PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Multiphasic Regulation of Systemic and Peripheral Organ Metabolic Responses to Cardiac Hypertrophy.

Abstract Reduced fat oxidation in hypertrophied hearts coincides with a shift of carnitine palmitoyl transferase I from muscle to increased liver isoforms. Acutely increased carnitine palmitoyl transferase I in normal rodent hearts has been shown to recapitulate the reduced fat oxidation and elevated atrial natriuretic peptide message of cardiac hypertrophy.
PMID
Related Publications

Heart Failure With Preserved Ejection Fraction Induces Beiging in Adipose Tissue.

Gsα deficiency in adipose tissue improves glucose metabolism and insulin sensitivity without an effect on body weight.

Obesity resistance and increased energy expenditure by white adipose tissue browning in Oga(+/-) mice.

Inhibition of Sam68 triggers adipose tissue browning.

Ablation of ghrelin receptor reduces adiposity and improves insulin sensitivity during aging by regulating fat metabolism in white and brown adipose tissues.

Authors

Mayor MeshTerms
Keywords

adipose tissue

hypertrophy

insulin resistance

metabolism

pressure overload

Journal Title circulation. heart failure
Publication Year Start




PMID- 28404627
OWN - NLM
STAT- MEDLINE
DA  - 20170413
DCOM- 20170418
LR  - 20170418
IS  - 1941-3297 (Electronic)
IS  - 1941-3289 (Linking)
VI  - 10
IP  - 4
DP  - 2017 Apr
TI  - Multiphasic Regulation of Systemic and Peripheral Organ Metabolic Responses to
      Cardiac Hypertrophy.
LID - e003864 [pii]
LID - 10.1161/CIRCHEARTFAILURE.117.003864 [doi]
AB  - BACKGROUND: Reduced fat oxidation in hypertrophied hearts coincides with a shift 
      of carnitine palmitoyl transferase I from muscle to increased liver isoforms.
      Acutely increased carnitine palmitoyl transferase I in normal rodent hearts has
      been shown to recapitulate the reduced fat oxidation and elevated atrial
      natriuretic peptide message of cardiac hypertrophy. METHODS AND RESULTS: Because 
      of the potential for reduced fat oxidation to affect cardiac atrial natriuretic
      peptide, and thus, induce adipose lipolysis, we studied peripheral and systemic
      metabolism in male C57BL/6 mice model of transverse aortic constriction in which 
      left ventricular hypertrophy occurred by 2 weeks without functional decline until
      16 weeks (ejection fraction, -45.6%; fractional shortening, -22.6%). We report
      the first evidence for initially improved glucose tolerance and insulin
      sensitivity in response to 2 weeks transverse aortic constriction versus sham,
      linked to enhanced insulin signaling in liver and visceral adipose tissue
      (epididymal white adipose tissue [WAT]), reduced WAT inflammation, elevated
      adiponectin, mulitilocular subcutaneous adipose tissue (inguinal WAT) with
      upregulated oxidative/thermogenic gene expression, and downregulated lipolysis
      and lipogenesis genes in epididymal WAT. By 6 weeks transverse aortic
      constriction, the metabolic profile reversed with impaired insulin sensitivity
      and glucose tolerance, reduced insulin signaling in liver, epididymal WAT and
      heart, and downregulation of oxidative enzymes in brown adipose tissue and
      oxidative and lipogenic genes in inguinal WAT. CONCLUSIONS: Changes in insulin
      signaling, circulating natriuretic peptides and adipokines, and varied expression
      of adipose genes associated with altered insulin response/glucose handling and
      thermogenesis occurred prior to any functional decline in transverse aortic
      constriction hearts. The findings demonstrate multiphasic responses in
      extracardiac metabolism to pathogenic cardiac stress, with early iWAT browning
      providing potential metabolic benefits.
CI  - (c) 2017 American Heart Association, Inc.
FAU - Liew, Chong Wee
AU  - Liew CW
AD  - From the Department of Physiology and Biophysics (C.W.L., S.X., M.M., H.W.K.,
      A.C.C., J.M.O., E.D.L.) and Center for Cardiovascular Research (X.W., A.C.C.,
      J.M.O., E.D.L.), University of Illinois College of Medicine at Chicago;
      Department of Kinesiology and Nutrition, University of Illinois at Chicago
      College of Applied Health Sciences (J.P., G.F.); and Sanford Burnham Prebys
      Medical Discovery Institute, Orlando, FL (A.C.C., E.D.L.).
FAU - Xu, Shanshan
AU  - Xu S
AD  - From the Department of Physiology and Biophysics (C.W.L., S.X., M.M., H.W.K.,
      A.C.C., J.M.O., E.D.L.) and Center for Cardiovascular Research (X.W., A.C.C.,
      J.M.O., E.D.L.), University of Illinois College of Medicine at Chicago;
      Department of Kinesiology and Nutrition, University of Illinois at Chicago
      College of Applied Health Sciences (J.P., G.F.); and Sanford Burnham Prebys
      Medical Discovery Institute, Orlando, FL (A.C.C., E.D.L.).
FAU - Wang, Xuerong
AU  - Wang X
AD  - From the Department of Physiology and Biophysics (C.W.L., S.X., M.M., H.W.K.,
      A.C.C., J.M.O., E.D.L.) and Center for Cardiovascular Research (X.W., A.C.C.,
