The role of muscle in appetite control
Published on 10 December 2010 in Food, health and wellbeing
Introduction
Diet and lifestyle change are likely to be the most pragmatic approaches to reducing obesity and improving outcomes for co-morbidities such as diabetes. Dieting is often the primary approach to weight loss, however, dieting in most cases is ineffective over the long term, with lost weight regained when dieting ceases. This is due to a combination of a reduced metabolic rate experienced during weight loss and the action of a powerful homeostatic system in the brain to defend a perceived appropriate body mass. Exercise is a lifestyle change that is often tried alone or in conjunction with diet to reduce weight and has beneficial effects on metabolic health in addition to weight loss, including improvement in insulin sensitivity. Exercise combined with dieting is often the most effective intervention at weight loss maintenance.
Depending upon the level of exercise, food intake may or may not be adjusted to compensate for energy expended. In humans the relationship between exercise and food intake seems poorly connected at least over short timescales and in the longer term energy expenditure may be compensated for by increased food intake in some individuals and not in others.
Skeletal muscle is the largest pool of protein in the body and constitutes nearly 50% of total body mass, contributing up to 40% of energy expended in the resting state. During growth protein is required to provide the building blocks of increased muscle mass. Studies in juvenile rodents at RINH have shown that during growth when lean mass (muscle) is increasing, protein content of a diet determines the level of food intake. This would implicate lean mass as an important determinant of food intake and suggests that food intake is set by the requirement to satisfy the need to maintain or increase lean tissue. This is important as lean mass varies as a result of obesity, dieting and exercise as well as lifestage, increasing dramatically in early years during growth and decreasing in later life, leading to sarcopenia (loss of muscle) in the elderly.
Recently the discovery of the cytokine, IL-6 as a circulating hormone produced and secreted from contracting muscle supports the contention that hormones produced and secreted from muscle can influence metabolism and establishes muscle as an endocrine organ. This discovery provides a conceptual basis for communication between exercised muscle and organs of the body including the brain. Until now we have not appreciated the potential influence of muscle on the ability to regulate appetite and that muscle derived factors produced during exercise, growth or in response to nutrient availability could relay a signal either directly or indirectly to the brain to adjust feeling of hunger and behaviour, including amount or type of food consumed for short-term and long-term needs.
Key Points
- Regulation of food intake is controlled by the brain and is an integration of hormones signalling hunger or satiety originating from peripheral tissues such as muscle, gut and adipose tissue, together with hunger inducing and satiety inducing neuropeptide hormones produced in the brain.
- Muscle has not been considered as a major endocrine organ until recent research identified several hormonal signals originating from muscle with the potential to alter metabolism.
- The hormone interlukin-6 originating from muscle during exercise acts within the brain as a satiety factor reducing short-term food intake, demonstrating the potential of muscle as a source of hormones that have a role in the regulation of food intake.
Research Undertaken
Recent work has been performed in a rodent model of body weight regulation that is set by the duration of exposure to short (winter-like) or long (summer-like) days. In our model, lean and fat mass accrue during long days and this is reversed by short day exposure. The model also demonstrates a remarkable ability to overcome short day induced body weight loss if given access to a running wheel and regain both lean and fat mass with a concomitant increase in food intake. This strongly suggests a result of exercise, a hormone from muscle increases either dependently or independently of an increase in lean mass to drive food intake.
Our current work is aimed at identifying this hormone produce from muscle and understanding how this acts at on peripheral tissue and the brain to bring about increase in food intake and muscle mass.
Policy Implications
Exercise has been advocated to reduce the rise in obesity, but for some individuals, exercise is followed by a compensatory increase in food intake. The reason for this is not fully understood, but in part may be due to over-estimation of energy expenditure or undervaluing the energy content of food types. This may in part be driven by biased assessments influenced by hormone actions on reward centres of the brain leading unwittingly to inappropriate decisions on food selection at the next the meal. Therefore understanding the interaction between muscle as an endocrine organ and the brain and the impact diet and exercise on this interaction, may lead to interventions that provide a sustainable loss of body mass (fat) without compensatory increases in food intake. This research has relevance to `Preventing Overweight and Obesity in Scotland - A Route Map Towards Healthy Weight Management’ as it can lead to understanding why physical activity may not be intuitively as effective in preventing or reducing obesity.
During aging, in addition to a reduction of appetite, muscle mass also declines. These two events may not be unrelated. Therefore understanding the relationship between muscle mass and food intake may lead to interventions to reverse or limit a decline in muscle tissue, driving up appetite and help to maintain health as we age.
Author
Dr. Perry Barrett P.Barrett@abdn.ac.uk
