|Stern, Judith - UNIV OF CALIFORNIA DAVIS|
|Havel, Peter - UNIV OF CALIFORNIA DAVIS|
Submitted to: American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 10, 1998
Publication Date: N/A
Interpretive Summary: It has been estimated that more than 30% of the US adult population is overweight or obese, and statistics show that obesity is on the rise. Attempts to reduce body weight with modifications of diet and/or physical activity have not yielded successful long-term, permanent reductions in body weight. A potential breakthrough for the treatment of obesity occurred in 1995 with the discovery of the hormone leptin. In studies conducted with experimental animals, leptin boosted metabolism and curbed food intake. However, we still know very little about leptin's influence on eating and activity in humans. We controlled the food intake of 12 women for 12 weeks by providing a diet that was restricted in calories, and the womens, leptin levels dropped. During this time, those women who had larger decreases in leptin reported being more hungry, and those who had smaller decreases were less hungry. We think these observations are the first to demonstrate a link between leptin, human eating behavior and hunger. Studies must be done to determine if the administration of leptin to obese individuals is an effective means for controlling appetite and limiting food intake.
Technical Abstract: Based on observations in rodents, leptin is thought to play a key role in the regulation of energy expenditure and food intake, but less is known of its influence on ingestive behavior and energy balance in humans. We examined the effect of a chronic energy deficit on plasma leptin and self-reported appetite in women and explored possible relationships between leptin and appetite sensations. Twelve healthy women (BMI=23-37) participated in a metabolic ward study with 3 wk of neutral energy balance followed by 12 wk of energy deficit (energy intake reduced by 2 MJ-d-1 and energy expenditure increased by 0.8 MJ-d-1). During the study, body weight and composition were monitored, fasting leptin concentrations were measured 4 times, and feelings of hunger, fullness, desire to eat, and prospective consumption were monitored hourly throughout the day, on 7 selected days. Adiposity-adjusted leptin decreased by 54% after 1 wk of moderate energy deficiency and remained low after 6 and 12 wks. Leptin was associated with self-reported hunger, desire to eat, and prospective consumption (range of r= -0.6 to -0.7; p<0.01). The greatest hunger increase coincided with the largest percent drop in circulating leptin and the lowest final leptin concentration. The relationship between leptin and hunger was not influenced by amount of weight or body fat loss. These findings support the idea that leptin is a physiological regulator of hunger during an energy deficit in humans, and its role in long-term food intake regulation warrants further study.