1599-1929 http://localhost:8080/xmlui/handle/123456789/5032 2026-04-26T03:48:33Z 2026-04-26T03:48:33Z Hadtstein, Felix Vrolijk, Misha http://localhost:8080/xmlui/handle/123456789/5057 2023-06-16T08:30:32Z 2021-01-01T00:00:00Z

Title: Vitamin B-6-Induced Neuropathy: Exploring the Mechanisms of Pyridoxine Toxicity Authors: Hadtstein, Felix; Vrolijk, Misha Abstract: Vitamin B-6 in the form of pyridoxine (PN) is commonly used by the general population. The use of PN-containing supplements has gained lots of attention over the past years as they have been related to the development of peripheral neuropathy. In light of this, the number of reported cases of adverse health effects due to the use of vitamin B-6 have increased. Despite a long history of study, the pathogenic mechanisms associated with PN toxicity remain elusive. Therefore, the present review is focused on investigating the mechanistic link between PN supplementation and sensory peripheral neuropathy. Excessive PN intake induces neuropathy through the preferential injury of sensory neurons. Recent reports on hereditary neuropathy due to pyridoxal kinase (PDXK) mutations may provide some insight into the mechanism, as genetic deficiencies in PDXK lead to the development of axonal sensory neuropathy. High circulating concentrations of PN may lead to a similar condition via the inhibition of PDXK. The mechanism behind PDXK-induced neuropathy is unknown; however, there is reason to believe that it may be related to γ -aminobutyric acid (GABA) neurotransmission. Compounds that inhibit PDXK lead to convulsions and reductions in GABA biosynthesis. The absence of central nervous systemrelated symptoms in PDXK deficiency could be due to differences in the regulation of PDXK, where PDXK activity is preserved in the brain but not in peripheral tissues. As PN is relatively impermeable to the blood–brain barrier, PDXK inhibition would similarly be confined to the peripheries and, as a result, GABA signaling may be perturbed within peripheral tissues, such as sensory neurons. Perturbed GABA signaling within sensory neurons may lead to excitotoxicity, neurodegeneration, and ultimately, the development of peripheral neuropathy. For several reasons, we conclude that PDXK inhibition and consequently disrupted GABA neurotransmission is the most plausible mechanism of toxicity.

2021-01-01T00:00:00Z Turner, Laurent Santosa, Sylvia http://localhost:8080/xmlui/handle/123456789/5056 2023-06-16T08:27:12Z 2021-01-01T00:00:00Z

Title: Putting ATM to BED: How Adipose Tissue Macrophages Are Affected by Bariatric Surgery, Exercise, and Dietary Fatty Acids Authors: Turner, Laurent; Santosa, Sylvia Abstract: With increasing adiposity in obesity, adipose tissue macrophages contribute to adipose tissue malfunction and increased circulating proinflammatory cytokines. The chronic low-grade inflammation that occurs in obesity ultimately gives rise to a state of metainflammation that increases the risk of metabolic disease. To date, only lifestyle and surgical interventions have been shown to be somewhat effective at reversing the negative consequences of obesity and restoring adipose tissue homeostasis. Exercise, dietary interventions, and bariatric surgery result in immunomodulation, and for some individuals their effects are significant with or without weight loss. Robust evidence suggests that these interventions reduce chronic inflammation, in part, by affecting macrophage infiltration and promoting a phenotypic switch from the M1- to M2- like macrophages. The purpose of this review is to discuss the impact of dietary fatty acids, exercise, and bariatric surgery on cellular characteristics affecting adipose tissue macrophage presence and phenotypes in obesity.

2021-01-01T00:00:00Z Cai, Shuang Quan, Shuang Yang, Guangxin Chen, Meixia Ye, Qianhong Wang, Gang Yu, Haitao Wang, Yuming Qiao, Shiyan Zeng, Xiangfang http://localhost:8080/xmlui/handle/123456789/5055 2023-06-16T08:23:41Z 2021-01-01T00:00:00Z

Title: Nutritional Status Impacts Epigenetic Regulation in Early Embryo Development: A Scoping Review Authors: Cai, Shuang; Quan, Shuang; Yang, Guangxin; Chen, Meixia; Ye, Qianhong; Wang, Gang; Yu, Haitao; Wang, Yuming; Qiao, Shiyan; Zeng, Xiangfang Abstract: With the increasing maternal age and the use of assisted reproductive technology in various countries worldwide, the influence of epigenetic modification on embryonic development is increasingly notable and prominent. Epigenetic modification disorders caused by various nutritional imbalance would cause embryonic development abnormalities and even have an indelible impact on health in adulthood. In this scoping review, we summarize the main epigenetic modifications in mammals and the synergies among different epigenetic modifications, especially DNA methylation, histone acetylation, and histone methylation.We performed an in-depth analysis of the regulation of various epigenetic modifications on mammals fromzygote formation to cleavage stage and blastocyst stage, and reviewed the modifications of key sites and their potential molecular mechanisms. In addition, we discuss the effects of nutrition (protein, lipids, and one-carbon metabolism) on epigenetic modification in embryos and emphasize the importance of various nutrients in embryonic development and epigenetics during pregnancy. Failures in epigenetic regulation have been implicated in mammalian and human early embryo loss and disease. With the use of reproductive technologies, it is becoming even more important to establish developmentally competent embryos. Therefore, it is essential to evaluate the extent to which embryos are sensitive to these epigenetic modifications and nutrition status. Understanding the epigenetic regulation of early embryo development will help us make better use of reproductive technologies and nutrition regulation to improve reproductive health in mammals.

2021-01-01T00:00:00Z Stokes, Alexandra Campbell, Karen J Yu, Hong-Jie Szymlek-Gay, Ewa A Abbott, Gavin He, Qi-Qiang Zheng, Miaobing http://localhost:8080/xmlui/handle/123456789/5054 2023-06-16T08:19:41Z 2021-01-01T00:00:00Z

Title: Protein Intake from Birth to 2 Years and Obesity Outcomes in Later Childhood and Adolescence: A Systematic Review of Prospective Cohort Studies Authors: Stokes, Alexandra; Campbell, Karen J; Yu, Hong-Jie; Szymlek-Gay, Ewa A; Abbott, Gavin; He, Qi-Qiang; Zheng, Miaobing Abstract: Emerging evidence shows an association between protein intake during infancy and later obesity risk, and that association may differ by protein sources. This systematic review summarized and evaluated prospective cohort studies assessing the long-term association of total protein intake and protein sources during infancy (from birth to 2 y) with subsequent obesity outcomes in childhood or adolescence. Literature searches were conducted in Embase,Medline, Scopus, andWeb of Science. Sixteen studies that reported associations between total protein intake and/or protein intake from different sources from birth to 2 y and ≥1 obesity outcomes in childhood or adolescence from 9 cohorts were identified. Most studies (11/16) were rated as high quality. The most frequently reported association was total protein intake and BMI (up to 10 y) with 6 out of 7 cohorts showing significant positive associations. Similar associations were found for animal protein, but not for plant protein. Limited studies examined the association between protein intake (both total and sources) and body composition (body fat, fat mass, and fat-free mass) and revealed inconsistent findings. Overall, higher intakes of total and animal protein during infancy were associated with higher BMI in childhood and adolescence. Future studies investigating the contribution of protein sources in long-term obesity development are needed. This review was registered at PROSPERO as CRD42020166540. Adv

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