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The global rise in obesity and metabolic diseases presents a major public health challenge, underscoring the need for innovative preventive and therapeutic strategies. While genetic predisposition and lifestyle factors are well-established contributors, increasing evidence highlights the critical influence of early-life nutritional environments on long-term metabolic health. However, the molecular mechanisms underlying this developmental programming remain incompletely defined. Our recent work investigates how early-life metabolic cues shape adipose tissue development, with a particular focus on thermogenic beige adipocytes—specialized cells within white adipose tissue that dissipate energy through mitochondrial uncoupling. These cells are emerging as key regulators of systemic energy balance and metabolic resilience. During the early postnatal period, mammals experience a transient state of elevated ketone bodies. Traditionally regarded as alternative energy substrates, ketone bodies are now recognized to have signaling functions. We demonstrate that β-hydroxybutyrate (βHB) acts as a regulatory metabolite that promotes beige adipocyte development. Mechanistically, βHB remodels the epigenetic landscape of adipose progenitor cells, modulating gene expression programs associated with thermogenesis and cellular differentiation. Collectively, these findings reveal a previously underappreciated role of early-life metabolism in programming adipose tissue plasticity and long-term metabolic health, providing new insights into the interplay between metabolism, epigenetics, and disease susceptibility.