      J.M.O., E.D.L.), University of Illinois College of Medicine at Chicago;
      Department of Kinesiology and Nutrition, University of Illinois at Chicago
      College of Applied Health Sciences (J.P., G.F.); and Sanford Burnham Prebys
      Medical Discovery Institute, Orlando, FL (A.C.C., E.D.L.).
FAU - McCann, Maximilian
AU  - McCann M
AD  - From the Department of Physiology and Biophysics (C.W.L., S.X., M.M., H.W.K.,
      A.C.C., J.M.O., E.D.L.) and Center for Cardiovascular Research (X.W., A.C.C.,
      J.M.O., E.D.L.), University of Illinois College of Medicine at Chicago;
      Department of Kinesiology and Nutrition, University of Illinois at Chicago
      College of Applied Health Sciences (J.P., G.F.); and Sanford Burnham Prebys
      Medical Discovery Institute, Orlando, FL (A.C.C., E.D.L.).
FAU - Whang Kong, Hyerim
AU  - Whang Kong H
AD  - From the Department of Physiology and Biophysics (C.W.L., S.X., M.M., H.W.K.,
      A.C.C., J.M.O., E.D.L.) and Center for Cardiovascular Research (X.W., A.C.C.,
      J.M.O., E.D.L.), University of Illinois College of Medicine at Chicago;
      Department of Kinesiology and Nutrition, University of Illinois at Chicago
      College of Applied Health Sciences (J.P., G.F.); and Sanford Burnham Prebys
      Medical Discovery Institute, Orlando, FL (A.C.C., E.D.L.).
FAU - Carley, Andrew C
AU  - Carley AC
AD  - From the Department of Physiology and Biophysics (C.W.L., S.X., M.M., H.W.K.,
      A.C.C., J.M.O., E.D.L.) and Center for Cardiovascular Research (X.W., A.C.C.,
      J.M.O., E.D.L.), University of Illinois College of Medicine at Chicago;
      Department of Kinesiology and Nutrition, University of Illinois at Chicago
      College of Applied Health Sciences (J.P., G.F.); and Sanford Burnham Prebys
      Medical Discovery Institute, Orlando, FL (A.C.C., E.D.L.).
FAU - Pang, Jingbo
AU  - Pang J
AD  - From the Department of Physiology and Biophysics (C.W.L., S.X., M.M., H.W.K.,
      A.C.C., J.M.O., E.D.L.) and Center for Cardiovascular Research (X.W., A.C.C.,
      J.M.O., E.D.L.), University of Illinois College of Medicine at Chicago;
      Department of Kinesiology and Nutrition, University of Illinois at Chicago
      College of Applied Health Sciences (J.P., G.F.); and Sanford Burnham Prebys
      Medical Discovery Institute, Orlando, FL (A.C.C., E.D.L.).
FAU - Fantuzzi, Giamila
AU  - Fantuzzi G
AD  - From the Department of Physiology and Biophysics (C.W.L., S.X., M.M., H.W.K.,
      A.C.C., J.M.O., E.D.L.) and Center for Cardiovascular Research (X.W., A.C.C.,
      J.M.O., E.D.L.), University of Illinois College of Medicine at Chicago;
      Department of Kinesiology and Nutrition, University of Illinois at Chicago
      College of Applied Health Sciences (J.P., G.F.); and Sanford Burnham Prebys
      Medical Discovery Institute, Orlando, FL (A.C.C., E.D.L.).
FAU - O'Donnell, J Michael
AU  - O'Donnell JM
AD  - From the Department of Physiology and Biophysics (C.W.L., S.X., M.M., H.W.K.,
      A.C.C., J.M.O., E.D.L.) and Center for Cardiovascular Research (X.W., A.C.C.,
      J.M.O., E.D.L.), University of Illinois College of Medicine at Chicago;
      Department of Kinesiology and Nutrition, University of Illinois at Chicago
      College of Applied Health Sciences (J.P., G.F.); and Sanford Burnham Prebys
      Medical Discovery Institute, Orlando, FL (A.C.C., E.D.L.).
FAU - Lewandowski, E Douglas
AU  - Lewandowski ED
AD  - From the Department of Physiology and Biophysics (C.W.L., S.X., M.M., H.W.K.,
      A.C.C., J.M.O., E.D.L.) and Center for Cardiovascular Research (X.W., A.C.C.,
      J.M.O., E.D.L.), University of Illinois College of Medicine at Chicago;
      Department of Kinesiology and Nutrition, University of Illinois at Chicago
      College of Applied Health Sciences (J.P., G.F.); and Sanford Burnham Prebys
      Medical Discovery Institute, Orlando, FL (A.C.C., E.D.L.).
      [email protected]
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Circ Heart Fail
JT  - Circulation. Heart failure
JID - 101479941
SB  - IM
MH  - Adipose Tissue, Brown/metabolism
MH  - Adipose Tissue, White/metabolism
MH  - Animals
MH  - Cardiomegaly/*metabolism
MH  - Energy Metabolism/physiology
MH  - Insulin Resistance/*physiology
MH  - Lipid Metabolism/*physiology
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Obesity/metabolism
MH  - Oxidation-Reduction
MH  - Signal Transduction/physiology
OTO - NOTNLM
OT  - adipose tissue
OT  - hypertrophy
OT  - insulin resistance
OT  - metabolism
OT  - pressure overload
EDAT- 2017/04/14 06:00
MHDA- 2017/04/19 06:00
CRDT- 2017/04/14 06:00
PHST- 2016/10/28 [received]
PHST- 2017/03/22 [accepted]
AID - CIRCHEARTFAILURE.117.003864 [pii]
AID - 10.1161/CIRCHEARTFAILURE.117.003864 [doi]
PST - ppublish
SO  - Circ Heart Fail. 2017 Apr;10(4). pii: e003864. doi:
      10.1161/CIRCHEARTFAILURE.117.003864.

<?xml version="1.0" encoding="UTF-8"?>
<b:Sources SelectedStyle="" xmlns:b="http://schemas.openxmlformats.org/officeDocument/2006/bibliography"  xmlns="http://schemas.openxmlformats.org/officeDocument/2006/bibliography" >
</b:Sources>