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Life sciences · Journal article
Molecular Biology of the Cell · September 16, 2026
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Metabolic diseases such as type 2 diabetes are often associated with adipose tissue dysfunction and obesity. Disorders of the primary cilium, or ciliopathies, can lead to obesity and the development of metabolic disease, as these signaling organelles regulate both the satiety pathway and adipose tissue expansion. Alström syndrome, a ciliopathy caused by loss of function of the Alms1 gene, is linked to hyperphagia, obesity, and early-onset type 2 diabetes, though how ALMS1 functions throughout the body to maintain energy homeostasis and metabolic health remains unclear. Here we demonstrate that ALMS1 loss in cultured preadipocytes and primary adipocyte progenitor cells from visceral, but not subcutaneous, mouse white adipose tissue depots inhibits their ability to undergo adipogenesis. Isolated primary adipocyte progenitor cells and cultured preadipocytes exhibit reduced ciliation and decreased centriole cohesion in the absence of ALMS1. Further, ALMS1 knockout preadipocytes retain the ciliary localization of G protein-coupled receptors known to influence adipogenesis, yet fail to undergo the changes in adipogenesis expected with their activation, consistent with a defect in ciliary transduction downstream of receptor localization. These findings demonstrate a new role for the ciliopathy gene Alms1 in directly regulating adipose tissue expansion through the regulation of ciliary signals required for adipogenesis.