Metabolic diseases articles within Nature

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  • Article |

    Experiments using conserved tumour models show that the G-protein-coupled receptor TkR99D in Drosophila Malphigian tubular stellate cells and NK3R in mouse renal tubules link malignant tumours to defective excretory functions.

    • Wenhao Xu
    • , Gerui Li
    •  & Wei Song

  • Article |

    Integration of multiomics data with functional analysis of pancreatic tissues from individuals with early-stage type 2 diabetes indicates that the genetic risk converges on RFX6, which regulates chromatin architecture at multiple risk loci.

    • John T. Walker
    • , Diane C. Saunders
    •  & Marcela Brissova

  • Article |

    A study shows that clonal haematopoiesis of indeterminate potential is associated with an increased risk of chronic liver disease specifically through the promotion of liver inflammation and injury.

    • Waihay J. Wong
    • , Connor Emdin
    •  & Pradeep Natarajan

  • Article
    | Open Access

    Serine deficiency can increase small fibre neuropathy in wild-type mice and serine replacement in diabetic mice alleviates diabetic neuropathy, directly linking amino acid metabolism to peripheral nerve disorders.

    • Michal K. Handzlik
    • , Jivani M. Gengatharan
    •  & Christian M. Metallo

  • Article
    | Open Access

    Metabolomics analysis of the mouse embryo shows a metabolic shift towards the tricarboxylic acid cycle between gestational days 10.5 and 11.5, leading to the subsequent development of organ-specific metabolic programmes.

    • Ashley Solmonson
    • , Brandon Faubert
    •  & Ralph J. DeBerardinis

  • Article |

    A single-cell atlas of white adipose tissue from mouse and human reveals diverse cell types and similarities and differences across species and dietary conditions.

    • Margo P. Emont
    • , Christopher Jacobs
    •  & Evan D. Rosen

  • Article |

    Whole-genome sequencing analysis of somatic mutations in liver samples from patients with chronic liver disease identifies driver mutations in metabolism-related genes such as FOXO1, and shows that these variants frequently exhibit convergent evolution.

    • Stanley W. K. Ng
    • , Foad J. Rouhani
    •  & Peter J. Campbell

  • Article |

    A role and mechanism of action are identified for INSP3R1 in the stimulation of hepatic gluconeogenesis and mitochondrial oxidation by glucagon, suggesting that INSP3R1 may be a target for ameliorating dysregulation of hepatic glucose metabolism.

    • Rachel J. Perry
    • , Dongyan Zhang
    •  & Gerald I. Shulman

  • Article |

    The chimeric cytokine IC7Fc combines the beneficial effects of the cytokines IL-6 and CNTF on weight loss and metabolism in mice, with no obvious side effects in mice and non-human primates.

    • Maria Findeisen
    • , Tamara L. Allen
    •  & Mark A. Febbraio

  • Letter |

    The Forkhead transcription factors FOXK1 and FOXK2, which are induced by starvation, reprogram cellular metabolism to induce aerobic glycolysis.

    • Valentina Sukonina
    • , Haixia Ma
    •  & Sven Enerbäck

  • Article |

    Genetic or pharmacological inhibition of α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase increases NAD+ and improves mitochondrial function in nematodes and mice, and may have therapeutic potential in kidney and liver disease.

    • Elena Katsyuba
    • , Adrienne Mottis
    •  & Johan Auwerx

  • Letter |

    The activation of lipid X receptors (LXRs) in mouse liver not only promotes cholesterol efflux but also inhibits cholesterol synthesis simultaneously; this is mediated by the lipid-responsive long non-coding RNA LeXis, which is induced by a Western diet and orchestrates crosstalk between LXRs and the cholesterol biosynthetic pathway.

    • Tamer Sallam
    • , Marius C. Jones
    •  & Peter Tontonoz

  • Letter |

    Fat-resident regulatory T cells (fTreg cells) accumulate in adipose tissue of mice as a function of age, but not obesity; mice without fTreg cells are protected against age-associated insulin resistance, but remain susceptible to obesity-associated insulin resistance and metabolic disease, indicating different aetiologies of age-associated versus obesity-associated insulin resistance.

    • Sagar P. Bapat
    • , Jae Myoung Suh
    •  & Ye Zheng

  • Letter |

    Blocking ERK/MAP kinases improves insulin sensitivity thorough a mechanism similar to the actions of the anti-diabetic thiazolidinediones drugs on PPARγ.

    • Alexander S. Banks
    • , Fiona E. McAllister
    •  & Bruce M. Spiegelman

  • Article |

    The structure of human GLUT1 in an inward-open conformation is reported; access to the structure of the human protein, instead of just a bacterial homologue, made it possible to map (inactivating) mutations associated with GLUT1 deficiency syndrome onto the structure.

    • Dong Deng
    • , Chao Xu
    •  & Nieng Yan

  • Article |

    Bariatric surgical procedures, such as vertical sleeve gastrectomy (VSG), are the most effective therapy for the treatment of obesity; now bile acids, and the presence of the nuclear bile acid receptor FXR, are shown to underpin the mechanism of VSG action, and the ability of VSG to reduce body weight and improve glucose tolerance is substantially reduced if FXR is absent.

    • Karen K. Ryan
    • , Valentina Tremaroli
    •  & Randy J. Seeley

  • News & Views |

    Mice receiving low doses of certain antibiotics gain weight and accumulate fat. This could be because some gut bacteria survive the treatment better than others, shifting digestion towards greater energy provision. See Article p.621

    • Harry J. Flint

  • News & Views |

    Fat cells are usually thought of as being either energy-storing white fat cells or food-burning brown fat cells. The identification of a third type of fat cell in mice and humans might open up new avenues for combating obesity.

    • Barbara Cannon
    •  & Jan Nedergaard

  • Article |

    Synthetic REV-ERB agonists can alter the circadian expression of core clock genes in the hypothalami of mice, which changes the expression of metabolic genes in liver, skeletal muscle and adipose tissue, and results in increased energy expenditure.

    • Laura A. Solt
    • , Yongjun Wang
    •  & Thomas P. Burris

  • Letter |

    Mice deficient in the lipid sensor GPR120 develop obesity, glucose intolerance and fatty liver when fed a high-fat diet, and a loss-of-function variant in the GPR120 gene strongly contributes to increased obesity in human.

    • Atsuhiko Ichimura
    • , Akira Hirasawa
    •  & Philippe Froguel

  • 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

  • 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

  • Letter |

    Heat shock protein 70 (Hsp70) is a molecular chaperone which, by inhibiting lysosomal membrane permeabilization, promotes the survival of stressed cells. Hsp70 is now shown to stabilize lysosomes by binding to an anionic phospholipid, BMP, resulting in stimulation of acid sphingomyelinase (ASM) activity. Notably, the decreased ASM activity and lysosomal stability seen in patients with Niemann–Pick disease can be corrected by treatment with recombinant Hsp70.

    • Thomas Kirkegaard
    • , Anke G. Roth
    •  & Marja Jäättelä

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