Metabolic syndrome is a global health problem in adults and its prevalence among children and adolescents is rising. It is strongly linked to a lifestyle with high-caloric food, which causes obesity and lipid metabolism anomalies. Molecular damage due to excessive oxidative stress plays a major role during the development of metabolic syndrome complications. Among the different hormones, melatonin presents strong antioxidant properties, and it is used to treat metabolic diseases. However, there is not a consensus about its use as a metabolic syndrome treatment. The aim of this study was to identify melatonin effects in a metabolic syndrome model. Golden hamsters were fed with 60% fructose-enriched food to induce metabolic syndrome and were compared to hamsters fed with regular chow diet. Both groups were also treated with melatonin. Fructose-fed hamsters showed altered blood lipid levels (increased cholesterol and LDL) and phenotypes restored with the melatonin treatment. The Harderian gland (HG), which is an ideal model to study autophagy modulation through oxidative stress, was the organ that was most affected by a fructose diet. Redox balance was altered in fructose-fed HG, inducing autophagic activation. However, since LC3-II was not increased, the impairment must be in the last steps of autophagy. Lipophagy HG markers were also disturbed, contributing to the dyslipidemia. Melatonin treatment improved possible oxidative homeostasis through autophagic induction. All these results point to melatonin as a possible treatment of the metabolic syndrome.

Aims: The objective of this work was to apply the proteomic approach for identification of animal-based stress biomarkers during pig muscle maturation. Study Design: Pigs were subjected to management treatments that may promote stress, like mixing unfamiliar animals on farm and/or during transport and lairage before slaughter. Three pre-slaughter treatments were applied: UF-UTL (Unmixed on Farm - Unmixed during Transport and at Lairage), MF-UTL (Mixed in Farm - Unmixed during Transport and at Lairage) and MF-MTL (Mixed in Farm - Mixed during Transport and at Lairage). Methodology: Fifteen entire male pigs were used in this experiment. At slaughter, blood samples were taken for biochemical analysis. Meat quality traits (pH, electrical conductivity, drip loss, meat colour) were measured and muscle samples from the Longissimus thoracis were taken within the first 24 h post-mortem and used for analysis of total antioxidant activity (TAA) and sarcoplasmic protein profile study by SDS-PAGE. Results: Mixing treatments (MF-UTL and MF-MTL) provoked faster muscle pH post-mortem decline (P= .009), lower total antioxidant activity (P< .001) and changes in some key proteins, like the heat shock 70kDa protein-1B (P= .040), glyceraldehyde-3-phosphate dehydrogenase “GAPDH” (P= .047), lactate dehydrogenase-A “LDH-A” (P< .001) and adenylate kinase isoenzyme-1 “AK-1” (P< .001). Furthermore, serum molecules related to fat metabolism (LDL-cholesterol and triglycerides) and changes of muscle proteins involved in the adenine nucleotide metabolism (AK-1) and glycolysis regulation (piruvate kinase “PK” and GAPDH) allowed accurate prediction of muscle pH and discriminated correctly 87% of meat samples into “no-mixing” or “mixing” treatments. Conclusions: Early monitorization (within 24 h after slaughter) of selected biomarkers could be used in the meat industry as a tool for detection of situations of pre-slaughter stress related to animal mixing practices. However more research is needed in order to validate these results on a broader animal population.

Leptin is critically compromised in the major common forms of obesity. Skeletal muscle is the main effector tissue for energy modification that occurs as a result of the effect of endocrine axes, such as leptin signaling. Our study was carried out using skeletal muscle from a leptin-deficient animal model, in order to ascertain the importance of this hormone and to identify the major skeletal muscle mechanisms affected. We also examined the therapeutic role of melatonin against leptin-induced muscle wasting. Here, we report that leptin deficiency stimulates fatty acid β-oxidation, which results in mitochondrial uncoupling and the suppression of mitochondrial oxidative damage; however, it increases cytosolic oxidative damage. Thus, different nutrient-sensing pathways are disrupted, impairing proteostasis and promoting lipid anabolism, which induces myofiber degeneration and drives oxidative type I fiber conversion. Melatonin treatment plays a significant role in reducing cellular oxidative damage and regulating energy homeostasis and fuel utilization. Melatonin is able to improve both glucose and mitochondrial metabolism and partially restore proteostasis. Taken together, our study demonstrates melatonin to be a decisive mitochondrial function-fate regulator in skeletal muscle, with implications for resembling physiological energy requirements and targeting glycolytic type II fiber recovery.

Despite efforts to elucidate the cellular adaptations induced by obesity, cellular bioenergetics is currently considered a crucial target. New strategies to delay the onset of the hazardous adaptations induced by obesity are needed. Therefore, we evaluated the effects of 4 weeks of melatonin treatment on mitochondrial function and lipid metabolism in the livers of leptin-deficient mice. Our results revealed that the absence of leptin increased lipid storage in the liver and induced significant mitochondrial alterations, which were ultimately responsible for defective ATP production and reactive oxygen species overproduction. Moreover, leptin deficiency promoted mitochondrial biogenesis, fusion, and outer membrane permeabilization. Melatonin treatment reduced the bioenergetic deficit found in ob/ob mice, alleviating some mitochondrial alterations in the electron transport chain machinery, biogenesis, dynamics, respiration, ATP production, and mitochondrial outer membrane permeabilization. Given the role of melatonin in maintaining mitochondrial homeostasis, it could be used as a therapeutic agent against adipogenic steatosis.