REGULATION
OF ENERGY BALANCE
Variations in energy stores or energy balance reflect the difference between energy intake and energy expenditure and are generally associated with changes in body weight and, variations in fat mass. Given the high degree of fat mass stability throughout adult life, despite the tremendous amount of energy flowing through the organism, it can be argued that the level of energy stores is regulated. Brain circuitries involved in the control of energy intake (food intake) and energy expenditure (thermogenesis) seem capable of integrating peripheral signals, produced by perturbations of adipose tissue mass, into messages to effectors of food intake and energy expenditure, so as to prevent substantial variations in the level of energy reserves.
D. Richard studies the regulation of energy balance. Related to his research program
are the following general and specific objectives:
1. Study of the neurosystems involved in the control of food intake and
thermogenesis
i) Determination of the mechanisms governing the action of the
corticotropin-releasing hormone (CRH), neuropeptide Y (NPY), melanin-concentrating hormone
(MCH), thyrotropin-releasing hormone (TRH), serotonin (5-hydroxytryptamine, 5-HT), and
proopiomelanocortin (POMC) in the control of food intake and thermogenesis
ii) Determination of the neuronal circuits involved in the regulation of
energy balance through the identification of sites of synthesis (neuronal bodies) and
action (receptors) of the above mentioned neuromolecules
iii) Identification and determination of the role of new neuromolecules
in the regulation of energy balance
2. Study of the periphery-central nervous system interrelationships in the
regulation of energy balance
i) Determination of the sites and mechanisms of action of leptin,
corticosteroids (corticosterone, cortisol, aldosterone), and insulin in the control of
food intake and energy expenditure
3. Study of the effectors of food intake and thermogenesis
i) Determination of the effectors of food intake and description of the
circuitries coupling the regulatory centres with effectors of thermogenesis via the
sympathetic nervous system
ii) Role of the uncoupling proteins (UCP1, 2, 3) in the regulation of
energy balance
These projects are supported by the Medical Research Council of Canada, the Natural Sciences and Engineering Research Council of Canada, Canadian Diabetes Association, the Human Frontier Science Program and the Fonds FCAR.
Richard D, Rivest R, Naïmi N, Timofeeva H, Rivest S (1996) Expression of corticotropin-releasing factor and its receptors in the brain of lean and obese Zucker rats. Endocrinology 137: 4786-4795.
Naïmi N, Rivest S, Racotta I, Richard D (1997) Neuronal activation of the hypothalamic magnocellular system in response to oropharyngeal stimuli in the rat. J Neuroendo. 9: 329-340.
Timofeeva E, Richard D. (1997) Functional activation of CRH neurons and expression of the genes encoding CRH and its receptors in food-deprived lean (Fa/?) and obese (fa/fa) Zucker rats. Neuroendocrinology 66: 327-340.
Huang Q, Rivest R, Richard D (1998) Effects of leptin on corticotropin-releasing factor (CRF) synthesis and CRF neuron activation in the paraventricular hypothalamic nucleus of obese (ob/ob) mice. Endocrinology 139: 1524-1532.
Arvaniti K, Deshaies Y, Richard D The effects of leptin on energy balance does not require the presence of intact adrenals. Am J Physiol., in press.