#METABOLOMICS WORKBENCH jwalejko_20210126_095433 DATATRACK_ID:2423 STUDY_ID:ST001665 ANALYSIS_ID:AN002717 PROJECT_ID:PR001070
VERSION             	1
CREATED_ON             	January 28, 2021, 11:13 am
#PROJECT
PR:PROJECT_TITLE                 	Branched-chain alpha-ketoacids are preferentially reaminated and activate
PR:PROJECT_TITLE                 	protein synthesis in the heart
PR:PROJECT_SUMMARY               	Branched-chain amino acids (BCAA) and their cognate α-ketoacids (BCKA) are
PR:PROJECT_SUMMARY               	elevated in an array of cardiometabolic diseases. Here we demonstrate that the
PR:PROJECT_SUMMARY               	major metabolic fate of uniformly-13C-labeled α-ketoisovalerate ([U-13C]KIV) in
PR:PROJECT_SUMMARY               	the heart is reamination to valine. Activation of cardiac branched-chain
PR:PROJECT_SUMMARY               	α-ketoacid dehydrogenase (BCKDH) by treatment with the BCKDH kinase inhibitor,
PR:PROJECT_SUMMARY               	BT2, does not impede the strong flux of [U-13C]KIV to valine. Sequestration of
PR:PROJECT_SUMMARY               	BCAA and BCKA away from mitochondrial oxidation is likely due to low levels of
PR:PROJECT_SUMMARY               	expression of the mitochondrial BCAA transporter SLC25A44 in the heart, as its
PR:PROJECT_SUMMARY               	overexpression significantly lowers accumulation of [13C]-labeled valine from
PR:PROJECT_SUMMARY               	[U-13C]KIV. Finally, exposure of perfused hearts to levels of BCKA found in
PR:PROJECT_SUMMARY               	obese rats increased increases phosphorylation of the translational repressor
PR:PROJECT_SUMMARY               	4E-BP1 as well as multiple proteins in the MEK-ERK pathway, leading to a
PR:PROJECT_SUMMARY               	doubling of total protein synthesis. These data suggest that elevated BCKA
PR:PROJECT_SUMMARY               	levels found in obesity may contribute to pathologic cardiac hypertrophy via
PR:PROJECT_SUMMARY               	chronic activation of protein synthesis.
PR:INSTITUTE                     	Duke University
PR:DEPARTMENT                    	Medicine
PR:LAST_NAME                     	Walejko
PR:FIRST_NAME                    	Jacquelyn
PR:ADDRESS                       	300 N Duke St Durham NC 27701
PR:EMAIL                         	jacquelyn.walejko@duke.edu
PR:PHONE                         	6086097615
#STUDY
ST:STUDY_TITLE                   	Branched-chain alpha-ketoacids are preferentially reaminated and activate
ST:STUDY_TITLE                   	protein synthesis in the rat heart
ST:STUDY_SUMMARY                 	Branched-chain amino acids (BCAA) and their cognate α-ketoacids (BCKA) are
ST:STUDY_SUMMARY                 	elevated in an array of cardiometabolic diseases. Here we demonstrate that the
ST:STUDY_SUMMARY                 	major metabolic fate of uniformly-13C-labeled α-ketoisovalerate ([U-13C]KIV) in
ST:STUDY_SUMMARY                 	the heart is reamination to valine. Activation of cardiac branched-chain
ST:STUDY_SUMMARY                 	α-ketoacid dehydrogenase (BCKDH) by treatment with the BCKDH kinase inhibitor,
ST:STUDY_SUMMARY                 	BT2, does not impede the strong flux of [U-13C]KIV to valine.
ST:INSTITUTE                     	Duke University
ST:LAST_NAME                     	Walejko
ST:FIRST_NAME                    	Jacquelyn
ST:ADDRESS                       	300 N Duke St
ST:EMAIL                         	jacquelyn.walejko@duke.edu
ST:PHONE                         	9194792304
#SUBJECT
SU:SUBJECT_TYPE                  	Mammal
SU:SUBJECT_SPECIES               	Rattus norvegicus
SU:TAXONOMY_ID                   	10116
SU:AGE_OR_AGE_RANGE              	10 weeks
SU:GENDER                        	Male
#SUBJECT_SAMPLE_FACTORS:         	SUBJECT(optional)[tab]SAMPLE[tab]FACTORS(NAME:VALUE pairs separated by |)[tab]Raw file names and additional sample data
SUBJECT_SAMPLE_FACTORS           	-	199	Treatment:Control	
SUBJECT_SAMPLE_FACTORS           	-	200	Treatment:Control	
SUBJECT_SAMPLE_FACTORS           	-	207	Treatment:Control	
SUBJECT_SAMPLE_FACTORS           	-	208	Treatment:Control	
SUBJECT_SAMPLE_FACTORS           	-	215	Treatment:Control	
SUBJECT_SAMPLE_FACTORS           	-	205	Treatment:BT-2	
SUBJECT_SAMPLE_FACTORS           	-	206	Treatment:BT-2	
SUBJECT_SAMPLE_FACTORS           	-	216	Treatment:BT-2	
SUBJECT_SAMPLE_FACTORS           	-	217	Treatment:BT-2	
SUBJECT_SAMPLE_FACTORS           	-	210	Treatment:LY	
SUBJECT_SAMPLE_FACTORS           	-	211	Treatment:LY	
SUBJECT_SAMPLE_FACTORS           	-	212	Treatment:LY	
SUBJECT_SAMPLE_FACTORS           	-	213	Treatment:LY	
SUBJECT_SAMPLE_FACTORS           	-	214	Treatment:LY	
SUBJECT_SAMPLE_FACTORS           	-	218	Treatment:LY	
#COLLECTION
CO:COLLECTION_SUMMARY            	Fed male Wistar rats were anesthetized with 5% isoflurane, and isolated hearts
CO:COLLECTION_SUMMARY            	were perfused in the Langendorff mode at 37°C with non-recirculating perfusate.
