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Li Zhao, Chunfang Zhu, Meng Lu, Chi Chen, Xiaomin Nie, Buatikamu Abudukerimu, Kun Zhang, Zhiyuan Ning, Yi Chen, Jing Cheng, Fangzhen Xia, Ningjian Wang, Michael D Jensen, and Yingli Lu

disorders than is subcutaneous fat, the body fat distributions between visceral and subcutaneous fat, especially lower-body fat, play an important role in the occurrence of metabolic diseases. The Goto-Kakizaki (GK) rat line is established by repeated

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Xiaoqin Shi, Xinyu Li, Yi Hou, Xuemei Cao, Yuyao Zhang, Heng Wang, Hongyin Wang, Chuan Peng, Jibin Li, Qifu Li, Chaodong Wu, and Xiaoqiu Xiao

Introduction In the past decades, the global prevalence of obesity and other metabolic diseases (MS) has dramatically increased in both children and adults ( Friend et al . 2013 , Jaacks et al . 2016 ). The disproportionately early-onset of

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Joan Villarroya, Rubén Cereijo, Aleix Gavaldà-Navarro, Marion Peyrou, Marta Giralt, and Francesc Villarroya

intervention strategies for complex metabolic diseases such as obesity, diabetes, and cardiovascular diseases. Supplementary data This is linked to the online version of the paper at . Declaration of interest

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Esther Nuñez-Durán, Belén Chanclón, Silva Sütt, Joana Real, Hanns-Ulrich Marschall, Ingrid Wernstedt Asterholm, Emmelie Cansby, and Margit Mahlapuu

Introduction Type 2 diabetes, characterised by hyperglycaemia in the context of insulin resistance, is one of the most common metabolic diseases in the world. Insulin production from pancreatic β-cells plays a vital role in maintaining the

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Chia-Lei Lin, Lyda Williams, Yoshinori Seki, Harpreet Kaur, Kirsten Hartil, Ariana Fiallo, A Scott Glenn, Ellen B Katz, Maureen J Charron, and Patricia M Vuguin

of MetS in G4+/− and WT offspring ( Hartil et al . 2009 , Vuguin et al . 2013 ). Although both animal models developed features of metabolic disease, genotype-dependent differences were observed. Specifically, WT fetuses exposed to a HFD in utero

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Bushra Taqui, Farzad Asadi, Evangelina Capobianco, Daniel Barry Hardy, Alicia Jawerbaum, and Edith Juliana Arany

transcriptional activity are impaired in the placenta and different fetal organs, with further influence on the postnatal stage (i.e. the fetal origins of metabolic diseases) ( Rees et al. 2008 , Jawerbaum & Capobianco 2011 , Jawerbaum & White 2017 ). PPARs

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Abigail Wolf Greenstein, Neena Majumdar, Peng Yang, Papasani V Subbaiah, Rhonda D Kineman, and Jose Cordoba-Chacon

: implications for metabolic disease . Physiological Reviews 90 367 – 417 . ( doi:10.1152/physrev.00003.2009 ) Guo J Jou W Gavrilova O Hall KD 2009 Persistent diet-induced obesity in male C57BL/6 mice resulting from temporary obesigenic

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Anthony M Belenchia, Sarah A Johnson, Mark R Ellersieck, Cheryl S Rosenfeld, and Catherine A Peterson

The fetal period represents an important window of susceptibility for later obesity and metabolic disease. Maternal vitamin D deficiency (VDD) during pregnancy is a global concern that may have long-lasting consequences on offspring metabolic health. We sought to determine whether a VDD in utero environment affects fetal adipose tissue development and offspring metabolic disease predisposition in adulthood. Furthermore, we sought to explore the extent to which the VDD intrauterine environment interacts with genetic background or postnatal environment to influence metabolic health. Eight-week-old P0 female C57BL/6J mice were fed either a VDD diet or sufficient diet (VDS) from four weeks before pregnancy (periconception) then bred to male A vy /a mice. Females were maintained on the diets throughout gestation. At weaning, A vy /a and a/a male F1 offspring were randomized to low-fat (LFD) or high-fat diet (HFD) until 19 weeks of age, at which point serum and adipose tissue were harvested for analyses. Mice born to VDD dams weighed less at weaning than offspring born to VDS dams but experienced rapid weight gain in the four weeks post weaning, and acquired a greater ratio of perigonadal (PGAT) to subcutaneous (SQAT) than control offspring. Additionally, these mice were more susceptible to HFD-induced adipocyte hypertrophy. Offspring of VDD dams also had greater expression of Pparg transcript. These novel findings demonstrate that in utero VDD, an easily correctable but highly prevalent health concern, predisposes offspring to long-term adipose tissue consequences and possible adverse metabolic health complications.

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R. E. Oakey

Human steroid sulphatase is a widely distributed enzyme, located in the microsome, which catalyses the hydrolysis of sulphate esters of 3β-hydroxy-Δ5-steroids. It may be identical to aryl sulphatase C (Burns, 1983) which hydrolyses phenolic oestrogen sulphates, but is different from the lysosomal aryl sulphatases A and B which hydrolyse cerebrosides and oligosaccharides respectively.

Deficiency of steroid sulphatase is a metabolic disease with a recessive X-linked mode of inheritance. The disease was discovered in a pregnancy with an affected fetus and placenta (France & Liggins, 1969) and was subsequently found to be associated with an inherited variant of a scaly condition of the skin, recessive X-linked ichthyosis (RXLI). This observation (Jobsis, van Duuren, de Vries et al. 1976; Shapiro, Weiss, Webster & France, 1978) affirmed the recessive X-linked mode of inheritance of steroid sulphatase deficiency and provided an estimate of the incidence – 1 in 6000 total births (Wells

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Yu Wu, Tingting Wu, Jun Wu, Lei Zhao, Qing Li, Zac Varghese, John F Moorhead, Stephen H Powis, Yaxi Chen, and Xiong Z Ruan

Inflammatory stress is closely related to metabolic disease and insulin resistance. The precise cellular mechanism linking obesity and diabetes is largely unknown, but about 14–20% of obese individuals develop diabetes. In this study, we investigated whether chronic inflammation exacerbated glucose metabolism disorder by impairing β cell function in high-fat diet (HFD)-fed C57BL/6J mice. We used s.c. casein injection to induce chronic inflammation in HFD-fed C57BL/6J mice; 14 weeks on a HFD resulted in weight gain, hyperlipidemia, and low insulin sensitivity in these mice which nevertheless had normal blood glucose and serum inflammatory cytokines levels. Casein injection in the background of HFD elevated serum tumor necrosis factor α (TNFα) and serum amyloid A levels and increased TNFα and MCP1 expression in the adipose tissue, liver, and muscle of HFD-fed mice. Chronic inflammation induced by casein injection further decreased insulin sensitivity and insulin signaling, resulting in insulin deficiency and hyperglycemia in these mice. Islet mass and insulin content were markedly increased in HFD mice. However, in contrast with HFD-fed alone, chronic inflammation in HFD-fed mice decreased both islet mass and insulin content, reduced the genetic expression of insulin synthesis and secretion, and increased β cell apoptosis. We conclude that chronic inflammation exacerbated glucose metabolism disorders by impairing β cell function in HFD-fed C57BL/6J mice, suggesting that this mechanism may operate in obese individuals with chronic inflammation, making them prone to hyperglycemia.