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They found that these esters inhibited adipogenesis-fat accumulation, specifically at the mitotic clonal expansion stage in 3T3-L1 adipocyte cells.

The defective gene encodes the adipocyte hormone leptin, and the children do not produce it.

However, Zeng et al. found that loss of Clstn3b does not affect the expression of genes involved in adipocyte development, thermogenesis or mitochondrial function, including the gene that encodes UCP1.

Despite the well-documented association between adipocyte hypertrophy and hypoxia, the authors found that intracellular oxygen tension — a measure of the concentration of oxygen in the cell, which is decreased in hypoxia — was higher in Ant2-mutant mice than in controls.

The improved adipocyte oxygen tension in the Ant2-mutant mice was independent of ATP synthase, indicating that it did not relate to changes in coupled mitochondrial respiration.