Friday, December 28, 2007

Sugars: hedonic aspects, neuroregulation, and energy balance -- Levine et al. 78 (4): 834S -- American Journal of Clinical Nutrition

Sugars: hedonic aspects, neuroregulation, and energy balance -- Levine et al. 78 (4): 834S -- American Journal of Clinical Nutrition..

ABSTRACT
The prevalence of obesity has increased dramatically in recent years in the United States, with similar patterns seen in several other countries. Although there are several potential explanations for this dramatic increase in obesity, dietary influences are a contributing factor. An inverse correlation between dietary sugar intake and body mass index has been reported, suggesting beneficial effects of carbohydrate intake on body mass index. In this review we discuss how sugars interact with regulatory neurochemicals in the brain to affect both energy intake and energy expenditure. These neurochemicals appear to be involved in dietary selection, and sugars and palatable substances affect neurochemical changes in the brain. For example, rats that drink sucrose solutions for 3 wk have major changes in neuronal activity in the limbic area of the brain, a region involved in pleasure and other emotions. We also investigate the relations between sucrose (and other sweet substances), drugs of abuse, and the mesolimbic dopaminergic system. The presence of sucrose in an animal’s cage can affect the animals desire to self-administer drugs of abuse. Also, an animal’s level of sucrose preference can predict its desire to self-administer cocaine. Such data suggest a relation between sweet taste and drug reward, although the relevance to humans is unclear. Finally, we address the influence of sugar on body weight control. For example, sucrose feeding for 2 wk decreases the efficiency of energy utilization and increases gene expression of uncoupling protein 3 in muscle, suggesting that sucrose may influence uncoupling protein 3 activity and contribute to changes in metabolic efficiency and thus regulation of body weight.

Key Words: WORDSSucrose • neuropeptides • dopamine • reward • energy expenditure • uncoupling proteins • substance abuse • carbohydrates

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Sugars provide energy and a pleasant taste. It should not be surprising, therefore, that the intake of sugars is influenced by 2 types of brain systems: those associated with the regulation of feeding and energy homeostasis and those associated with reward. During the past 3 decades, it has become clear that a host of neuromodulators are involved in the regulation of both energy and reward pathways. Many of these substances increase feeding (orexigenic agents) or decrease feeding (anorexic agents), and some also affect energy expenditure. In this review we focus on how sugars interact with regulatory neurochemicals in the brain to affect both energy intake and energy expenditure. We also examine the relations between sucrose (and other sweet substances), drugs of abuse, and the mesolimbic dopaminergic system. Finally, we discuss the influence of sugar on body weight regulation.

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NEUROCHEMICAL CHANGES INDUCED BY SUGARS

Several laboratories have published data suggesting that ingestion of sweet tastants results in neurochemical changes indicative of a change in opioid- or dopamine-mediated responses. Pomonis et al (36) gave rats access to a 10% sucrose solution or water for 3 wk and injected the rats with 10 mg naloxone or saline/kg. The rats’ brains were subsequently analyzed for c-Fos immunoreactivity in limbic and autonomic regions in the forebrain and hindbrain. c-Fos is an early gene transcription factor, and an increase in c-Fos concentrations is thought to reflect neural activation. Pomonis et al found that c-Fos concentrations in the central nucleus of the amygdala after naloxone injection were elevated more in the rats that drank 10% sucrose than in those that drank water. This suggests that this area is activated when sucrose is ingested. Thus, the central nucleus of the amygdala may participate in the integration of gustatory, hedonic, and autonomic signals as they relate to sucrose consumption.

Colantuoni et al (37) daily gave rats a 25% glucose solution with laboratory food pellets for 12 h, followed by 12 h of food deprivation. The rats doubled their glucose intake in 10 d and developed a pattern of excessive intake in the first hour of daily access. After 30 d, receptor binding in several brain areas of the glucose-exposed animals was compared with that in controls fed food pellets. Dopamine D-1 receptor binding increased significantly in the accumbens core and shell. In contrast, D-2 binding decreased in the dorsal striatum. Binding to dopamine transporter increased in the midbrain. Opioid mu-1 receptor binding increased significantly in the cingulate cortex, hippocampus, locus coeruleus, and accumbens shell. These data indicate neurochemical and region-specific responses to glucose intake and suggest a complex interplay between dopamine and opioids in the neural response to sugar. Colantuoni et al (38) also noted behavior changes associated with opiate withdrawal, such as teeth chattering in rats injected with naloxone after chronic glucose imbibition. Thus, chronic ingestion of sugars by laboratory animals may result in a state that resembles mild opioid dependence.

