Thermogenesis is a term which can be used to describe any form of heat production, but is normally applied to adaptive or regulatory components of metabolic rate, namely non-shivering thermogenesis (NST) and diet-induced thermogenesis (DIT). NST and DIT are activated in response to physiological stimuli and are largely dependent on sympathetic activation of heat production in brown adipose tissue (BAT). The quantitative importance and thermogenic mechanisms of BAT will be reviewed by others participating in this symposium. The objective of the present review is to discuss our current knowledge of the central mechanisms involved in the control of BAT thermogenesis, and how they are affected by physiological or pathological conditions.Of all aspects of BAT thermogenesis it is the central control which is probably the least understood, partly as a result of its complexity, but also because it has received relatively little direct attention. Considerable information and insight into this area can, however, be gained from studies concerned with feeding behaviour and temperature regulation, both of which are closely related and show many common features with sympatheticallymediated thermogenesis. Over the past few years, our understanding of central thermogenic mechanisms has improved considerably, due mainly to studies specifically designed to investigate this problem.
Areas of the brain controlling BATThe hypothalamus is the major area concerned with the control of autonomic functions, particularly feeding behaviour and thermoregulation, and has been the primary focus for studies on BAT thermogenesis. A close association between the ventromedial hypothalamus (VMH) and the regulation of body-weight or energy balance was first demonstrated almost 40 years ago, when destruction of the ventromedial nucleus was shown to result in hyperphagia and obesity. For a long time thereafter the VMH was referred to as a 'satiety' centre, acting reciprocally with the lateral hypothalamus (LH; known as the hunger centre) to control food intake (Stellar, 1954). However, obesity will develop in response to VMH lesions in the absence of hyperphagia, indicating that energy expenditure was simultaneously reduced (Han et al.