Huddling can be defined as "an active and close aggregation of animals". It is a cooperative group behaviour, permitting individuals involved in social thermoregulation to minimize heat loss and thereby lower their energy expenditure, and possibly allowing them to reallocate the saved energy to other functions such as growth or reproduction. Huddling is especially important in the case of animals faced with high heat loss due to a high surface-to-volume ratio, poor insulation, or living in cold environments. Although numerous experimental studies have focused on the huddling behaviour of a wide range of species, to our knowledge, this is the first attempt to review the various implications of this widely used behavioural strategy. Huddling allows individuals to maximise energy savings by (1) decreasing their cold-exposed body surface area, (2) reducing their heat loss through warming of ambient temperatures surrounding the group, and (3) eventually lowering their body temperature through physiological processes. Huddling provides substantial energy savings and is estimated to reduce energy expenditure by between 6 and 53%. Broad variations in the energetic benefits of huddling depend on the number of individuals and species involved in huddles, the ambient temperatures to which individuals are exposed and the density of the aggregations. It has been shown that huddling individuals have increased survival, a lower food intake, a decreased body mass loss, increased growth rate, reduced water loss, and/or a more constant body temperature together with a significant reduction in metabolic rate. Though huddling has been studied widely, this review reveals the intricacies of this adaptive behaviour.

The role of the tumor suppressor retinoblastoma protein (pRb) has been firmly established in the control of cell cycle, apoptosis, and differentiation. Recently, it was demonstrated that lack of pRb promotes a switch from white to brown adipocyte differentiation in vitro. We used the Cre-Lox system to specifically inactivate pRb in adult adipose tissue. Under a high-fat diet, pRb-deficient (pRb ad؊/؊ ) mice failed to gain weight because of increased energy expenditure. This protection against weight gain was caused by the activation of mitochondrial activity in white and brown fat as evidenced by histologic, electron microscopic, and gene expression studies. Moreover, pRb ؊/؊ mouse embryonic fibroblasts displayed higher proliferation and apoptosis rates than pRb ؉/؉ mouse embryonic fibroblasts, which could contribute to the altered white adipose tissue morphology. Taken together, our data support a direct role of pRb in adipocyte cell fate determination in vivo and suggest that pRb could serve as a potential therapeutic target to trigger mitochondrial activation in white adipose tissue and brown adipose tissue, favoring an increase in energy expenditure and subsequent weight loss.brown adipose tissue ͉ mitochondria ͉ pocket proteins ͉ obesity