Regulation of Appetite in the Elderly

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Regulation of appetite is a sophisticated process that involves feedback from peripheral sensory endings and the interaction of a variety of neurotransmitters in the central nervous system [1]. Numerous studies have shown that food intake declines over the human lifespan, with males having a greater decrease in food intake than females. A large part of the anorexia of aging seems to be related to the changes in gastrointestinal activity that occurs with aging [1].

During a meal, the fundus distends to accommodate food, a process termed adaptive relaxation. Food is then passed to the antrum after mixing with stomach secretions. Antral distension is the major signal for termination of a meal [1]. With aging, there appears to be impaired gastric fundal accommodation [6] due to impaired adaptive relaxation, which is caused by a decline in the local release of nitric oxide. Older mice have decreased nitric oxide synthase activity in their fundus [7]. The decline in adaptive relaxation that occurs with aging leads to more rapid antral filling. In addition, some studies suggested that large-

Table 1. Comparison of the major features of starvation, sarcopenia, cachexia and dehydration

Starvation (Anorexia of aging)

Sarcopenia

Cachexia

Dehydration

Weight loss

++

+

+++

++

Loss of lean mass

+

+

+++

0

Loss of fat mass

++

0

++

0

Cytokine excess

+/-

+

+++

0

Albumin

_

0

__

0

Anaemia

+/-

0

++

0

Hypogonadism

+/-

+

++

0

volume solid meals delay the rate of gastric emptying in the elderly [8-11]. This will eventually lead to prolongation of antral distension, which results in satiety (Fig. 1).

Infusion of lipid into the duodenum leads to the release of the peptide hormone cholecys-tokinin (CCK), which, in turn, leads to satiety. Evidence from animal studies indicates that CCK suppresses appetite in older animals more than in younger animals [12, 13]. This finding was also confirmed in humans. In addition, the basal circulating concentration of CCK and its response to lipids increases with aging, mainly due to a decline in the CCK clearance rate. CCK exerts its effects by increasing contractile activity in the pylorus, leading to slowing of gastric emptying and increasing the antral response to gastric distension [14]. CCK also directly stimulates the ascending vagal fibres that carry satiating signals to the nucleus tractus solitarii and to the hypothalamus [15].

Glucagon-like peptide is another gastrointestinal hormone involved with satiation, but its levels do not change with aging [16]. In contrast, amylin levels, which in mice decreases food intake in young and old mice, increase from middle age to old age [17].

The hormone leptin is released from adipose tissue [18] and exerts its effects by decreasing food intake and increasing the metabolic rate. Circulating leptin levels increase in older men and decrease in older women [19]. The increase in lep-tin levels in men is related to the decrease in testosterone that occurs with aging [1], which, in turn, is associated with muscle loss [20] and an increase in body fat [21]. Testosterone replacement in older men leads to a decline in leptin levels [1]. The increase in leptin with aging in men is considered a major factor in the increased anorexia of aging that occurs in males compared to females.

Although animal studies suggest that a decline

Nitric Oxide, Adaptive Relaxation, and Appetite

Fig. 1. Alterations in stomach motility that lead to the anorexia of aging

in opioid activity in the central nervous system may be associated with anorexia in older animals [22, 23], a study in humans did not show any difference in the effect of naloxone on food intake [12]. In humans, alteration in the thirst drive, which is modulated by ^-opioid receptors, appears to play a role in the development of age-related hypodipsia. Similarly, numerous neurotransmitters, such as neuropeptide Y, norepinephrine, and serotonin are involved in appetite regulation, although their role in the pathogenesis of the anorexia of the aging has been poorly investigated. An excess of corticotropin releasing factor is thought to be involved in the pathogenesis of the severe anorexia associated with depression in older persons.

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