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Difference between revisions of "Gancheva 2019 Nat Commun"

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|abstract=The mechanisms underlying improved insulin sensitivity after surgically-induced weight loss are still unclear. We monitored skeletal muscle metabolism in obese individuals before and over 52 weeks after metabolic surgery. Initial weight loss occurs in parallel with a decrease in muscle oxidative capacity and respiratory control ratio. Persistent elevation of intramyocellular lipid intermediates, likely resulting from unrestrained adipose tissue lipolysis, accompanies the lack of rapid changes in insulin sensitivity. Simultaneously, alterations in skeletal muscle expression of genes involved in calcium/lipid metabolism and mitochondrial function associate with subsequent distinct DNA methylation patterns at 52 weeks after surgery. Thus, initial unfavorable metabolic changes including insulin resistance of adipose tissue and skeletal muscle precede epigenetic modifications of genes involved in muscle energy metabolism and the long-term improvement of insulin sensitivity.
|abstract=The mechanisms underlying improved insulin sensitivity after surgically-induced weight loss are still unclear. We monitored skeletal muscle metabolism in obese individuals before and over 52 weeks after metabolic surgery. Initial weight loss occurs in parallel with a decrease in muscle oxidative capacity and respiratory control ratio. Persistent elevation of intramyocellular lipid intermediates, likely resulting from unrestrained adipose tissue lipolysis, accompanies the lack of rapid changes in insulin sensitivity. Simultaneously, alterations in skeletal muscle expression of genes involved in calcium/lipid metabolism and mitochondrial function associate with subsequent distinct DNA methylation patterns at 52 weeks after surgery. Thus, initial unfavorable metabolic changes including insulin resistance of adipose tissue and skeletal muscle precede epigenetic modifications of genes involved in muscle energy metabolism and the long-term improvement of insulin sensitivity.
|editor=[[Plangger M]],
|editor=[[Plangger M]],
|mipnetlab=DE Duesseldorf Roden M, US PA Pittsburgh DeLany JP, DE Cologne Pesta D
}}
}}
{{Labeling
{{Labeling
|area=Respiration
|area=Respiration, nDNA;cell genetics, mt-Medicine, Patients
|diseases=Obesity
|organism=Human
|tissues=Skeletal muscle
|preparations=Permeabilized tissue
|couplingstates=LEAK, OXPHOS, ET
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|additional=Labels, 2019-10,
|additional=Labels, 2019-10,
}}
}}

Latest revision as of 14:50, 7 June 2022

Publications in the MiPMap
Gancheva S, Ouni M, Jelenik T, Koliaki C, Szendroedi J, Toledo FGS, Markgraf DF, Pesta DH, Mastrototaro L, De Filippo E, Herder C, Jähnert M, Weiss J, Strassburger K, Schlensak M, Schürmann A, Roden M (2019) Dynamic changes of muscle insulin sensitivity after metabolic surgery. Nat Commun 10:4179.

» PMID: 31519890 Open Access

Gancheva S, Ouni M, Jelenik T, Koliaki C, Szendroedi J, Toledo FGS, Markgraf DF, Pesta DH, Mastrototaro L, De Filippo E, Herder C, Jaehnert M, Weiss J, Strassburger K, Schlensak M, Schuermann A, Roden M (2019) Nat Commun

Abstract: The mechanisms underlying improved insulin sensitivity after surgically-induced weight loss are still unclear. We monitored skeletal muscle metabolism in obese individuals before and over 52 weeks after metabolic surgery. Initial weight loss occurs in parallel with a decrease in muscle oxidative capacity and respiratory control ratio. Persistent elevation of intramyocellular lipid intermediates, likely resulting from unrestrained adipose tissue lipolysis, accompanies the lack of rapid changes in insulin sensitivity. Simultaneously, alterations in skeletal muscle expression of genes involved in calcium/lipid metabolism and mitochondrial function associate with subsequent distinct DNA methylation patterns at 52 weeks after surgery. Thus, initial unfavorable metabolic changes including insulin resistance of adipose tissue and skeletal muscle precede epigenetic modifications of genes involved in muscle energy metabolism and the long-term improvement of insulin sensitivity.

Bioblast editor: Plangger M O2k-Network Lab: DE Duesseldorf Roden M, US PA Pittsburgh DeLany JP, DE Cologne Pesta D


Labels: MiParea: Respiration, nDNA;cell genetics, mt-Medicine, Patients  Pathology: Obesity 

Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 


Coupling state: LEAK, OXPHOS, ET 

HRR: Oxygraph-2k 

Labels, 2019-10