Diabetes articles within Nature

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  • News & Views |

    An innovative method for probing the genomes of the vast community of microorganisms that inhabit the human gut provides an alternative approach to identifying risk factors for type 2 diabetes. See Letter p.55

    • Julia Oh
    •  & Julia A. Segre

  • Article |

    The authors have developed a new method, metagenome-wide association study (MGWAS), to compare the combined genetic content of the faecal microbiota of healthy people versus patients with type 2 diabetes; they identify multiple microbial species and metabolic pathways that are associated with either cohort and show that some of these may be used as biomarkers.

    • Junjie Qin
    • , Yingrui Li
    •  & Jun Wang

  • Outlook |

    The number of people living with, and dying of, diabetes across the world is shocking: 90 million Chinese live with diabetes and 1.3 million died in 2011; 23% of Qatari adults have developed diabetes. Here we chart the extent of the global epidemic and present some of the implications for national governments by Tony Scully.

    • Tony Scully

  • Outlook |

    Decades of study into the causes of diabetes have produced no definitive answers.

    • Erika Jonietz

  • Outlook |

    While type 1 diabetes might be promising ground for a vaccine, the most effective way to avoid type 2 remains good old-fashioned diet and exercise.

    • Scott P. Edwards

  • Outlook |

    Artificial pancreases promise to take the decision-making — and human mistakes — out of managing type 1 diabetes.

    • Elie Dolgin

  • Outlook |

    Promising drugs to treat diabetes stumble in the latter stages of clinical testing. Thomas Mandrup-Poulsen explains why — and how to fix it.

    • Thomas Mandrup-Poulsen

  • Article |

    Downregulation of the glucose transporter GLUT4 in adipose tissue occurs early in the development of type 2 diabetes; here GLUT4-mediated glucose uptake is shown to induce a novel form of the transcription factor ChREBP, which regulates de novo lipogenesis and systemic glucose metabolism.

    • Mark A. Herman
    • , Odile D. Peroni
    •  & Barbara B. Kahn

  • News |

    Profiles of a researcher's genes, proteins and more show personalized genomic medicine in action.

    • Carina Dennis

  • Editorial |

    The soaring incidence of diabetes is driving the United Arab Emirates' science ambitions.

  • News & Views Forum |

    Variation in a genomic region that contains the cancer-associated gene ATM affects a patient's response to the diabetes drug metformin. Two experts discuss the implications for understanding diabetes and the link to cancer.

    • Morris J. Birnbaum
    •  & Reuben J. Shaw

  • Letter |

    A non-coding region on chromosome 9p21 was previously shown to associate with coronary artery disease and type 2 diabetes, and the region has been implicated in regulating neighbouring genes. Here, 33 distinct enhancers within this region are identified, showing that SNPs in one of the enhancers affect STAT1 binding. Furthermore, it is shown that in human vascular endothelial cells the enhancer interval physically interacts with a number of specific loci and that IFN-γ activation strongly affects the chromatin structure and transcriptional regulation of the 9p21 locus, including STAT1 binding, long-range enhancer interactions and expression of neighbouring genes.

    • Olivier Harismendy
    • , Dimple Notani
    •  & Kelly A. Frazer

  • News & Views |

    With the spread of fast-food outlets and more sedentary lifestyles, the prevalence of diabetes in India is rising alarmingly. But the subpopulations at risk and the symptoms of the disease differ from those in the West.

    • Jared Diamond

  • News & Views |

    Impaired insulin action, combined with its insufficient secretion, can cause diabetes. In a surprising extension of this notion, decreased insulin action in the kidney's podocyte cells may contribute to renal complications in diabetes.

    • Christian Rask-Madsen
    •  & George L. King

  • Letter |

    Here it is shown that the consumption of a high-fat diet by male rats has an intergenerational effect: it leads to the dysfunction of pancreatic β-cells in female offspring. Relative to controls, these offspring showed an early onset of impaired insulin secretion and glucose tolerance, which worsened with time. The results add to our understanding of the complex genetic and environmental factors that are leading to the global epidemic of obesity and type 2 diabetes.

    • Sheau-Fang Ng
    • , Ruby C. Y. Lin
    •  & Margaret J. Morris

  • Editorial |

    The controversy surrounding diabetes drugs highlights the importance of comparative studies.

  • News & Views |

    Antidiabetic drugs that activate the protein PPARγ had a bright start but soon lost their appeal because of undesirable side effects. Subtle modifications may once again make them suitable for treating diabetes.

    • Riekelt H. Houtkooper
    •  & Johan Auwerx

  • Letter |

    Circadian rhythms control many physiological functions. During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis — a rhythmic process that is disturbed in people with diabetes. These authors show that pancreatic islets contain their own clock: they have self-sustained circadian oscillations of CLOCK and BMAL1 genes and proteins, which are vital for the regulation of circadian rhythms. Without this clock, a cascade of cellular failure and pathology initiates the onset of diabetes mellitus.

    • Biliana Marcheva
    • , Kathryn Moynihan Ramsey
    •  & Joseph Bass

  • News & Views |

    Most insulin-secreting pancreatic β-cells are irreplaceably lost in type 1 diabetes. In a mouse model, pancreatic α-cells seem to sacrifice their identity to replenish the low stock of β-cells1. Two experts discuss what this means for understanding the basic cell biology involved and its relevance to treating diabetes.boxed-text

    • Kenneth S. Zaret
    •  & Morris F. White

  • Article |

    Pancreatic β-cells release insulin, which controls energy homeostasis in vertebrates, and its lack causes diabetes mellitus. The transcription factor neurogenin 3 (Neurog3) initiates differentiation of β-cells and other islet cell types from pancreatic endoderm; here, the transcription factor Rfx6 is shown to direct islet cell differentiation downstream of Neurog3 in mice and humans. This may be useful in efforts to generate β-cells for patients with diabetes.

    • Stuart B. Smith
    • , Hui-Qi Qu
    •  & Michael S. German

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