Fromme 2017 Abstract MITOEAGLE Barcelona

From Bioblast
Jump to: navigation, search
COST Action MITOEAGLE
Source depot and dietary status influence oxidative phosphorylation capacity in permeabilized, mature adipocytes. Fromme_Presentation

Link: MitoEAGLE

Schoettl T, Fromme T, Braun K, Kappler L, Pachl F, Kuester B, Klingenspor M (2017)

Event: MitoEAGLE Barcelona 2017

COST Action MITOEAGLE

Altered bioenergetic properties of white adipocyte mitochondria during obesity have repeatedly been hypothesized to cause perturbations of glucose homeostasis. In this respect, visceral adipose tissue depots are considered to pose a greater risk than subcutaneous fat. We assessed bioenergetic parameters of subcutaneous inguinal and visceral epididymal white adipocytes employing a comprehensive respirometry setup of intact and permeabilized adipocytes as well as isolated mitochondria. Samples were taken from normal weight mice as well as from four different murine obesity models, both genetic and diet-induced.

Inguinal adipocytes clearly featured a higher respiratory capacity attributable to increased mitochondrial respiratory chain content compared with epididymal adipocytes. The lower capacity of mitochondria from epididymal adipocytes was accompanied by an increased generation of reactive oxygen species per oxygen consumed.

Maximal respiration capacity and cell respiratory control ratios were diminished in white adipocytes of each of the four murine obesity models, both in the absence and the presence of impaired glucose tolerance. In a parallel proteomic analysis, feeding a high fat diet led to a massive, global loss in respiratory chain components, demonstrating that altered bioenergetic parameters are not only adaptively regulated on the activity level, but consequence of extensive mitochondrial remodeling. This phenomenon was more pronounced in visceral than subcutaneous adipocytes.

We conclude that reduced respiratory capacity due to mitochondrial remodeling in white adipocytes is a hallmark of murine obesity, stronger in visceral adipose tissue and causally independent from glucose tolerance status. Impaired respiratory capacity in white adipocytes solely is not sufficient for the development of systemic glucose intolerance.


O2k-Network Lab: DE Freising Klingenspor M, DE Tuebingen Weigert C


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style  Pathology: Obesity  Stress:Oxidative stress;RONS  Organism: Mouse  Tissue;cell: Fat  Preparation: Intact cells, Permeabilized cells, Isolated mitochondria 



HRR: Oxygraph-2k  Event: A3 


Affiliations

Schöttl T(1), Fromme T(1), Braun K(1), Kappler L(1), Pachl F(2), Küster B(2), Klingenspor M(1)
  1. Molecular Nutritional Medicine, Technical Univ Munich, Else Kröner Fresenius Center Nutritional Medicine, Freising
  2. Chair Proteomics and Bioanalytics, Technical Univ Munich, Freising, Germany. - fromme@tum.de