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Sökning: WFRF:(Hagberg CE)

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  • Abreu-Vieira, G, et al. (författare)
  • Adrenergically stimulated blood flow in brown adipose tissue is not dependent on thermogenesis
  • 2015
  • Ingår i: American journal of physiology. Endocrinology and metabolism. - : American Physiological Society. - 1522-1555 .- 0193-1849. ; 308:9, s. E822-E829
  • Tidskriftsartikel (refereegranskat)abstract
    • Brown adipose tissue (BAT) thermogenesis relies on blood flow to be supplied with nutrients and oxygen and for the distribution of the generated heat to the rest of the body. Therefore, it is fundamental to understand the mechanisms by which blood flow is regulated and its relation to thermogenesis. Here, we present high-resolution laser-Doppler imaging (HR-LDR) as a novel method for noninvasive in vivo measurement of BAT blood flow in mice. Using HR-LDR, we found that norepinephrine stimulation increases BAT blood flow in a dose-dependent manner and that this response is profoundly modulated by environmental temperature acclimation. Surprisingly, we found that mice lacking uncoupling protein 1 (UCP1) have fully preserved BAT blood flow response to norepinephrine despite failing to perform thermogenesis. BAT blood flow was not directly correlated to systemic glycemia, but glucose injections could transiently increase tissue perfusion. Inguinal white adipose tissue, also known as a brite/beige adipose tissue, was also sensitive to cold acclimation and similarly increased blood flow in response to norepinephrine. In conclusion, using a novel noninvasive method to detect BAT perfusion, we demonstrate that adrenergically stimulated BAT blood flow is qualitatively and quantitatively fully independent of thermogenesis, and therefore, it is not a reliable parameter for the estimation of BAT activation and heat generation.
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  • Andersson, ER, et al. (författare)
  • Gender Bias Impacts Top-Merited Candidates
  • 2021
  • Ingår i: Frontiers in research metrics and analytics. - : Frontiers Media SA. - 2504-0537. ; 6, s. 594424-
  • Tidskriftsartikel (refereegranskat)abstract
    • Expectations of fair competition underlie the assumption that academia is a meritocracy. However, bias may reinforce gender inequality in peer review processes, unfairly eliminating outstanding individuals. Here, we ask whether applicant gender biases peer review in a country top ranked for gender equality. We analyzed peer review assessments for recruitment grants at a Swedish medical university, Karolinska Institutet (KI), during four consecutive years (2014–2017) for Assistant Professor (n = 207) and Senior Researcher (n = 153). We derived a composite bibliometric score to quantify applicant productivity and compared this score with subjective external (non-KI) peer reviewer scores of applicants' merits to test their association for men and women, separately. To determine whether there was gender segregation in research fields, we analyzed publication list MeSH terms, for men and women, and analyzed their overlap. There was no gendered MeSH topic segregation, yet men and women with equal merits are scored unequally by reviewers. Men receive external reviewer scores resulting in stronger associations (steeper slopes) between computed productivity and subjective external reviewer scores, meaning that peer reviewers “reward” men's productivity with proportional merit scores. However, women applying for assistant professor or senior researcher receive only 32 or 92% of the score men receive, respectively, for each additional composite bibliometric score point. As productivity increases, the differences in merit scores between men and women increases. Accumulating gender bias is thus quantifiable and impacts the highest tier of competition, the pool from which successful candidates are ultimately chosen. Track record can be computed, and granting organizations could therefore implement a computed track record as quality control to assess whether bias affects reviewer assessments.
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  • Ioannidou, A, et al. (författare)
  • The multifaceted roles of the adipose tissue vasculature
  • 2022
  • Ingår i: Obesity reviews : an official journal of the International Association for the Study of Obesity. - : Wiley. - 1467-789X. ; 23:4, s. e13403-
  • Tidskriftsartikel (refereegranskat)
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  • Mehlem, A, et al. (författare)
  • PGC-1α Coordinates Mitochondrial Respiratory Capacity and Muscular Fatty Acid Uptake via Regulation of VEGF-B
  • 2016
  • Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 65:4, s. 861-873
  • Tidskriftsartikel (refereegranskat)abstract
    • Vascular endothelial growth factor (VEGF) B belongs to the VEGF family, but in contrast to VEGF-A, VEGF-B does not regulate blood vessel growth. Instead, VEGF-B controls endothelial fatty acid (FA) uptake and was identified as a target for the treatment of type 2 diabetes. The regulatory mechanisms controlling Vegfb expression have remained unidentified. We show that peroxisome proliferator–activated receptor γ coactivator 1α (PGC-1α) together with estrogen-related receptor α (ERR-α) regulates expression of Vegfb. Mice overexpressing PGC-1α under the muscle creatine kinase promoter (MPGC-1αTG mice) displayed increased Vegfb expression, and this was accompanied by increased muscular lipid accumulation. Ablation of Vegfb in MPGC-1αTG mice fed a high-fat diet (HFD) normalized glucose intolerance, insulin resistance, and dyslipidemia. We suggest that VEGF-B is the missing link between PGC-1α overexpression and the development of the diabetes-like phenotype in HFD-fed MPGC-1αTG mice. The findings identify Vegfb as a novel gene regulated by the PGC-1α/ERR-α signaling pathway. Furthermore, the study highlights the role of PGC-1α as a master metabolic sensor that by regulating the expression levels of Vegfa and Vegfb coordinates blood vessel growth and FA uptake with mitochondrial FA oxidation.
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  • Resultat 1-17 av 17

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