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Cold‐Induced Lipokines in Energy Metabolism
Author(s) -
Tseng Yu-Hua
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.00202
Subject(s) - brown adipose tissue , thermogenesis , endocrinology , medicine , adipose tissue , paracrine signalling , white adipose tissue , biology , autocrine signalling , type 2 diabetes , lipid metabolism , chemistry , diabetes mellitus , receptor
Obesity and metabolic syndrome are rapidly increasing worldwide, leading to high morbidity and mortality in type 2 diabetes, cardiovascular disease, renal failure, and even some cancers. Centered to these pathologies is the adipose tissue. In addition to the energy‐storing white adipose tissue, brown and brown‐like beige adipose tissue (BAT) are specialized for thermogenic energy expenditure. Due to the high capacity of BAT in consuming glucose and fatty acids to generate heat and dissipate energy and the presence of BAT in adult humans, increasing the amount or activity of BAT has been considered an appealing approach for the treatment or prevention of obesity and its related metabolic disorders. Besides energy dissipation, at least part of the beneficial effects of BAT is due to its secretory function and consequent capacity to affect metabolic functions in other tissues such as muscle, WAT, and liver. Thermogenic adipocytes can synthesize and release factors such as peptides, lipids, or other metabolites, which may act as endocrine, paracrine, or autocrine agents to regulate physiological functions required for adaptive thermogenesis. Cold exposure is one of the most efficient ways to activate BAT and increases energy consumption. Short‐term cold exposure leads to significant improvement in insulin sensitivity. By utilizing mass spectrometry‐based lipidomics, we have identified novel lipid mediators (i.e., lipokines) derived from BAT, whose concentrations are increased in the circulation of cold exposed mice and humans. These lipokines act as a marker and stimulator of thermogenic activity and negatively correlates with body mass index and insulin sensitivity. Mechanistic studies demonstrate that cold‐induced lipokines can regulate glucose and fatty acid metabolism. These findings provide novel therapeutic approaches for the treatment of metabolic diseases by mimicking cold exposure. Support or Funding Information NIH (R01DK077097, R01DK102898, P30DK036836), US Army (W81XWH‐17‐1‐0428)