Skip to main content
. 2018 Aug 1;2018:7515767. doi: 10.1155/2018/7515767

Figure 2.

Figure 2

Potential crosstalk between melatonin hormone and fructose. Fructose induces lipogenesis via SREBP-1c stimulation [26, 29], hypertension [8, 10, 25–27, 33, 34], gluconeogenesis [23, 29], hyperuricemia, and reactive oxygen species (ROS) [8, 28]. Besides, it induces chrono-disruption [67, 68], and the impairment expression of clock genes modifies the circadian output of PGC1α, PPAR α, NRF, SIRT1, and UCP1 [1, 48–50]. The molecular inhibition of PGC1α, PPAR α, NRF, SIRT1, and UCP1 by fructose [8, 22, 26, 28, 29, 32, 82, 83] can be reverted by melatonin exposition [44, 51, 54–56]. Similarly, melatonin reverted the chrono-disruption, hyperuricemia, hypertension, and impaired expression of clock genes [72–74, 84–86], finally modulating the negative effects of fructose on metabolism.