BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Memento EPFL//
BEGIN:VEVENT
SUMMARY:Resistin: the Pièce de Résistance of the Metabolic Syndrome?”
DTSTART:20131125T121500
DTSTAMP:20260916T043946Z
UID:ee7dbe563b09ac51fd58967bdce2e294c2ef85a97b30d321990164d9
CATEGORIES:Conferences - Seminars
DESCRIPTION:Joseph Rutkowski\, PhD\, University of Texas Southwestern Medi
 cal Center\, Dallas\, TX (USA)\nBio: With training and degrees in Chemical
  and Biomedical Engineering\, Dr. Rutkowski brings to the Touchstone Diabe
 tes Center at UTSW a strong background in interdisciplinary physiology res
 earch and a desire to incorporate new approaches towards the understanding
  of adipose tissue biology. His past work in the physiology of lymphatic c
 irculation ranged from fluid transport and the pathology of lymphedema to 
 inflammation and mechanisms of immune cell trafficking. His current work s
 eeks to integrate both the biochemical and biophysical roles of the inters
 titial microenvironment and microvascular biology in modulating tissue met
 abolism and inflammation: local factors that regulate systemic well-being.
 \nResistin was originally identified as an adipocyte-derived factor upregu
 lated during obesity and a contributor to obesity-associated insulin resis
 tance. Clinically\, resistin has been implicated in cardiovascular disease
  in a number of different patient populations. To address these phenomena\
 , we generated an adipocyte-specific resistin production model with modera
 te overexpression to probe the impact of resistin signaling on atheroscler
 otic and metabolic read outs. We found increased atherosclerosis when we o
 verexpress resistin in LDL-Receptor (LDL-R)-/- mice. This is in part relat
 ed to elevated serum triglyceride levels and a reduced ability to clear tr
 iglycerides upon a challenge. Further phenotypes\, independent of the LDL-
 R-/- background\, confirmed increased adiposity associated with a more pro
 nounced insulin resistance. A hallmark of the model is a disproportionate 
 increase in circulating leptin levels. These mice thus recapitulate both t
 he proposed negative cardiovascular correlation and that of insulin resist
 ance. A unifying mechanism for this complex phenotype is a resistin-mediat
 ed central leptin resistance that we demonstrate directly both in vivo as 
 well as in organotypic brain slices. In line with reduced sympathetic nerv
 e system (SNS) outflow\, we find decreased brown adipose tissue activity. 
 Resistin overexpression leads to a complex metabolic phenotype driven by r
 esistin-mediated central leptin resistance\, leading to reduced brown adip
 ose tissue activity. The resistin-mediated hypothalamic leptin resistance 
 is therefore a likely underlying mechanism for resistin action in both ath
 erosclerosis and insulin resistance
LOCATION:SV1717A http://map.epfl.ch/?room=sv1717a
STATUS:CONFIRMED
END:VEVENT
END:VCALENDAR