].
Fructose has been claimed to be of concern due to several factors: First, in the 1980’s, sucrose was replaced to a large extent, particularly in North America, by high fructose corn syrup (HFCS) in carbonated beverages. The intake of soft drinks containing HFCS has risen in parallel with the epidemic of obesity[7]. Second, dietary fructose has been implicated in risk factors for cardiovascular disease (CVD): 1. Plasma triglycerides (TG) and VLDL-TG increased following the ingestion of large quantities of fructose; 2. Fructose intake has been found to predict LDL particle size in overweight schoolchildren[8]. 3. A positive relationship has been demonstrated between fructose intake and uric acid levels[9]. Third, the use of fructose as a sweetener has increased. The third National Health Examination Survey (NHANES) demonstrated that over 10% of Americans’ daily calories were from fructose[10]. These studies suggest that the relationship between fructose and health needs re-evaluation. Rise of fructose consumption Fructose consumption has been escalating over the past several decades and is believed to play a role in the rising epidemic of metabolic disorders[14]. Fructose is a simple monosaccharide that occurs naturally in fruit, though the two main sources of dietary fructose in the Western diet are sucrose (table sugar) and high-fructose corn syrup (HFCS)[14]. Sucrose is cleaved enzymatically during digestion to produce one fructose molecule and one glucose molecule. HFCS, on the contrary, contains free fructose and glucose in varying ratios. A popular type of HFCS that is used to sweeten beverages in the United States – HFCS-55 – contains 55% fructose, 42% glucose and 3% oligosaccharides[15]. The 1999–2004 data from the National Health and Nutrition Examination Survey (NHANES) show that the average daily intake of fructose in the United States is now approximately 49 g, which equates to 9.1% of total energy intake[16]. In comparison, the average daily intake of fructose during 1977–1978 was 37 g[16]. The highest consumers of fructose are 19–22-year-olds, largely due to excess consumption of sugar-sweetened beverages. Fructose consumption as a percentage of total energy intakes amongst male and female 19–22-year-olds in the 95th percentile is 17.5 and 17.9%, respectively[16]. Fructose and diseases Fructose and hyperuricemia
Increased intake of fructose is associated with hyperuricemia. Various studies indicate that that increased intake of sugar sweetened soft drinks and fructose is associated with risk of hyperuricemia in men[24].
Fructose and metabolic syndrome
It is hypothesized that fructose induces metabolic syndrome in health individuals. Study was carried out to investigate the role of uric acid in the hypertensive response. In this study, allopurinol was given to patients to lower the serum uric acid level. Ultimately it was found that excessive intake of fructose can increase the blood pressure and is responsible of metabolic syndrome but the lowering of serum uric acid level by allopurinol prevents the increase in mean arterial blood pressure[25].
Fructose and obesity
Fructose is almost similar to glucose because they are isomers to each other. Difference is in their metabolic pathway due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. In initial period when science was not so progressed, the diabetics patients were using fructose due to its low glycemic index. It has been observed now that obesity, diabetes mellitus, insulin resistance and hypertension are associated with chronic consumption of fructose. Dyslipidemia and impairment in hepatic insulin resistance are also due to increase intake of fructose in the diet. Adverse metabolic effects of fructose are responsible for hepatic de novo lipogenesis, hyperuricemia, oxidative stress and lipotoxicity. Epidemiological studies show that obesity, metabolic and cardiovascular disorders are also due to consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose). Adverse metabolic effects of fructose are usually on high consumption and there is lack of evidence of adverse effect on moderate consumption of fructose. Study shows that free fructose is more dangerous than consumption of fructose consumed with sucrose[26].
Fructose and hypertension
The rise in fructose intake has been paralleled by a rise in hypertension. A study of the US population during 2007–2008 found that 29% of adults were hypertensive, compared to 11–13% in 1939 and 24% during 1988–1994[27,28]. Epidemiological studies have hinted at a link between fructose consumption and hypertension. Jalal et al.[29] reported that excess dietary fructose (>74 g/day) in the form of added sugar was associated with higher blood pressure (BP) values in US adults who did not have a history of hypertension. Similarly, a study of 4867 adolescents found that SBP rose by 2mmHg from the lowest to the highest category of sugar-sweetened beverage intake[30]. In a prospective study of US adults, Chen et al.[31] found that drinking one less sugar-sweetened beverage per day was associated with a 1.8mmHg reduction in SBP and a 1.1mmHg reduction in DBP over 18 months. References
- Wang, Y.M.; van Eys, J. Nutritional significance of fructose and sugar alcohols. Annu. Rev. Nutr. 1981, 1, 437–475.
- Hanover, L.M.; White, J.S. Manufacturing, composition, and applications of fructose. Am. J. Clin. Nutr. 1993, 58 (Suppl. S5), 724S–732S.
- Bray GA, Nielsen SJ, Popkin BM: Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr 2004, 79:537-543.
