In the Western world, consumption of soft drinks has increased the last three decades and is partly responsible for the epidemic-like increase in obesity. Soft drinks, originally sweetened by sucrose, are now sweetened by other caloric sweeteners, such as fructose. In this study, we investigated the short-term effect of sucrose, glucose or fructose solutions on food intake and body weight in rats, and on peripheral and central appetite signals. Rats received water containing either of the sugars and standard rat chow for two weeks. Rats receiving water alone and standard chow were controls. All rats offered the sugar solutions increased their total caloric intake. The increased caloric intake occurred despite the fact that the rats offered either of the sugar solutions consumed less chow. As a consequence of the increased caloric intake, the sugar-drinking rats had elevated serum levels of free fatty acids, triglycerides and cholesterol. In addition, consuming sugar solutions resulted in increased serum leptin, decreased serum PYY and down-regulated hypothalamic NPY mRNA. Serum ghrelin was increased in rats receiving fructose solution. Moreover, consumption of sucrose or fructose solution resulted in up-regulated hypothalamic CB1 mRNA. Hypothalamic POMC mRNA was down-regulated in rats receiving glucose or fructose. In conclusion, consumption of glucose, sucrose or fructose solution results in caloric overconsumption and body weight gain through activation of hunger signals and depression of satiety signals as well as activation of reward components. The weight-promoting effect of these sugar solutions may possibly be ameliorated by the down-regulation of NPY mRNA and increased serum leptin.
"Whether or not sugar consumption has caused metabolic changes may have implications for the mechanisms underlying sugarinduced cognitive changes. For example, the onset of obesity may also alter levels of satiety peptides such as leptin, ghrelin, and neuropeptide Y (Lindqvist et al., 2008; Lindqvist, de la Cour, Stegmark, Hakanson, & Erlanson-Albertsson, 2005), which may in turn alter how food rewards are appraised. Studying the effects of sugar on the functioning of these homeostatic systems – with or without obesity – will be important in understanding what underlies effects on behavioural tasks that use food reinforcers. "
[Show abstract][Hide abstract] ABSTRACT: The pronounced global rise in sugar consumption in recent years has been driven largely by increased consumption of sugar-sweetened beverages. Although high sugar intakes are recognised as increasing the risk of obesity and related metabolic disturbances, less is known about how sugar might also impair cognition and learned behaviour. This review considers the effects of sugar in rodents on measures of learning and memory; reward processing, anxiety and mood. The parallels between sugar consumption and addictive behaviours are also discussed. The available evidence clearly indicates that sugar consumption can induce cognitive dysfunction. Deficits have been found most consistently on tasks measuring spatial learning and memory. Younger animals appear to be particularly sensitive to the effects of sugar on reward processing, yet results vary according to what reward-related behaviour is assessed. Sugar does not appear to produce long-term effects on anxiety or mood. Importantly, cognitive impairments have been found when intake approximates levels of sugar consumption in people and without changes to weight gain. There remain several caveats when extrapolating from animal models to putative effects of sugar on cognitive function in people. These issues are discussed in conjunction with potential underlying neural mechanisms and directions for future research.
"It is used in the preparation of a variety of food, drinks, and as a diet sweetener  . Determination of fructose in food  and in biological fluids   is therefore of great importance. Several conventional analytical methods for the determination of d-fructose have been largely described in literature , such as gas-chromatography , liquid chromatography , fluorimetric , near infrared spectroscopy  and electrochemistry . "
[Show abstract][Hide abstract] ABSTRACT: This paper describes the development and performance of the first fructose biosensor based on a commercial screen-printed graphene electrode (SPGE). The electrode was modified with an osmium-polymer, which allowed the efficient wiring of the enzyme fructose dehydrogenase (FDH). The immobilization of both osmium-polymer and FDH was realized in an easy way. Aliquots of 10 μL Os-polymer and 10 μL FDH were thoroughly mixed with poly(ethylene glycol) (400) diglycidyl ether (PEDGE) and deposited on the electrode surface and left there to dry overnight. The biosensor exhibits a detection limit of 0.8 μM, a linear range between 0.1 and 8 mM, high sensitivity to fructose (2.15 μA cm−2/mM), good reproducibility (RSD = 1.9%), fast response time (3 s) and a stability of 2 months when stored in the freezer.
The proposed fructose biosensor was tested in real food samples and validated with a commercial spectrophotometric enzymatic kit. No significant interference was observed with the proposed biosensor.
Sensors and Actuators B Chemical 05/2014; 195:287–293. DOI:10.1016/j.snb.2014.01.050 · 4.10 Impact Factor
"c o m / l o c a t e / p h b Animal models allow for examination of the long-term effects of sucrose consumption with strict control over diet and external factors in ways that are less feasible in human studies. In rodents, chronic consumption of sucrose solution induces metabolic disturbances similar to those observed in humans     ; however, as in humans, the relationship between sucrose consumption and body weight gain is variable . Wistar rats given sucrose solutions can reduce their solid chow intake to a sufficient degree to prevent excess weight gain, but this compensation may not be sufficient to prevent obesity when highly concentrated solutions (i.e. "
[Show abstract][Hide abstract] ABSTRACT: The metabolic consequences of providing rats with extended access to sugar solutions have varied across studies. The two experiments in this study examined the effects of 8weeks of 24-h access to 10% sucrose solution on adult Wistar rats. This was followed by 6weeks of food restriction with no access to sucrose during which the behavioural effects of prior sucrose consumption on reward-oriented behaviour (Experiment 1) and reversal learning (Experiment 2) were assessed. In a comparison between rat strains, Experiment 1 found that sucrose accelerated weight gain in Albino but not Hooded Wistar rats, while sucrose-fed rats of both strains exhibited elevated fasting blood glucose and resistance to insulin. Importantly, at cull retroperitoneal fat deposits were elevated in sucrose-fed rats, at which point glucose and insulin had resolved to control levels and liver triglyceride content did not differ between groups. Experiment 2 also found that retroperitoneal fat content was higher in sucrose-fed rats at cull, after 6weeks of behavioural testing without sucrose and with restricted access to food, and found a similar effect for epididymal fat. Behavioural testing in Experiment 1 found that sucrose exposure had no effect on habit formation assessed using an outcome devaluation paradigm. However, instrumental responding by sucrose-fed Albino rats was the least affected by pre-feeding, indicating a relationship between sucrose-induced obesity and food-seeking behaviour. In Experiment 2, sucrose-fed and control rats did not differ on a discrimination reversal task. In conclusion, this study demonstrates that the behavioural and metabolic effects of sucrose consumption vary with strain. Further, results indicate that sucrose consumption can lead to lasting increases in adipose tissue stores, a finding which has significant implications for human diets.
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