Do B Vitamins Enhance the Effect of Omega-3 Polyunsaturated Fatty Acids on Cardiovascular Diseases? A Systematic Review of Clinical Trials.

Studies have suggested that B vitamins or omega-3 polyunsaturated fatty acids (PUFAs) may deter the development of cardiovascular disease (CVD). This systematic review aims to examine whether the combined supplementation of both B vitamins and omega-3 PUFAs could provide additional beneficial effects to prevent CVD beyond the effect of each supplement based on clinical trials published up to December 2021. The overall findings are inconsistent and inconclusive, yet the combined supplementation of these two nutrients may be more effective at reducing plasma homocysteine, triglyceride, and low-density lipoprotein-cholesterol than the individual components. The underlying mechanisms mainly include alleviating endothelial dysfunction, inhibiting atherosclerosis and lesion initiation, reducing oxidative stress, suppressing activation of pro-inflammatory cytokines, regulating endothelial nitric oxide synthase, and interfering with methylation of genes that promote atherogenesis. Although biologically plausible, the existing literature is insufficient to draw any firm conclusion regarding whether B vitamins can further enhance the potential beneficial effects of omega-3 PUFA intake on either primary or secondary prevention of CVD. The inconsistent findings may be largely explained by the methodological challenges. Therefore, well-designed high-quality trials that will use the combined supplementation of B vitamins and omega-3 PUFAs or dietary patterns rich in these two types of nutrients are warranted.

Ethanol extracts from Hemerocallis citrina attenuate the decreases of brain-derived neurotrophic factor, TrkB levels in rat induced by corticosterone administration.

ETHNOPHARMACOLOGICAL RELEVANCE: Hemerocallis citrina, a traditional herbal medicine, has been used for the improvement of behavioral and emotional status in Eastern-Asia countries. AIM OF THE STUDY: Our previous studies have demonstrated that the ethanol extracts of H. citrina flowers (HCE) reversed the behavioral alterations and monoamine neurotransmitter dysfunctions in stressed mice. However, the relation of its antidepressant-like action with neurotrophic molecular expressions remains unknown. MATERIALS AND METHODS: To clarify this, we explored the effect of HCE (32.5, 65, 130mg/kg, p.o.) on the behavior, brain-derived neurotrophic factor (BDNF) and its receptor (TrkB) in depression-like rats induced by exogenous administration of the stress hormone corticosterone (40mg/kg, s.c.). RESULTS: It was observed that repeated administration of corticosterone induced an elevation on the serum corticosterone levels, which caused the abnormalities observed in the sucrose preference test and forced swimming test (FST). Administration of HCE (65 and 130mg/kg) reversed the changes above and up-regulated the BDNF and TrkB receptor protein expressions in the brain region of frontal cortex and hippocampus. CONCLUSION: These findings confirm that HCE produce an antidepressant-like effect in corticosterone-induced depression-like model of rats and this effect is at least partly mediated by BDNF-TrkB signaling in the frontal cortex and hippocampus.

Prenatal and early postnatal exposure to high-saturated-fat diet represses Wnt signaling and myogenic genes in offspring rats.

The prenatal and early postnatal period is a key developmental window for nutrition status, and high-fat exposure in this period has been shown to be associated with type 2 diabetes, obesity and other features of metabolic disorders later in life. The present study was designed to investigate the underlying molecular mechanisms and role of relative genes involved in this process. We investigated the impact of prenatal and early postnatal exposure to a high-saturated-fat diet on the regulation of the Wnt signaling pathway and myogenic genes in skeletal muscle of rat offspring as well as the serum and muscle physiological outcomes. Timed-pregnant Sprague-Dawley rats were fed either a control (C, 16% kcal fat) or high-saturated-fat diet (HF, 45% kcal fat) throughout gestation and lactation. After weaning, female offspring were fed a control diet to generate two offspring groups: control diet-fed offspring of control diet-fed dams (C/C) and control diet-fed offspring of HF diet-fed dams (HF/C). The serum glucose of the HF/C offspring (5.58 ± 0.26 mmol/L) was significantly higher than that of C/C offspring (4.97 ± 0.28 mmol/L), and the Homeostasis Model Assessment-Insulin Resistance of HF/C offspring (2.00 ± 0.11) was also significantly higher when compared with C/C (1.84 ± 0.09). Furthermore, HF/C offspring presented excessive intramuscular fat accumulation (1.8-fold, P < 0.05) and decreased muscle glycogen (1.3-fold, P < 0.05), as well as impairment of muscle development at the age of 12 weeks. Meanwhile, we observed the repression of Wnt/ß-catenin signaling and myogenic genes in HF/C offspring. The present study indicates that prenatal and early postnatal exposure to a high-saturated-fat diet suppresses the development of skeletal muscle and myogenic genes via Wnt/ß-catenin signaling, and the inappropriate muscle development could potentially contribute to the predisposition of offspring to develop metabolic-syndrome-like phenotype in adulthood.

Maternal high-fat diet programs Wnt genes through histone modification in the liver of neonatal rats.

Maternal high-fat (HF) diets during gestation and lactation have been shown to contribute to metabolic disorders in offspring. Molecular and epigenetic mechanisms underlying this connection may be essential for the prevention and treatment of the fetal origins of metabolic diseases. The current study examined the impact of maternal HF diets on Wnt signaling and histone modification in offspring. Time-pregnant Sprague-Dawley rats were fed either control diet or HF diet during gestation and lactation and then the neonatal offspring of both groups were investigated. The neonatal offspring born to dams fed on HF diets exhibited increases in serum glucose and liver triglyceride levels. Maternal exposure to the HF diet also repressed the mRNA expression of Wnt1 and nuclear ß-catenin protein in the liver of offspring. The altered Wnt1 gene expression may be due to the changes of acetylation of H4 at its promoter as well as acetylation of H4 and methylation of H3K9 at coding region. Maternal exposure to the HF diet induced suppression of the Wnt/ß-catenin signaling pathway through histone modification, potentially increasing the risk of metabolic syndrome.