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      Nutritional Biomarkers, Gene-Diet Interaction, and Risk Factors for Type 2 Diabetes

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          Abstract

          Prevalence of type 2 diabetes (T2D) has been increasing globally, gaining high public health priority [1]. T2D is a complex disease, resulting from an interplay between lifestyle and genetic factors. Evidence from several randomized controlled trials suggests that physical activity and dietary intervention could prevent or delay progression of T2D [2–4]. In addition, genome-wide association studies have identified hundreds of genetic variants associated with T2D [5]. In the present special issue, each paper investigated different aspects of T2D prevention strategy, ranging from physical activity and diet/nutritional biomarker to gene-epigenetic mechanisms, in animal models and human studies. J. Qi et al. revealed that, in rats with insulin resistance induced by a high-fat diet, swimming exercise could improve insulin sensitivity, potentially via a reduction of TRIM72 expression, and upregulation of PI3-K/AKT signaling pathway, including IRS-1, p-AKTSer473, and AKT expression. The PI3-K/AKT signaling pathway is critically important for the regulation of insulin sensitivity and other biological processes related to aging [6, 7]. This study further showcased the intricate mechanism linking physical activity (swimming in this study) to insulin resistance. With similar design in a high-fat induced nonalcoholic fatty liver disease rodent model, Y. Xie et al. found that total alkaloid from Nelumbinis Plumula (NPA) could reduce insulin resistance via mechanism of restoring IRS1 and suppressing the JNK phosphorylation. Indeed, natural products derived from food resources have been proved to be promising natural remedies for T2D prevention and treatment [8]. Objectively measured nutritional biomarker may overcome recall bias and measurement error resulting from traditional dietary assessment tools, such as food frequency questionnaires. Emerging metabolomics studies are revealing more and more promising nutritional biomarkers and linking them to health outcomes. One of the examples is Branched-Chain Amino Acid (BCAA). In this issue, X. Zhao et al. systematically reviewed the current evidence on the relationship between BCAA and insulin resistance and concluded that circulating BCAAs (including valine, leucine, and isoleucine) are positively associated with insulin resistance and are useful biomarkers to predict future T2D cases. In a recent Mendelian randomization analysis, researchers identified a causal association of high circulating BCAAs with T2D risk and proved the causal role of BCAA metabolism in the T2D etiology [9]. Thus, use of nutritional biomarkers has obtained increasing popularity given their nature of objective measurement and potential usage to test causality in observational studies. Lastly, L. Yang et al. updated the association of genetic variations in LEPR gene with T2D risk with a meta-analysis, providing robust evidence for the association between rs1137101 at LEPR and T2D risk. In addition, T. Matsha et al. demonstrated the role of DNA methylation-genetic variations in screen-detected diabetes or known diabetes on treatment in an African population. All the above efforts add to the current knowledge on the role of genetic and epigenetic modulation on T2D etiology [10]. Taken together, articles in this special issue highlight several important fields in the prevention and treatment of T2D, focusing on the important role of diet and physical activity, incorporating natural remedies from food resources and new omics (metabolomics and genomics) strategies. The issue also suggests the importance of integrative strategies for the prevention and treatment of T2D in future research. Ju-Sheng Zheng Kaijun Niu Simone Jacobs Hassan Dashti Tao Huang

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          Natural Products for the Treatment of Type 2 Diabetes Mellitus.

