Brown adipose tissue in the treatment of obesity and diabetes: Are we hot enough? - PubMed (original) (raw)

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Brown adipose tissue in the treatment of obesity and diabetes: Are we hot enough?

Chong Yew Tan et al. J Diabetes Investig. 2011.

Abstract

The identification of functional brown adipose tissue in human adults has intensified interest in exploiting thermogenic energy expenditure for the purpose of weight management. However, food intake and energy expenditure are tightly regulated and it is generally accepted that variation in one component results in compensatory changes in the other. In the context of weight loss, additional biological adaptations occur in an attempt to further limit weight loss. In the present review, we discuss the relationship between increasing energy expenditure and body weight in humans, including the effects of cold exposure. The data raise the possibility that some processes, particularly those involved in thermogenesis, induce less compensatory food intake for a given magnitude of additional energy expenditure, a state we term the 'thermogenic disconnect'. Although cold exposure increases thermogenesis and can putatively be exploited to induce weight loss, there are multiple adaptive responses to cold, of which many actually reduce energy expenditure. In order to optimally exploit either cold itself or agents that mimic cold for thermogenic energy expenditure, these non-thermogenic cold responses must be considered. Finally, the relative contribution of brown adipose tissue vs other thermogenic processes in humans remains to be defined. However, overall the data suggest that activation of cold-induced thermogenic processes are promising targets for interventions to treat obesity and its secondary metabolic complications. (J Diabetes Invest, doi:10.1111/j.2040-1124.2011.00158.x, 2011).

Keywords: Brown adipose tissue; Energy expenditure; Weight loss.

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Figures

Figure 1

Figure 1

Components contributing to total daily energy expenditure and the role of cold‐induced thermogenesis (CIT). The bar graph on the left depicts the relative contribution of various components to total daily energy expenditure (TDEE), namely activity energy expenditure (AEE), thermal energy of feeding (TEF), diet‐induced thermogenesis (DIT), CIT, and basal metabolic rate (BMR). The BMR is measured in a lightly clothed subject at rest in a thermoneutral environment. Below thermoneutrality, CIT is evoked to defend core body temperature. In this situation, the measured energy expenditure at rest is termed the resting metabolic rate (RMR). The graph on the right shows the magnitude of the RMR for a given environmental temperature. At thermoneutral temperatures (TN), RMR = BMR. At cooler temperature, CIT (shaded area) is evoked. The magnitude of CIT is determined by the severity of cold exposure (dotted line).

Figure 2

Figure 2

Physiological responses to cold exposure. From left to right, cold stimuli are sensed by peripheral and central thermal receptors. Within the central nervous system (CNS), neurobehavioral and endocrine responses are activated to defend core body temperature, including the hypothalamic–pituitary–thyroid axis, the sympathetic nervous system, behavioral responses, hypothermic cold adaptation, and appetite regulation. In turn, these produce physiological responses that support thermogenesis (A), activate thermogenic effector tissues (B), conserve heat (C) and increase caloric intake (D). For maximal thermogenic induced weight loss, Processes A and B should be optimal, whereas Processes C and D should be minimized. BAT, brown adipose tissue; FFA, free fatty acids.

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