Yin 2014 J Clin Endocrinol Metab: Difference between revisions
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{{Publication | {{Publication | ||
|title=Yin X, Lanza IR, Swain JM, Sarr MG, Nair KS, Jensen MD (2014) Adipocyte mitochondrial function is reduced in human obesity independent of fat cell size. J Clin Endocrinol Metab 99:E209-16. | |title=Yin X, Lanza IR, Swain JM, Sarr MG, Nair KS, Jensen MD (2014) Adipocyte mitochondrial function is reduced in human obesity independent of fat cell size. J Clin Endocrinol Metab 99:E209-16. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/24276464 PMID: 24276464] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/24276464 PMID: 24276464 Open Access] | ||
|authors=Yin X, Lanza IR, Swain JM, Sarr MG, Nair KS, Jensen MD | |authors=Yin X, Lanza IR, Swain JM, Sarr MG, Nair KS, Jensen MD | ||
|year=2014 | |year=2014 | ||
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}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration, Exercise physiology;nutrition;life style | ||
|organism=Human | |organism=Human | ||
|tissues=Fat | |tissues=Fat | ||
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|diseases=Obesity | |diseases=Obesity | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
| | |pathways=NS | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Latest revision as of 12:25, 8 November 2016
Yin X, Lanza IR, Swain JM, Sarr MG, Nair KS, Jensen MD (2014) Adipocyte mitochondrial function is reduced in human obesity independent of fat cell size. J Clin Endocrinol Metab 99:E209-16. |
Yin X, Lanza IR, Swain JM, Sarr MG, Nair KS, Jensen MD (2014) 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.
โข O2k-Network Lab: US MN Rochester Nair KS
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Pathology: Obesity
Stress:Mitochondrial disease
Organism: Human
Tissue;cell: Fat
Preparation: Isolated mitochondria
Coupling state: OXPHOS
Pathway: NS
HRR: Oxygraph-2k