CO:COLLECTION_SUMMARY            	The hearts were allowed to beat spontaneously throughout the perfusion. At the
CO:COLLECTION_SUMMARY            	end of each perfusion, hearts were immediately freeze-clamped in liquid nitrogen
CO:COLLECTION_SUMMARY            	using the Wollenberger technique and stored at -80 oC for further analysis.
CO:SAMPLE_TYPE                   	Heart
#TREATMENT
TR:TREATMENT_SUMMARY             	All heart perfusions underwent an initial 15-minute equilibration period with
TR:TREATMENT_SUMMARY             	Krebs Ringer bicarbonate buffer containing 119 mM NaCl, 4.8 mM KCl, 2.6 mM
TR:TREATMENT_SUMMARY             	CaCl2, 1.2 mM KH2PO4, 1.2 mM MgSO4, 25 mM NaHCO3, 11 mM glucose, and 0.05 mM
TR:TREATMENT_SUMMARY             	L-carnitine at a flow rate of 12 ml/minute. After the equilibrium period, hearts
TR:TREATMENT_SUMMARY             	were perfused for 30 minutes with 3% BSA, 100 µU/mL insulin, 0.4 mM palmitate,
TR:TREATMENT_SUMMARY             	physiologic concentrations of amino acids, and either DMSO (Veh), BT2, or
TR:TREATMENT_SUMMARY             	LY3351337.
#SAMPLEPREP
SP:SAMPLEPREP_SUMMARY            	Frozen tissues were pulverized under liquid nitrogen using a mortar and pestle.
SP:SAMPLEPREP_SUMMARY            	Metabolites were then extracted using sequential 500 μL additions of -20°C
SP:SAMPLEPREP_SUMMARY            	MeOH, chilled water, and chloroform. After each addition, tissue lysates were
SP:SAMPLEPREP_SUMMARY            	prepared with a Tissue Lyser (Qiagen) for 60 seconds at 30Hz. Similarly, plasma
SP:SAMPLEPREP_SUMMARY            	metabolites (20 μL) were extracted by sequential 500 μL additions of -20°C
SP:SAMPLEPREP_SUMMARY            	MeOH, chilled water, and chloroform. After each addition, samples were vortexed
SP:SAMPLEPREP_SUMMARY            	for 30 seconds. Tissue and plasma extracts were then centrifuged at 4°C and
SP:SAMPLEPREP_SUMMARY            	14400 x g for 20 minutes and the clarified aqueous phase was transferred to a
SP:SAMPLEPREP_SUMMARY            	fresh Eppendorf and stored in -80°C until processing for GC-MS analysis. For
SP:SAMPLEPREP_SUMMARY            	GC-MS analysis, the extracted tissue was dried under N2 gas-flow at 37°C using
SP:SAMPLEPREP_SUMMARY            	an evaporator. Amino and organic acids were derivatized via methoximation and
SP:SAMPLEPREP_SUMMARY            	silylation. Briefly, metabolites were resuspended in 25 μL of methoxylamine
SP:SAMPLEPREP_SUMMARY            	hydrochloride (2% (w/v) in pyridine) and incubated at 40°C for 90 minutes on a
SP:SAMPLEPREP_SUMMARY            	heating block. After brief centrifugation, 35 μL of MTBSTFA + 1% TBDMS was
SP:SAMPLEPREP_SUMMARY            	added and the samples were incubated at 60°C for 30 minutes.
#CHROMATOGRAPHY
CH:CHROMATOGRAPHY_TYPE           	GC
CH:INSTRUMENT_NAME               	Agilent 7890B
CH:COLUMN_NAME                   	Agilent HP5-MS (30m x 0.25mm, 0.25 um)
#ANALYSIS
AN:ANALYSIS_TYPE                 	MS
#MS
MS:INSTRUMENT_NAME               	Agilent 5977A
MS:INSTRUMENT_TYPE               	Single quadrupole
MS:MS_TYPE                       	EI
MS:ION_MODE                      	UNSPECIFIED
MS:MS_COMMENTS                   	Masshunter used for data acquisition and processing.
#MS_METABOLITE_DATA
MS_METABOLITE_DATA:UNITS	Concentration of 13C (uM)
MS_METABOLITE_DATA_START
Samples	199	200	207	208	215	205	206	216	217	210	211	212	213	214	218
Factors	Treatment:Control	Treatment:Control	Treatment:Control	Treatment:Control	Treatment:Control	Treatment:BT-2	Treatment:BT-2	Treatment:BT-2	Treatment:BT-2	Treatment:LY	Treatment:LY	Treatment:LY	Treatment:LY	Treatment:LY	Treatment:LY
Valine	16.939	12.568	18.676	14.727	12.347	10.748	10.096	11.053	15.856	4.176	4.224	4.233	3.852	5.549	6.445
3-HIB	6.819	3.813	8.878	4.769	3.682	14.683	17.516	11.537	13.416	12.090	7.288	8.646	8.145	8.789	16.124
Citrate	0.132	0.061	0.095	0.129	0.151	0.816	0.564	0.437	0.327	0.085	0.102	0.158	0.072	0.103	0.113
Succinate	0.156	0.057	0.076	0.062	0.111	0.528	0.652	0.278	0.243	0.026	0.018	0.082	0.011	0.026	0.068
MS_METABOLITE_DATA_END
#METABOLITES
METABOLITES_START
metabolite_name	KEGG
Valine	C00183
3-HIB	C06001
Citrate	C00158
Succinate	C00042
METABOLITES_END
#END