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Background: The enhanced consumption of fructose as added sugar represents a major health concern. Due to the complexity and multiplicity of hypothalamic functions, we aim to point out early molecular alterations triggered by a sugar-rich diet throughout adolescence, and to verify their persistence until the young adulthood phase. Methods: Thirty days old rats received a high-fructose or control diet for 3 weeks. At the end of the experimental period, treated animals were switched to the control diet for further 3 weeks, and then analyzed in comparison with those that were fed the control diet for the entire experimental period. Results: Quantitative proteomics identified 19 differentially represented proteins, between control and fructose-fed groups, belonging to intermediate filament cytoskeleton, neurofilament, pore complex and mitochondrial respiratory chain complexes. Western blotting analysis confirmed proteomic data, evidencing a decreased abundance of mitochondrial respiratory complexes and voltage-dependent anion channel 1, the coregulator of mitochondrial biogenesis PGC-1α, and the protein subunit of neurofilaments α-internexin in fructose-fed rats. Diet-associated hypothalamic inflammation was also detected. Finally, the amount of brain-derived neurotrophic factor and its high-affinity receptor TrkB, as well as of synaptophysin, synaptotagmin, and post-synaptic protein PSD-95 was reduced in sugar-fed rats. Notably, deregulated levels of all proteins were fully rescued after switching to the control diet. Conclusions: A short-term fructose-rich diet in adolescent rats induces hypothalamic inflammation and highly affects mitochondrial and cytoskeletal compartments, as well as the level of specific markers of brain function; above-reported effects are reverted after switching animals to the control diet. [ABSTRACT FROM AUTHOR]

Accumulated lipid droplets in liver cause nonalcoholic fatty liver disease (NAFLD). Deep ocean water (DOW) containing high levels of magnesium, calcium, and potassium, etc. was proven to suppress hepatic lipid in obese rats fed high fat diet in the previous study. However, the effect of mineral compositions of DOW on the prevention of NAFLD is still unclear. This study removed calcium and potassium from DOW for modulating the mineral composition, and further compared the effects of DOW (D1(Mg + Ca + K)), DOW with low potassium (D2(Mg + Ca)), and DOW with low calcium and potassium (D3(Mg)) on the prevention of NAFLD in the mice model fed with high fat diet. In these results, DOW with high magnesium levels reduced serum and liver triglyceride and cholesterol levels and serum AST and ALT activities. However, when the calcium and/or potassium minerals were removed from DOW, the effects of reduction of triglyceride level, inhibition of acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and peroxisome proliferator-activated receptor-alpha (PPAR-α) expressions, and activation of superoxide dismutase, catalase, and glutathione reductase activities would be weaker. In conclusion, DOW including magnesium, calcium and potassium minerals has the strongest preventive effect on NAFLD in a mouse model by increasing the antioxidant system and inhibiting fatty acid biosynthesis. [ABSTRACT FROM AUTHOR]

Consumption of 2,4-decadienal (2,4-DD) delays gastric emptying (GE) rate in animals. Oil heating produces 2,4-DD and other aldehydes. Here we examined whether heated oil affects GE rate and food intake in humans, and whether it is mediated by 2,4-DD. In the first experiment, 10 healthy volunteers consumed 240-g pumpkin soup with 9.2 g of heated (HO) or non-heated corn oil (CO). Subsequently, 17 participants consumed pumpkin soup containing 3.1 g of either heated corn oil (HO), 1 mg 2,4-DD + non-heated corn oil (2,4-DD), or non-heated corn oil (CO). Sixty minutes following pumpkin soup, cod roe spaghetti was provided, and then energy intake was determined. To evaluate GE rate, 13C breath test (Experiment 1) and ultrasonography (Experiments 1 and 2) were used. The results from the Experiment 1 confirmed that consumption of heated corn oil reduced GE rate. Experiment 2 showed a delayed GE rate in HO and 2,4-DD trials compared with CO trial (p < 0.05). Energy intake was approximately 600–650 kJ lower in HO and 2,4-DD trials compared with CO trial (p < 0.05). These findings suggest that 2,4-DD, either formed by oil heating or added to food, contributes to suppressing GE rate and energy intake. [ABSTRACT FROM AUTHOR]

Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is expressed in skeletal muscles and regulates systemic metabolism. Thus, nutraceuticals targeting skeletal muscle PGC-1α have attracted attention to modulate systemic metabolism. As auraptene contained in citrus fruits promotes lipid metabolism and improves mitochondrial respiration, it could increase mitochondrial function through PGC-1α. Therefore, we hypothesized that PGC-1α is activated by auraptene and investigated its effect using Citrus hassaku extract powder (CHEP) containing >80% of auraptene. C2C12 myotubes were incubated with vehicle or CHEP for 24 h; C57BL/6J mice were fed a control diet or a 0.25% (w/w) CHEP-containing diet for 5 weeks. PGC-1α protein level and mitochondrial content increased following CHEP treatment in cultured myotubes and skeletal muscles. In addition, the number of oxidative fibers increased in CHEP-fed mice. These findings suggest that CHEP-mediated PGC-1α upregulation induced mitochondrial biogenesis and fiber transformation to oxidative fibers. Furthermore, as CHEP increased the expression of the protein sirtuin 3 and of phosphorylated AMP-activated protein kinase (AMPK) and the transcriptional activity of PGC-1α, these molecules might be involved in CHEP-induced effects in skeletal muscles. Collectively, our findings indicate that CHEP mediates PGC-1α expression in skeletal muscles and may serve as a dietary supplement to prevent metabolic disorders. [ABSTRACT FROM AUTHOR]

Fructose consumption has drastically increased during the last decades due to the extensive commercial use of high-fructose corn syrup as a sweetener for beverages, snacks and baked goods. Fructose overconsumption is known to induce obesity, dyslipidemia, insulin resistance and inflammation, and its metabolism is considered partially responsible for its role in several metabolic diseases. Indeed, the primary metabolites and by-products of gut and hepatic fructolysis may impair the functions of extrahepatic tissues and organs. However, fructose itself causes an adenosine triphosphate (ATP) depletion that triggers inflammation and oxidative stress. Many studies have dealt with the effects of this sugar on various organs, while the impact of fructose on brain function is, to date, less explored, despite the relevance of this issue. Notably, fructose transporters and fructose metabolizing enzymes are present in brain cells. In addition, it has emerged that fructose consumption, even in the short term, can adversely influence brain health by promoting neuroinflammation, brain mitochondrial dysfunction and oxidative stress, as well as insulin resistance. Fructose influence on synaptic plasticity and cognition, with a major impact on critical regions for learning and memory, was also reported. In this review, we discuss emerging data about fructose effects on brain health in rodent models, with special reference to the regulation of food intake, inflammation, mitochondrial function and oxidative stress, insulin signaling and cognitive function. [ABSTRACT FROM AUTHOR]