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Effects of sucrose, glucose and fructose on peripheral and central appetite signals

Department of Experimental Medical Science, Lund University, Lund, Sweden.
Regulatory Peptides (Impact Factor: 2.01). 10/2008; 150(1-3):26-32. DOI: 10.1016/j.regpep.2008.06.008
Source: PubMed

ABSTRACT 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.

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    • "For example, THC stimulates the intake of a high-fat or sweet-fat diet, but its effects are stronger for the fat diet (Koch 2001), and an antagonist decreases drinking of a lipid emulsion more than it does a sucrose solution (Thornton-Jones et al. 2007). Levels of 2-AG and binding to the cannabinoid CB1 receptor in the hypothalamus are also increased by a high-fat compared to low-fat diet (Higuchi et al. 2011; South and Huang 2008), while CB1 receptor expression is upregulated by sucrose intake (Lindqvist et al. 2008), suggesting that sucrose decreases endocannabinoid levels in this brain region. Also, like GAL and ENK, levels of anandamide in the hypothalamus are markedly elevated in female rats immediately prior to puberty onset (Wenger et al. 2002), when preference for fat is highest. "
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    ABSTRACT: Consummatory behavior is driven by both caloric and emotional need, and a wide variety of animal models have been useful in research on the systems that drive consumption of food and drugs. Models have included selective breeding for a specific trait, manipulation of gene expression, forced or voluntary exposure to a substance, and identification of biomarkers that predict which animals are prone to overconsuming specific substances. This research has elucidated numerous brain areas and neurochemicals that drive consummatory behavior. Although energy homeostasis is primarily mediated by the hypothalamus, reinforcement is more strongly mediated by nuclei outside the hypothalamus, in mesocorticolimbic regions. Orexigenic neurochemicals that control food intake can provide a general signal for promoting caloric intake or a more specific signal for stimulating consumption of a particular macronutrient, fat, carbohydrate, or protein. The neurochemicals involved in controlling fat ingestion--galanin, enkephalin, orexin, melanin-concentrating hormone, and the endocannabinoids--show positive feedback with this macronutrient, as these peptides both increase fat intake and are further stimulated by its intake. This positive association offers some explanation for why foods high in fat are so often overconsumed. Consumption of ethanol, a drug of abuse that also contains calories, is similarly driven by the neurochemical systems involved in fat intake, according to evidence that closely relates fat and ethanol consumption. Further understanding of the systems involved in consummatory behavior will enable the development of effective therapies for the treatment of both overeating and drug abuse.
    ILAR journal / National Research Council, Institute of Laboratory Animal Resources 03/2012; 53(1):35-58. DOI:10.1093/ilar.53.1.35 · 1.05 Impact Factor
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    • "Prior studies indicate that fructose has memory-enhancing properties (Messier and White, 1987; Rodriguez et al., 1994) and can act as a neuroprotectant under some circumstances (Sapolsky, 1986). Moreover, high fructose intake may alter hypothalamic appetitive systems (Lindqvist et al., 2008). "
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    ABSTRACT: Although fructose is commonly used as a sweetener, its effects on brain function are unclear. Using rat hippocampal slices, we found that fructose and mannose, like pyruvate, preserve ATP levels during 3-h of glucose deprivation. Similarly, fructose and mannose restored synaptic potentials (excitatory postsynaptic potential, EPSPs) depressed during glucose deprivation. However, restoration of synaptic responses was slow and only partial with fructose. EPSPs supported by mannose were inhibited by cytochalasin B (CCB), a glucose transport inhibitor, but were not inhibited by alpha-cyano-4-hydroxycinnamate (4-CIN), a monocarboxylate transport inhibitor, indicating that neurons use mannose via glucose transporters. In contrast, both CCB and 4-CIN depressed EPSPs supported by fructose, suggesting that fructose may be taken up by non-neuronal cells through CCB sensitive hexose transporters and metabolized to a monocarboxylate for subsequent use during neuronal respiration. Supporting this possibility, 20 minutes of oxygen deprivation in the presence of fructose resulted in functional and morphological deterioration whereas oxygen deprivation in the presence of glucose or mannose had minimal toxic effects. These results indicate that neuronal fructose utilization differs from glucose and mannose and likely involves release of monocarboxylates from glia.
    Neuroscience 05/2009; 161(3):847-54. DOI:10.1016/j.neuroscience.2009.04.008 · 3.33 Impact Factor
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    • "It can also be found together with sucrose and glucose in some root vegetables like beets, sweet potatoes, parsnips and onions. Today the largest source of fructose in the diet is though in the form of added fructose as a sweetener in desserts, candies and soft drinks (Lindqvist et al., 2008). Sucrose, which is a disaccharide consisting of 50 % fructose and 50 % glucose, also contributes to a portion of fructose when digested. "
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    ABSTRACT: Today the largest source of fructose can be found in soft drinks, desserts and candies where it serves as a sweetener together with glucose. Fructose is not metabolized the same way as glucose and does not stimulate production of several key-hormones such as insulin, leptin and ghrelin, regulating energy balance. Because of these differences it might be asked whether there is a connection between the increased consumption of high fructose corn syrup (HFCS), a common used sweetener, and the epidemic-like increase in obesity throughout the world. Several studies indicate that fructose gives rise to more deleterious metabolic effects than glucose, consequently leading to obesity. At the same time no differences between HFCS and sucrose has been shown indicating that HFCS are not likely contributing to the development of obesity as believed. The biggest use of fructose is in the form of HFCS, suggesting no reason to worry. Instead we should focus on our total consumption of sugar, try to stay away from soft-drinks and candy, and continue to eat adequate amounts of fruit. However, further investigations needs to be done to fully understand and determine the metabolic effects of prolonged consumption of fructose.
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