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Sucrose and reward

Human studies on the predictive potential of sucrose intake or preference on subsequent drug intake are relatively scarce and obviously cannot be conducted in a manner that precisely parallels the design of animal studies. Because of the established genetic influence on alcoholism (eg, 49), several studies examined taste preferences in subjects at risk for the development of alcoholism. Kampov-Polevoy et al (45) reported that subjects with a paternal history of alcohol dependence had a greater preference for strong sucrose solutions than did subjects with no paternal history of alcohol dependence. On the other hand, Scinska et al (50) and Kranzler et al (51) found no difference in the liking of sweets between sons of male alcoholics and control subjects. Scinska et al (50) did, however, note some differences in sensitivity to or preferences for salty and sour tastes. Therefore, the status of sweet taste preference as a marker for alcoholism is unclear, and we are not aware of any human studies in which sucrose preferences have been studied as potential markers for any other type of substance abuse.

Concurrent access to sweetened solutions and drugs of abuse
In rats, the intake of alcohol solutions with a concentration {approx}6% is low (52), and sucrose is often added to alcohol solutions to facilitate intake (eg, 53). However, when sucrose is provided as an alternative to alcohol, alcohol intake is reduced (53, 54). This effect is not specific to sucrose, because reductions in alcohol intake have also been obtained by the provision of saccharin and fat (54, 55). Given the differences between fat, sucrose, and saccharin in terms of caloric value and postingestive consequences, one may speculate that palatability is the salient factor in causing a reduction in intake. The effect is also not limited to alcohol, because the availability of palatable substances has been shown to reduce the intakes of orally self-administered phencyclidine in monkeys (56) and amphetamine in rats (57). The intravenous self-administration of cocaine is reduced by the availability of a glucose or saccharin solution

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EFFECTS OF SWEET SUBSTANCES ON THE MESOLIMBIC DOPAMINERGIC SYSTEM

The evidence reviewed above suggests a relation between sweet taste and drugs of abuse. Under certain laboratory conditions, a high preference for or intake of sweet-tasting substances can predict subsequent drug use, and the intake of these substances may modify the amount of drug self-administration. These relations may be consistent with the possibility that the rewarding effects of sweets and drugs of abuse are mediated by similar or overlapping mechanisms. The mesolimbic dopaminergic system is thought to play an important role in mediating the rewarding and incentive or motivational properties of drugs (68, 69). One effect common to many drugs of abuse is an increase in extracellular dopamine in the nucleus accumbens (69). The ingestion of food can also cause an increase in dopamine release in the nucleus accumbens, although, as pointed out by Wise (70), the effects are not as large as those produced by cocaine, heroin, or amphetamine.

Martel and Fantino (71) reported that the ingestion of a palatable food caused a greater increase in dopamine release than did the ingestion of standard laboratory food. However, a subsequent study indicated that this difference may have been due in part to differences in the amount consumed (72). When ingested in solution (73) or in granulated form (74), sucrose was also shown to increase dopamine release in the nucleus accumbens. Interestingly, increased dopamine release in response to granulated sugar was only observed in rats classified as high-sugar feeders; rats classified as low-sugar feeders did not have increased dopamine release (74). This difference, like that observed in the comparison between palatable food and usual laboratory food (71), may have been partially due to differences in intake during the microdialysis sessions. Similarly, the response to the ingestion of sucrose solution was compared with the response to water intake, and the different amounts of water and sucrose ingested may have been a factor (73). Nevertheless, these studies indicate some degree of activation by the ingestion of palatable food of the same system thought to be important in mediating drug reward. The observations that dopaminergic antagonists cause a reduction in the intake of sucrose solutions are also consistent with this view

Wow! What an interesting article. Carbs act in conjunction with brain chemicals to produce a kind of addiction, one that actually reshapes the brain and molds human behavior.

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