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Foz/foz mice are deficient for Alms1, a ubiquitous protein essential for proper primary cilium function. They are prone to insulin resistance, obesity and diabetes, a phenotype accelerated by high-fat diet (HFD) feeding. Their unique metabolic phenotype has been linked to hyperphagia resulting from abnormal ciliary function in the central nervous system [1]. The aim of our study is to verify the dependence of the phenotype on over-feeding and to explore the role of Alms1 deficiency in intestinal energy absorption.

Role of ciliary dysfunction in a new model of obesity and non-alcoholic steatohepatitis: the foz/fozmice