Leptin and the Anorexia of the Elderly

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Several cross-sectional and longitudinal studies have described a decline in food intake with aging in healthy elderly subjects [80-83]. This physiological decrease in food intake with age was defined as anorexia [80-83]. In the NHANES III an average decline in energy intake of about 1000 kcal/day (men) and 500 kcal/day (women) between the age of 20 and 75 years was described [84]. Aging was also associated with a decline in total energy expenditure that is accounted not only by a decline in physical activity but also by a decrease in resting metabolic rate [83]. When the decrease in energy intake is greater than the decrease in energy expenditure, involuntary weight loss may occur. Anorexia in the elderly and involuntary weight loss has been related to adverse outcomes, such as increased risk of sarcopenia, frailty, functional impairment, and mortality [80-83].

Anorexia has multiple causes including alterations in taste, flavor and palatability of food, increased gastrointestinal satiations signals, and decline in central feeding drive [80-83]. A role for leptin has been advanced in this multifactoral pathway due to its ability to decrease food intake and increase resting metabolic rate [80-83]. Thus, increased leptin level with age could play a role in anorexia of aging. Increased circulating leptin level in aging humans is largely due to increased fat mass. Adjustment for fat mass, however, eliminates this relationship in most [20-23, 25, 29] but not all studies [18, 24, 27]. Some investigators have speculated that increased leptin in males is due to the age-related decrease in testosterone that ultimately leads to decline in food intake.

A second hypothesis linking leptin to anorexia of aging is that aging may be associated with alteration in leptin sensitivity. Little information on this topic, however, is currently available. Ma et al. [85] hypothesized that the high plasma leptin level observed in different aging models may not be completely explained by the age related increase of body fat. This premise suggested the existence of a leptin-resistant state of aging because aging rats showed impaired leptin responsiveness with respect to food intake, fat mass, and distribution compared to young animals [85]. The impact of aging was also shown in adenovirus transfected hyperleptinemic diabetic rats [86]. In old rats the decline in food intake, body weight, and body fat following increased leptin levels was significantly lower than that observed in young rats [86]. Gabriely et al. [87] found a marked decrease in leptin's ability to decrease food intake in aging rats that underwent calorie restriction to maintain body fat and a metabolic pattern similar to that of young animals. Cumulatively, these results [85-87] imply a resistance to the effects of leptin with aging.

Fasting normally suppresses leptin level, thus, stimulating food intake. Reduced suppression of leptin level as well as a reduced increase in hypothalamic neuropeptide Y (NPY) by fasting has been reported in old versus young rats [88]. Monkeys on long-term caloric restriction did not have significantly lower food intake despite their low-leptin level when compared to controls [89].

Given the confusing animal experimental data in the above reports, it is very difficult to derive any definitive conclusion regarding the role of leptin in physiological anorexia of aging. Clearly further research including comprehensive human studies is mandatory to elucidate the contribution of leptin in decreased food intake with old age.

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