Yin 2014 J Clin Endocrinol Metab: Difference between revisions

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|organism=Human
|organism=Human
|tissues=Fat
|tissues=Fat
|preparations=Isolated Mitochondria
|preparations=Isolated mitochondria
|injuries=Mitochondrial Disease; Degenerative Disease and Defect
|injuries=Mitochondrial disease
|diseases=Obesity
|diseases=Obesity
|couplingstates=OXPHOS
|couplingstates=OXPHOS
|substratestates=CI+II
|substratestates=CI&II
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|additional=Labels
|additional=Labels
}}
}}

Revision as of 16:20, 10 February 2015

Publications in the MiPMap
[[Has title::Yin X, Lanza IR, Swain JM, Sarr MG, Nair KS, Jensen MD (2013) Adipocyte Mitochondrial Function is Reduced in Human Obesity Independent of Fat Cell Size. J Clin Endocrinol Metab [Epub ahead of print].]]

ยป [[Has info::PMID: 24276464]]

Yin X, Lanza IR, Swain JM, Sarr MG, Nair KS, Jensen MD (2013) J Clin Endocrinol Metab

Abstract: It has been suggested that mitochondrial dysfunctional in adipocytes contribute to obesity-related metabolic complications. However, obesity results in adipocyte hypertrophy, large and small adipocytes from the same depot have different characteristics, raising the possibility that obesity-related mitochondrial defects are an inherent function of large adipocytes.Objective:to examine whether obesity, independent of fat cell size and fat depot, is associated with mitochondria dysfunction.Design:cross-sectional comparison.Setting:Academic medical center.Patients or Other Participants:omental (OM) and/or abdominal subcutaneous (SQ) adipose samples were collected from 20, age-matched obese and non-obese non-diabetic men and women undergoing either elective abdominal surgery or research needle biopsy.Intervention:None.Main Outcome Measures:mitochondrial DNA abundance, oxygen consumption rates (OCR) and citrate synthase (CS) activity from populations of large and small adipocytes (separated with differential floatation).Results:For both omental and subcutaneous adipocytes, at the cell and organelle level, OCR and CS activity were significantly reduced in cells from obese compared with non-obese volunteers, even when matched for cell size by comparing large adipocytes from non-obese and small adipocytes from obese. Adipocyte mitochondrial content was not significantly different between obese and non-obese volunteers. Mitochondrial function and content parameters were not different between small and large cells, omental and subcutaneous adipocytes from the same person.Conclusion:Adipocyte mitochondrial oxidative capacity is reduced in obese compared to non-obese adults and this difference is not due to cell size differences. Adipocyte mitochondrial dysfunction in obesity is therefore related to overall adiposity rather than adipocyte hypertrophy.


โ€ข O2k-Network Lab: US MN Rochester Nair KS


Labels: MiParea: Respiration, Comparative MiP;environmental MiP, Exercise physiology;nutrition;life style  Pathology: Obesity  Stress:Mitochondrial disease  Organism: Human  Tissue;cell: Fat  Preparation: Isolated mitochondria 


Coupling state: OXPHOS 

HRR: Oxygraph-2k 

Labels 

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