          Type 2 diabetes mellitus is a metabolic disease characterized by persistent hyperglycemia. High blood sugar can produce long-term complications such as cardiovascular and renal disorders, retinopathy, and poor blood flow. Its development can be prevented or delayed in people with impaired glucose tolerance by implementing lifestyle changes or the use of therapeutic agents. Some of these drugs have been obtained from plants or have a microbial origin, such as galegine isolated from Galega officinalis, which has a great similarity to the antidiabetic drug metformin. Picnogenol, acarbose, miglitol, and voglibose are other antidiabetic products of natural origin. This review compiles the principal articles on medicinal plants used for treating diabetes and its comorbidities, as well as mechanisms of natural products as antidiabetic agents. Inhibition of α-glucosidase and α-amylase, effects on glucose uptake and glucose transporters, modification of mechanisms mediated by the peroxisome proliferator-activated receptor, inhibition of protein tyrosine phosphatase 1B activity, modification of gene expression, and activities of hormones involved in glucose homeostasis such as adiponectin, resistin, and incretin, and reduction of oxidative stress are some of the mechanisms in which natural products are involved. We also review the most relevant clinical trials performed with medicinal plants and natural products such as aloe, banaba, bitter melon, caper, cinnamon, cocoa, coffee, fenugreek, garlic, guava, gymnema, nettle, sage, soybean, green and black tea, turmeric, walnut, and yerba mate. Compounds of high interest as potential antidiabetics are: fukugetin, palmatine, berberine, honokiol, amorfrutins, trigonelline, gymnemic acids, gurmarin, and phlorizin.
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            Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile.

            Caloric restriction (CR) and down-regulation of the insulin/IGF pathway are the most robust interventions known to increase longevity in lower organisms. However, little is known about the molecular adaptations induced by CR in humans. Here, we report that long-term CR in humans inhibits the IGF-1/insulin pathway in skeletal muscle, a key metabolic tissue. We also demonstrate that CR induces dramatic changes of the skeletal muscle transcriptional profile that resemble those of younger individuals. Finally, in both rats and humans, CR evoked similar responses in the transcriptional profiles of skeletal muscle. This common signature consisted of three key pathways typically associated with longevity: IGF-1/insulin signaling, mitochondrial biogenesis, and inflammation. Furthermore, our data identify promising pathways for therapeutic targets to combat age-related diseases and promote health in humans. © 2013 John Wiley & Sons Ltd and the Anatomical Society.
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              Alterations of insulin signaling in type 2 diabetes: a review of the current evidence from humans.

              A generally accepted view posits that insulin resistant condition in type 2 diabetes is caused by defects at one or several levels of the insulin-signaling cascade in skeletal muscles, adipose tissue and liver, that quantitatively constitute the bulk of the insulin-responsive tissues. Hence, the gradual uncovering of the biochemical events defining the intracellular signaling of insulin has been quickly followed by clinical studies on humans attempting to define the molecular defect(s) responsible for the establishment of the insulin resistant state. While the existence of molecular defects within the insulin signal transduction machinery is undisputed, contrasting data exist on what is the principal molecular alteration leading to insulin resistance. Such discrepancies in the literature may depend on: 1) different subject characteristics, 2) methodological differences 3) small cohorts of subjects, and - not least - 4) intrinsic limitations in studying every detail of the insulin signaling cascade. Here, we review the studies on humans exploring the defects of the insulin signaling cascade generated by insulin resistance and type 2 diabetes, focusing on muscle and adipose tissue - which account for most of the glucose disposal capacity of the body - with focus on the unresolved discrepancies present in the literature.
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                Author and article information

                Journal
                J Diabetes Res
                J Diabetes Res
                JDR
                Journal of Diabetes Research
                Hindawi Publishing Corporation
                2314-6745
                2314-6753
                2016
                25 December 2016
                : 2016
                : 8610501
                Affiliations
                1MRC Epidemiology Unit, University of Cambridge, Cambridge, UK
                2Nutritional Epidemiology Institute, Tianjin Medical University, Tianjin, China
                3Institute of Public Health, University of Heidelberg, Heidelberg, Germany
                4Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
                5Saw Swee Hock School of Public Health, National University of Singapore, Singapore
                Author notes
                Author information
                http://orcid.org/0000-0001-6560-4890
                Article
                10.1155/2016/8610501
                5220505
                3499bafe-c7e9-4c28-aadf-16b068c0e877
                Copyright © 2016 Ju-Sheng Zheng et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 13 December 2016
                : 13 December 2016
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