Daniel Zeman-Meier retweetledi
Up front & free to read in our Jan issue #editorspicks: Targeting the NLRP3 inflammasome–IL-1β pathway in type 2 diabetes and obesity tinyurl.com/bdf9ec33
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Daniel Zeman-Meier
44 posts
Daniel Zeman-Meier
@zemanmeier
Family, Science, Nature. Studies how the immune system and metabolism regulate each other. PC1/3, insulin processing, HPA axis, islet amyloid and inflammation
Basel, Switzerland Katılım Ağustos 2022
88 Takip Edilen37 Takipçiler
Daniel Zeman-Meier retweetledi
Targeting the NLRP3 inflammasome–IL-1β pathway in #T2D + obesity. @zemanmeier et al review the role of IL-1β in physiology, pathology + clinical translation and the potential of IL-1β–NLRP3 inhibition to modify disease. @DepBiomedicine @UniBasel_en tinyurl.com/bdf9ec33 🔓
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Our newest addition: Review on the NLRP3/IL-1 pathway in health and disease and its clinical potential to treat #diabetes and its comorbidities. @DiabetologiaJnl @DepBiomedicine @UniBasel_en 🔓
link.springer.com/article/10.100…
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PC1/3 KO in Pomc-expressing tissues reproduced the phenotype of PC1/3 null mice, including an enlarged spleen size, reduced corticosterone and LPS hypersensitivity. We propose that lack of PC1/3 leads to hyperinflammation via reduced anti-inflammatory action of steroids.
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New: We investigated why lack of prohormone convertase 1/3 (PC1/3) in mice leads to sepsis hypersensitivity. We find that there is no role for PC1/3 in immune cells and that lack of PC1/3 in the HPA axis ➡️ less steroids is responsible for this phenotype. academic.oup.com/jes/article-ab…
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Based on the literature, we hypothesized that PC1/3 processes an anti-inflammatory peptide in immune cells. However, myeloid/hematopoietic PC1/3 KO did not do anything. We also doubt the literature showing that PC1/3 is expressed in the immune compartment.
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New: The cytokine IL-1beta promotes adiopogenesis in early-differentiation cells but not at later stages when IL-1b induces only inflammation. There is no metabolic role for IL-1beta in adult adipocytes 👉rdcu.be/dTF1J @UniBasel_en @DepBiomedicine @karolinskainst
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@DanielJDrucker @uoftmedicine @SinaiHealth @UofT_LMP Interestingly, we don't get a clear immune picture when we knock out gut hormones. Also not when LPS-provoked. This anti-inflammatoty action might be a feature of GLPra but probably not endogenous peptides.
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New from Susanna Fang and CK Wong @uoftmedicine Anti-Inflammatory Effects of Glucagon-Like Peptide-1 Receptor Agonists via the Neuroimmune Axis liebertpub.com/doi/10.1089/dn… @SinaiHealth @uoft_lmp
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Daniel Zeman-Meier retweetledi
March forth to our next seminar by @YCC_YiChunChen, postdoc in @BruceVerchere Lab and faculty candidate.✨ This Thursday at 12pm PT/2pm CT/3pm ET.
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@BaumannZora Luckily you will enlighten us soon about the missing topic 😉
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@CaATiER_Chop_ER @MouseCentral @VanderbiltU @JimJohnsonSci @KevinH_PhD @JohnSpeakman4 Probably more my interpretation and less the author's hypothesis, but the data suggest that insulin sensitivity is adapted to deal with temperature via change EE/insulin action. It's associative thus manipulating only one factor (sensitivity) might help to get more causation.
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@zemanmeier @MouseCentral @VanderbiltU @JimJohnsonSci @KevinH_PhD @JohnSpeakman4 And I wasn't too sure of your question of how to apply their hypothesis to your presumed conditions. Please elaborate.
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This is an excellent example of how indoor environmental changes can affect insulin and insulin sensitivity.
Very neat and meticulous study from @MouseCentral & colleagues @VanderbiltU.
A must read!!
@JimJohnsonSci @KevinH_PhD @JohnSpeakman4
Sable Systems International 🐭🐀🧝🏼♀️@SableSys
Gorgeous new Promethion-powered research from @MouseCentral & colleagues @VanderbiltU - on insulin-mediated glucose homeostasis during changes in EE caused by ↕️ ambient temperatures. "Insulin action adjusts to non-stressful changes in ambient temperature to contribute to the support of body temperature homeostasis without compromising glucose homeostasis." biorxiv.org/content/10.110…
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@JimJohnsonSci @BruceVerchere @YCC_YiChunChen Rip-cre (Herrera) and Pdx-creERT. Give the same result (supernatant of isolated islets). My constitutive whole-body PC1/3 KO was not viable and I did not analyze the wb inducible (UBC-ERT).
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Beautiful and important paper from @BruceVerchere and @YCC_YiChunChen . Top-Down Proteomics of Mouse Islets With Beta Cell CPE Deletion Reveals Molecular Details in Prohormone Processing | Endocrinology academic.oup.com/endo/article/1…
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Interested in #exocrine-#endocrine crosstalk? Our newest publication details a protocol on how to isolate and analyse (#immune) cells from both parts of the (mouse) #pancreas in parallel. Part of a bigger project driven by MD-PhD student @Laurasteiger14. star-protocols.cell.com/protocols/3068
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PS: Slc7a11 null and flox 🐭available from us right now...be quick if you are interested - colonies will be terminated in a few days.
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It was a difficult endeavor due to ex vivo/in vitro artefacts and lots of trial and error experiments. Now Axel is off to Boston for new adventures...
doi.org/10.1371/journa… 2/2
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Second (and last) publication by Axel deBaat about Cystine/Glutamate antiporter System Xc, this time with a focus on immune cells. We show that SXc is essential for maintaining glutathione levels, mitochondrial functionality and cytokine production. 👇1/2
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Great collaboration lead by Angela Bosch (Cavelti lab) and others @UniBasel_en @DepBiomedicine
link.springer.com/article/10.100…
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We find that CSF1r inhibition depletes macrophages of various "metabolic" tissues (including my favorite panc islets). In terms of metabolism, depletion lead to increased (liver) insulin sensitivity but to impaired insulin secretion. More to come about the mechanisms soon 👇
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Metabolic consequences of pharmacological depletion of tissue macrophages: A story that started many years with some curious PhD students in our lab. It didn't make sense why CSF1r inhibition should only target microglia (given that many other cells express this receptor). 👇
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