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Potential Crosstalk between Fructose and Melatonin: A New Role of Melatonin-Inhibiting the Metabolic Effects of Fructose - PubMed

  • ️Mon Jan 01 2018

Review

. 2018 Aug 1:2018:7515767.

doi: 10.1155/2018/7515767. eCollection 2018.

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Review

Potential Crosstalk between Fructose and Melatonin: A New Role of Melatonin-Inhibiting the Metabolic Effects of Fructose

Francisco J Valenzuela-Melgarejo et al. Int J Endocrinol. 2018.

Abstract

Increased consumption of energy-dense foods such as fructose-rich syrups represents one of the significant, growing concerns related to the alarming trend of overweight, obesity, and metabolic disorders worldwide. Metabolic pathways affected by fructose involve genes related to lipogenesis/lipolysis, beta-oxidation, mitochondrial biogenesis, gluconeogenesis, oxidative phosphorylation pathways, or altering of circadian production of insulin and leptin. Moreover, fructose can be a risk factor during pregnancy elevating the risk of preterm delivery, hypertension, and metabolic impairment of the mother and fetus. Melatonin is a chronobiotic and homeostatic hormone that can modulate the harmful effects of fructose via clock gene expression and metabolic pathways, modulating the expression of PPARγ, SREBF-1 (SREBP-1), hormone-sensitive lipase, C/EBP-α genes, NRF-1, PGC1α, and uncoupling protein-1. Moreover, this hormone has the capacity in the rat of reverting the harmful effects of fructose, increasing the body weight and weight ratio of the liver, and increasing the body weight and restoring the glycemia from mothers exposed to fructose. The aim of this review is to show the potential crosstalk between fructose and melatonin and their potential role during pregnancy.

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Figures

Figure 1
Figure 1

Metabolization of fructose in the liver cell. The main transporter of fructose in the liver is Glut-2, which translocates ketohexose to the cytoplasm and is transformed by the enzyme fructokinase to fructose-1-phosphate. After that, it is split into dihydroxyacetone phosphate and glyceraldehyde (triose phosphates). The final step is the production of pyruvate and their transformation to acetyl-CoA by pyruvate dehydrogenase; the latter product is a critical substrate for de novo lipogenesis.

Figure 2
Figure 2

Potential crosstalk between melatonin hormone and fructose. Fructose induces lipogenesis via SREBP-1c stimulation [26, 29], hypertension [, , –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 [, –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 [, , –56]. Similarly, melatonin reverted the chrono-disruption, hyperuricemia, hypertension, and impaired expression of clock genes [–, –86], finally modulating the negative effects of fructose on metabolism.

Figure 3
Figure 3

Effects of fructose and fructose plus melatonin over mothers and newborns in body weight and blood glucose levels. (a and b) show the body weight ratio (a) at term compared to the first day of pregnancy and blood glucose level (b) from 4 mothers maintained with standard diet (control) or supplemented daily with fructose (n = 4) or fructose plus melatonin (fructose + Mel, n = 4)). (c and d) show the body weight (c) and blood glucose level (d) from newborns (3–5 days). Wistar rats (200–250 g) were fed daily with standard diet (pellet) or supplemented with fructose-rich syrups equivalent to 2.7 g/kg/day (Great Value, USA) or fructose plus melatonin (Sigma-Aldrich, USA). Melatonin supplementation was given daily in drinking water at 0.1 mg/kg/day beginning at the third week and maintained after mating. Measurement of body weight and glycemia was performed from newborns euthanized by decapitation. We obtained the blood sampling in the tail tip, previously gently massaging the tail, and then using the Accu-Chek test strip system for glycemia measurement. The weight of the mothers as expressed with the ratio between body weights at term versus the first day after mating (grams at term/grams at day 1). ∗Different from control, P < 0.05, one-way ANOVA, Newman–Keuls posttest. ∗∗Fructose versus fructose + melatonin. The protocol was approved by the Ethics Committee of the University of Bío-Bío.

Figure 4
Figure 4

Effects of fructose and fructose plus melatonin in the heart/body weight ratio (a) and liver/body weight ratio (b) of the newborns (3–5 days), from mothers fed daily with standard diet (control) or supplemented with fructose-rich syrups or fructose plus melatonin. ∗Different from control, P < 0.05, one-way ANOVA, Newman–Keuls posttest. ∗∗Fructose versus fructose + melatonin. The protocol was approved by the Ethics Committee of the University of Bío-Bío.

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