Einleitung Adipose tissue is central to the regulation of energy balance. While white adipose
tissue is responsible for triglyceride storage, brown adipose tissue specializes in
energy expenditure. Deterioration of brown adipocyte function contributes to the development
of metabolic complications like obesity and diabetes. These disorders are also leading
symptoms of the Bardet–Biedl syndrome (BBS), a hereditary disorder in humans which
is caused by dysfunctions of Bbs gene products that form the BBSome supercomplex at
the base of the primary cilium. Cilia are hair-like organelles involved in cellular
signal transduction.
Methoden Effects of metabolic activation were analyzed in brown and subcutaneous white adipose
tissue of Bbs4 knockout mice to evaluate the role of cilia during adipose tissue remodeling.
Ergebnisse Ciliary dysfunction impairs the metabolic response of adipose tissue to adrenergic
stimulation, leading to significant loss of adipose tissue mass when Bbs4 knockout
mice are housed in a cold environment. This is accompanied by cold-intolerance and
alterations of fatty acid metabolism. Furthermore, pharmacologic β-adrenergic stimulation
uncovers impaired browning capacity of subcutaneous white adipose tissue.
Schlussfolgerung These findings taken together suggest that cilia-dependent signal transduction is
essential for the regulation of adipose tissue metabolism, representing a potential
target to treat metabolic disorders.
