Brain Systems Controlling Eating

The Hypothalamus. Current notions regarding the organization of the brain's feeding system derive from early animal studies aimed at identifying brain regions responsible for turning on or turning off feeding. One of the original findings in this regard was that destruction of the medial hypothalamus, in particular the ventromedial hypothalamic nucleus (VMH), produced a behavioral syndrome characterized by severe overeating and ultimately obesity (12). Humans with VMH tumors display a similar behavioral profile, confirming across species the importance of the VMH for eating.

Initially, the VMH was viewed as the brain's satiety center, but it is now recognized that both the psychological and neural characteristics of satiety are far too complex to be accounted for solely by the VMH. However, it is generally agreed that the VMH and its connections are important for relaying satiety signals from the periphery to neural systems involved in turning off feeding. Recent evidence indicates that VMH lesions also destroy fibers projecting to the pituitary stalk and brain stem, both of which are important in the control of various hormones. Of relevance here are findings showing that VMH lesions increase insulin secretion and decrease glucagon secretion, a combination associated with overeating. Thus the overeating associated with VMH lesions may be secondary to the peripheral hormonal and metabolic effects of the lesions rather than a direct result of the missing VMH.

In contrast to the inhibitory role ascribed to the VMH, the lateral hypothalamus (LH) has become associated with stimulation of eating. Animal experiments reveal that lesions of the LH produce aphagia and adipsia, whereas stimulation of the LH produces eating responses (12). Although LH lesions produce aphagia and adipsia, artificially fed animals can eventually recover and maintain close to normal eating habits; this recovery indicates that the central nervous system is sufficiently plastic to enable other brain areas to take over, to some extent, the feeding functions of the LH. It should be noted, however, that although eating deficits can eventually recover, LH-lesioned rats seldom return to their prelesion weight. This finding suggests that the LH contributes to the establishment and maintenance of a set point for body weight, which may be altered permanently by the lesion.

Other Hypothalamic Structures Involved in Eating. Another important structure implicated in eating behavior is the paraventricular nucleus (PVN) of the hypothalamus. In fact, many of the effects associated with VMH manipulations have more recently been interpreted as PVN effects, owing to the discovery that VMH lesions destroy fibers originating from the PVN, some of which are associated with control of hormonal functions already described and others of which project to brain stem mechanisms involved in the control of eating. Moreover, it has been demonstrated that PVN lesions have effects on eating similar to those of VMH lesions. For these reasons, as well as for reasons to be discussed next, researchers have begun to view the PVN as a critical structure for the control of feeding.

Neurotransmitters and Eating. Any description of the neural basis of eating would be incomplete without a discussion of the neurotransmitter systems implicated in eating. Neurotransmitters are responsible for interneuronal communication. Thus, the activity of cells within particular brain regions is determined by the neurotransmitters that stimulate or inhibit them.

Norepinephrine, endorphins, galanin, and neuropeptide Y are transmitters that act in the PVN to facilitate food intake (13). Of special interest here is the finding that the stimulatory effects of norepinephrine in the PVN appear to be specific to carbohydrate intake (13). Elsewhere, growth hormone-releasing factor in the medial preoptic area of the hypothalamus stimulates eating (14). Neurotransmitter signals involved in inhibiting eating include dopamine and norepinephrine in the perifornical region of the hypothalamus as well as serotonin in the PVN (13). Interestingly, serotonin's inhibitory effect, like norepinephrine's stimulatory effect, is carbohydrate selective (13).

Although exactly how these transmitter signals are integrated during normal eating is still unclear, it is assumed that these chemical signals reflect food-relevant information derived from the periphery. For example, consider the regulation of carbohydrate intake. A high-carbohydrate meal increases tryptophan uptake in the brain and ultimately the synthesis of serotonin, for which tryptophan is the precursor. Increased serotonin activity, as discussed earlier, suppresses food intake, particularly carbohydrates. Thus increased carbohydrate intake eventually feeds back negatively on further carbohydrate intake (probably through serotonin's action in the PVN), providing a mechanism for the short-term regulation of carbohydrate intake.

Extrahypothalamic Influences on Feeding. Nonhypothal-amic brain systems have also been implicated in the control of feeding. In particular, activation of the nigrostriatal and mesolimbic dopamine pathways, which use dopamine as a neurotransmitter, is associated with stimulatory effects on feeding. These pathways originate in the midbrain and project rostrally to striatal and limbic structures in the forebrain, with some of the axons involved coursing through the lateral hypothalamus en route. This anatomical fact has been taken to suggest that some of the feeding decrements associated with LH lesions may in fact be due to destruction of ascending dopamine neurons. Although the role of the nigrostriatal and mesolimbic dopamine pathways in feeding is not entirely understood, it is of interest to note that these pathways are crucial for reward and reinforcement functions in general (15), suggesting that activation of these systems may reinforce the sensory-motor associations involved in eating and also increase the rewarding properties of food or eating (16,17). Thus contrary to the conventional homeostatic view of eating regulation, these particular signals may be associated with nonregulatory influences on eating such as taste hedonics or learned feeding patterns.

Keep Your Weight In Check During The Holidays

Keep Your Weight In Check During The Holidays

A time for giving and receiving, getting closer with the ones we love and marking the end of another year and all the eating also. We eat because the food is yummy and plentiful but we don't usually count calories at this time of year. This book will help you do just this.

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