beiging

Beiging is a biological process in which white adipose tissue (WAT) develops beige, or brite, adipocytes that resemble brown adipose tissue (BAT) in function. Beige adipocytes are inducible within white fat depots and can contribute to non-shivering thermogenesis through the protein UCP1. The beiging phenomenon is of interest because it links adipose tissue plasticity to energy expenditure and metabolic health. It is distinct from constitutive BAT, which forms during development in dedicated regions; beiging represents a reversible transition in which white fat takes on brown-fat–like properties in response to stimuli such as cold exposure, β-adrenergic signaling, and certain hormones.

Key molecular drivers include the transcriptional regulators PRDM16 and PGC-1α, along with EBF2, which help reprogram adipocytes toward a brown-like gene expression profile. β-adrenergic signaling increases cAMP and activates protein kinase A, promoting UCP1 expression and mitochondrial biogenesis. Other contributors to beiging include BMP7, irisin (a myokine proposed to link exercise to beige fat formation), FGF21, and thyroid hormones. The beiging program is dynamic and can be reversed if the stimulating cues are removed.

Physiological and clinical relevance: In animal models, beiging elevates energy expenditure and improves insulin sensitivity; in humans, beige adipocytes have been detected in subcutaneous WAT and may participate in metabolic regulation, though individual capacity to undergo beiging declines with age and obesity. Therapeutic strategies aim to safely induce beiging or stabilize beige adipocytes to treat obesity and metabolic disorders, but challenges remain in achieving durable, widespread effects without adverse outcomes.

Terminology: Beiging is often used interchangeably with browning of white adipose tissue. Beige adipocytes are sometimes termed brite adipocytes, reflecting their origin from white fat depots.