Abstract
The aim of this article is to review the research into the main peripheral appetite signals altered in human obesity, together with their modifications after body weight loss with diet and exercise and after bariatric surgery, which may be relevant to strategies for obesity treatment. Body weight homeostasis involves the gut–brain axis, a complex and highly coordinated system of peripheral appetite hormones and centrally mediated neuronal regulation. The list of peripheral anorexigenic and orexigenic physiological factors in both animals and humans is intimidating and expanding, but anorexigenic glucagon-like peptide 1 (GLP-1), cholecystokinin (CCK), peptide YY (PYY) and orexigenic ghrelin from the gastrointestinal tract, pancreatic polypeptide (PP) from the pancreas and anorexigenic leptin from adiposites remain the most widely studied hormones. Homeostatic control of food intake occurs in humans, although its relative importance for eating behaviour is uncertain, compared with social and environmental influences. There are perturbations in the gut–brain axis in obese compared with lean individuals, as well as in weight-reduced obese individuals. Fasting and postprandial levels of gut hormones change when obese individuals lose weight, either with surgical or with dietary and/or exercise interventions. Diet-induced weight loss results in long-term changes in appetite gut hormones, postulated to favour increased appetite and weight regain while exercise programmes modify responses in a direction expected to enhance satiety and permit weight loss and/or maintenance. Sustained weight loss achieved by bariatric surgery may in part be mediated via favourable changes to gut hormones. Future work will be necessary to fully elucidate the role of each element of the axis, and whether modifying these signals can reduce the risk of obesity.
Highlights
Projections suggest that, by 2030, obesity prevalence may reach over 45% of the entire US population, and 48% in the United Kingdom.[1]
Original studies were identified from the two databases by searching for the following terms in the title or abstract: ‘appetite’, ‘satiety’, ‘satiation’, ‘satiety response’ or ‘post-meal satiety’; in conjunction with: ‘obesity’, ‘body fat’, ‘weight gain’, ‘weight reduction’, ‘weight loss’, ‘waist circumference’ or ‘body mass index’; and together with: ‘hormone (s)’, ‘peptide(s)’, ‘glucagon-like peptide 1’, ‘peptide YY’, ‘leptin’, ‘ghrelin’, ‘pancreatic polypeptide’, ‘obestatin’ or ‘cholecystokinin’
Obesity in humans arises from excess energy consumption relative to expenditure over long periods, with secondary hyperphagia that opposes weight loss
Summary
Projections suggest that, by 2030, obesity prevalence may reach over 45% of the entire US population, and 48% in the United Kingdom.[1]. Growing obesity research is shedding light on the complex and interrelated biological and psychosocial underpinnings of appetite regulation and eating behaviour. The changing food environment and food culture have a major role in the recent rise in obesity: with ready availability of attractive high-calorie foods, often in excessive portion sizes, and sedentary lifestyles all regarded as normal.[4] a body of evidence supports a continuing role for the gut–brain axis in regulation of food intake and the maintenance of body weight.[5,6,7,8] a complex array of signals from peripheral and central nervous systems, possibly under epigenetic programming, interacts with psychological and social factors to determine energy balance and body weight homeostasis.[5]
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