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Volume 13 Issue 2, February 2017

This image illustrates the human pancreatic microenvironment in type 2 diabetes mellitus. The pancreatic lobule, which was labelled for CD31 (vasculature) and glucagon (islet), was imaged by deep-tissue confocal microscopy with optical clearing (refractive index: 1.52) to illustrate the fatty infiltration (transmitted light signals) around the endocrine and exocrine pancreas. Image supplied by Shiue-Cheng Tang and Shih-Jung Peng at Department of Medical Science, National Tsing Hua University, Taiwan, and Luc Baeyens and Michael German at Diabetes Center, UCSF, USA.

Research Highlight

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In Brief

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Year in Review

  • Neuroendocrine networks were previously perceived mainly as transcriptionally controlled, neural regulatory pathways that are centred at the hypothalamus. However, multisystemic circuits encompassing the brain and peripheral tissues have now been uncovered that involve nonneuronal cells and nontranscriptional regulatory mechanisms, with previously unidentified functions, such as reward and behaviour. Several developments in 2016 have helped to consolidate these new advances.

    • Manuel Tena-Sempere
    Year in Review
  • Adipose tissues have a central role in energy homeostasis, as they secrete adipokines and regulate energy storage and dissipation. Novel adipokines from white, brown and beige adipocytes have been identified in 2016. Identifying the specific receptors for each adipokine is pivotal for developing greater insights into the fat-derived signalling pathways that regulate energy homeostasis.

    • Shingo Kajimura
    Year in Review
  • Type 2 diabetes mellitus (T2DM) is a major global health challenge. Development of more effective strategies for prevention and therapy depends on an improved understanding of its pathogenetic mechanisms. 2016 ends a period during which large-scale discovery of risk alleles for T2DM became routine and heralds a shift in research focus towards their exploitation to fuel mechanistic insights.

    • Mark I. McCarthy
    Year in Review
  • Although regular physical activity can prevent or reduce the risk of many age-related diseases, the molecular mechanisms underpinning the protective effects of exercise are largely unknown. In 2016, a series of studies demonstrated that crosstalk between tissues during exercise can protect against metabolic disease, cancer, retinal degeneration and memory loss. These studies provide a molecular basis for the concept of 'exercise as medicine'.

    • Mark A. Febbraio
    Year in Review
  • In 2016, four studies were published that provided crucial new information on the endocrine actions of the hormone fibroblast growth factor 21 (FGF21). These studies provide a framework for the nutritional stimuli that regulate FGF21 expression and demonstrate a major role for FGF21 in primates and humans in regulating food intake, macronutrient preference and central reward pathways.

    • Matthew J. Potthoff
    Year in Review
  • Obesity and ageing are major worldwide health challenges associated with lifestyle changes and an increase in age-related diseases, characterized by chronic inflammation dubbed metaflammation and inflammaging. However, the mechanistic link between these inflammatory processes is still unknown. New findings in 2016 shed light on these issues and indicate common targets for intervention.

    • Claudio Franceschi
    Year in Review
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Review Article

  • Dyslipidaemia is a major contributor to the onset of metabolic disease. Here, Meikle and Summers discuss lipidomic research into relationships between diet, lipid metabolism and metabolic disease. The Review also highlights promising potential therapeutics that target lipid metabolism to counteract obesity, insulin resistance and type 2 diabetes mellitus.

    • Peter J. Meikle
    • Scott A. Summers
    Review Article
  • Here, Chow and colleagues discuss the endocrine manifestations of mitochondrial diseases, a group of multisystem disorders characterized by great clinical, biochemical and genetic heterogeneity. The authors describe the clinical features, genetic causes and pathological mechanisms underlying these diseases, the understanding of which will be key to developing innovative therapies for these patients.

    • Jasmine Chow
    • Joyeeta Rahman
    • Shamima Rahman
    Review Article
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Consensus Statement

  • Silver–Russell syndrome (SRS) is an imprinting disorder that causes prenatal and postnatal growth retardation. This Consensus Statement summarizes recommendations for clinical diagnosis, investigation and management of patients with SRS, including the use of growth hormone and gonadotropin-releasing hormone analogues.

    • Emma L. Wakeling
    • Frédéric Brioude
    • Irène Netchine
    Consensus Statement Open Access
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