- Ischayek JI, Kern M. US honeys varying in glucose and fructose content elicit similar glycemic indexes. J Am Diet Assoc 2006; 106(8):1260—2.
- Faiq A. Carbohydrate metabolism. In: Biochemistry review. 1st ed. Karachi: Urdu Bazar; 2004. p. 1—100.
- Dubois L, Farmer A, Girard M, Peterson K. J Am Diet Assoc 2007;107:924—34.
- Bray G: How bad is fructose? Am J Clin Nutr 2007, 86:895-896 .
- Aeberli I, Zimmermann MB, Molinari L, et al: Am J Clin Nutr 2007, 86:1174-1178.
- Nakagawa T, Hu H, Zharikov S, et al: A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol Renal Physiol 2006, 290: F625-631.
- Vos M, Kimmons J, Gillespie C, Welsh J, Blanck H: Medscape J Med 2008, 10(7):160.
- Bray GA. How bad is fructose? Am J Clin Nutr 2007; 86: 895–6.
- Lustig RH. Fructose: it’s ‘alcohol without the buzz’. Adv Nutr 2013; 4: 226–35.
- Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc 2010; 110: 1307–21.
- Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang D-H, et al. Am J Clin Nutr 2007; 86:899–906.
- Hanover LM, White JS. Manufacturing, composition, and applications of fructose. Am J Clin Nutr 1993; 58:724S–732S.
- Marriott BP, Cole N, Lee E. National estimates of dietary fructose intake increased from 1977 to 2004 in the United States. J Nutr 2009; 139:1228S–1235S.
- Park YK, Yetley EA. Intakes and food sources of fructose in the United States. Am J Clin Nutr 1993;58(5):737—47.
- Choi HK, Willett W, Curhan G. Fructose-rich beverages and risk of gout in women. J Am Med Assoc 2010;24304(20):2270—8.
- Ali M, Rellos P, Cox TM. Hereditary fructose intolerance. J Med Genet 1998;35(5):353—565.
- Segebarth C, Grivegnée AR, Longo R, Luyten PR, den Hollander JA. Biochimie 1991;73(1):105—8.
- Angelopoulos TJ, Lowndes J, Zukley L, Melanson KJ, Nguyen V, Huffman A, et al. J Nutr 2009;139(6):1242—5.
- Huang D, Dhawan T, Young S, Yong WH, Boros LG, Lipids Health Dis 2011;24:10—20.
- Van der Meulen R, Makras L, Verbrugghe K, Adriany T, De Vuyst L. Appl Environ Microbiol 2006;72(2):1006—12.
- Akram M. Management of acute gout. Inter J Fam Med 2010;3(4):233—4.
- Perez S, Schold J. Int J Obes 2009;34:454—61.
- Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev 2010;90(1): 23—46.
- Egan BM, Zhao Y, Axon RN. Us trends in prevalence, awareness, treatment, and control of hypertension, 1988–2008. JAMA 2010; 303:2043–2050.
- Robinson SC, Brucer M. Range of normal blood pressure. A statistical and clinical study of 11,383 persons. Arch Intern Med 1939; 64:409–444.
- Jalal DI, Smits G, Johnson RJ, Chonchol M. J Am Soc Nephrol 2010; 21:1543–1549.
- Nguyen S, Choi HK, Lustig RH, Hsu C-y. J Pediatr 2009;154:807–813.
- Chen L, Caballero B, Mitchell DC, Loria C, Lin P-H, Champagne CM, et al. Circulation 2010; 121:2398–2406.
1. 性状：白色斜方棱柱状结晶或结晶性粉末。以呋喃糖型和吡喃糖型同时存在。糖类中味最甜。极易潮解。
2. 密度（g/mL,25/4℃）：1.60
3. 相对蒸汽密度（g/mL,空气=1）：未确定
4. 熔点（ºC）：103～105℃（分解）
5. 晶相相标准燃烧热(焓)(kJ·mol-1)：-2810.4
6. 晶相标准声称热(焓)( kJ·mol-1)：-1265.6
7. 折射率：未确定
8. 闪点（ºC）：未确定
9. 比旋光度（º）：[α]D20 －132°→－92°（C=2）
10. 自燃点或引燃温度（ºC）：未确定
11. 蒸气压（kPa,25ºC）：未确定
12. 饱和蒸气压（kPa,60ºC）：未确定
13. 燃烧热（KJ/mol）：未确定
14. 临界温度（ºC）：未确定
15. 临界压力（KPa）：未确定
16. 油水（辛醇/水）分配系数的对数值：未确定
17. 爆炸上限（%,V/V）：未确定
18. 爆炸下限（%,V/V）：未确定
19. 溶解性：易溶于水、热丙酮，1g产品可溶于15ml乙醇、14ml甲醇，溶于吡啶、乙胺和甲胺，微溶于冷丙酮。
![[2H4]-D-果糖](https://structimg.guidechem.com/7/31/293970.png)
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