Studies using mice with an adipose-specific depletion of Bmal1 show that hypothalamic sensing of circulating polyunsaturated fatty acids (PUFAs) and non-esterified polyunsaturated fatty acids is disturbed when the adipose clock is impaired, a situation which results in altered circadian energy intake and obesity in mice [197]. This evidence concerns the gene CLOCK and obesity due to melanocortin 4 receptor deficiency.