Adipose tissues are organs that have vital physiological roles in human health and disease. Functionally, white adipose tissue (WAT) is the principal repository for triglyceride energy, while brown adipose tissue (BAT) consumes fat and glucose to generate heat via chemical uncoupling and futile cycling (1). Excess calories stored in WAT lead to overweight and obesity and cause dysfunction in many organ systems, including WAT and BAT themselves. Reversing the ravages of obesity requires a net negative energy balance, which can be achieved through a combination of reduced food consumption, reduced caloric absorption, and increased energy expenditure. For decades, it has been recognized that chronic adrenergic stimulation of rodent BAT, either physiologically by cold exposure or pharmacologically via adrenergic receptor (AR) agonists, leads to a range of metabolic benefits, including resistance to diet-induced obesity (DIO), improved glycemia, and improved lipoprotein and cardiovascular risk profile (2). In this context, the question emerged: if adult humans had functional BAT, could its activation and growth be utilized to treat obesity and related metabolic diseases? The first step toward answering this question was conclusively established by 2009 with the demonstration of the presence of functional BAT in adult humans (3). More recently, investigators have devoted efforts to the next step, establishing at the cellular level that mouse and human adipocytes have similar genetic and functional features, particularly related to thermogenesis and the release of soluble endocrine mediators such as peptide hormones, bioactive lipids, and extracellular vesicles (4). In parallel with this second step, clinical researchers first showed that acute stimulation of human BAT by either mild cold exposure or activation of the β3-AR with mirabegron increased BAT thermogenesis and glucose uptake (5, 6). Next, they determined that chronic stimulation increased BAT mass and metabolic activity (6). By 2023, it is well accepted that adult humans have functional BAT, that it behaves like rodent BAT at the cellular level, and that it can be stimulated acutely and chronically. In addition, it is accepted that BAT has physiological relevance in human children, where it contributes to keeping them warm given their small size and limited muscle mass (7). However, a gnawing concern was that, despite similarities among the adipocytes, at the organismal level, rodent and adult human BAT were fundamentally different. Adult humans are three orders of magnitude larger than mice and therefore have a much smaller surface area–to–volume ratio that fundamentally alters their thermal dynamics: rodents must generate heat to maintain body temperature, and BAT plays a central role at 2%–5% of body weight. In contrast, humans generally maintain body temperature using what has been termed the “waste” heat from metabolic processes, with adult BAT typically only composing 0.1% to 0.5% of body weight (1). At this time, the field is in a state of balanced opposition, which led the organizers of ENDO 2023 to propose a debate between Dr. André Carpentier and me to address the question:“does activating BAT contribute to important metabolic benefits in humans?” Three specific benefits were addressed:(a) glucose metabolism;(b) cardiometabolic disease; and (c) obesity. The answer I defended was “Yes”, as detailed below.