Novel Browning Agents, Mechanisms, and Therapeutic Potentials of Brown Adipose Tissue
Table 1
Several browning agents (genes, microRNAs, and pharmacological, chemical, or plant-based products) that induce browning/browning in adipose tissue and provide protection from HFD-induced obesity.
Browning agents
Effect on browning and metabolic outcome
Reference
Gain of function/overexpression
Ucp1
Less lipid accumulation in adipocytes, resistance to HFD-induced obesity, beige cell phenotype in WAT, atrophy of BAT, and reduced Ucp1 and mitochondrial DNA content in BAT
Beige adipocyte induction in WAT when stimulated by b-AR, increased energy expenditure, limited weight gain, and improved glucose tolerance in response to a HFD
Ucp1 induction in WAT via stimulation of β-AR, increased thermogenesis, attenuated weight loss and energy expenditure, and protection against HFD-induced obesity
Overexpression in adipose tissue led to reduced acetylation of Pgc1α and favorable interaction between Pgc1α, Prdm16, and Ucp1 in adipocytes, induction of browning in WAT, and protection against HFD-induced obesity
Improved glucose homeostasis with induction of beige cells in WAT which provided protection against obesity and increased mitochondrial bioenergetic profile of WAT
Increased energy expenditure, cold-induced thermogenesis, Ucp1 expression in WAT, fatty acid oxidation, browning of WAT, protection against HFD-induced obesity, and associated complications
β3AR agonist induces browning in WAT, strong response to cold in the form of increased thermogenesis, increased Ucp1 mRNA in WAT and BAT upon treatment, weight loss, and improved energy expenditure
Acting via Prdm16 to regulate beige adipocyte induction, increasing Ucp1 expression, and promoting adipose thermogenesis resulting in increased energy expenditure
Acting via TRPV1 channel, increased the expression of Pgc1 and Prdm16 and induced browning in adipose tissue, and provided protection from HFD-induced obesity