Cardiac steatosis in diabetes mellitus: A 1H-magnetic resonance spectroscopy study

Jonathan M. McGavock, Ildiko Lingvay, Ivana Zib, Tommy Tillery, Naomi Salas, Roger H Unger, Benjamin D Levine, Philip Raskin, Ronald G. Victor, Lidia S. Szczepaniak

Research output: Contribution to journalArticle

380 Citations (Scopus)

Abstract

BACKGROUND - The risk of heart failure in type 2 diabetes mellitus is greater than can be accounted for by hypertension and coronary artery disease. Rodent studies indicate that in obesity and type 2 diabetes mellitus, lipid overstorage in cardiac myocytes produces lipotoxic intermediates that cause apoptosis, which leads to heart failure. In humans with diabetes mellitus, cardiac steatosis previously has been demonstrated in explanted hearts of patients with end-stage nonischemic cardiomyopathy. Whether cardiac steatosis precedes the onset of cardiomyopathy in individuals with impaired glucose tolerance or in patients with type 2 diabetes mellitus is unknown. METHODS AND RESULTS - To represent the progressive stages in the natural history of type 2 diabetes mellitus, we stratified 134 individuals (age 45±12 years) into 1 of 4 groups: (1) lean normoglycemic (lean), (2) overweight and obese normoglycemic (obese), (3) impaired glucose tolerance, and (4) type 2 diabetes mellitus. Localized H magnetic resonance spectroscopy and cardiac magnetic resonance imaging were used to quantify myocardial triglyceride content and left ventricular function, respectively. Compared with lean subjects, myocardial triglyceride content was 2.3-fold higher in those with impaired glucose tolerance and 2.1-fold higher in those with type 2 diabetes mellitus (P<0.05). Left ventricular ejection fraction was normal and comparable across all groups. CONCLUSIONS - In humans, impaired glucose tolerance is accompanied by cardiac steatosis, which precedes the onset of type 2 diabetes mellitus and left ventricular systolic dysfunction. Thus, lipid overstorage in human cardiac myocytes is an early manifestation in the pathogenesis of type 2 diabetes mellitus and is evident in the absence of heart failure.

Original languageEnglish (US)
Pages (from-to)1170-1175
Number of pages6
JournalCirculation
Volume116
Issue number10
DOIs
StatePublished - Sep 2007

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Type 2 Diabetes Mellitus
Diabetes Mellitus
Magnetic Resonance Spectroscopy
Glucose Intolerance
Heart Failure
Cardiomyopathies
Cardiac Myocytes
Triglycerides
Lipids
Left Ventricular Dysfunction
Left Ventricular Function
Stroke Volume
Coronary Artery Disease
Rodentia
Obesity
Magnetic Resonance Imaging
Apoptosis
Hypertension

Keywords

  • Magnetic resonance spectroscopy
  • Metabolism
  • Obesity

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Cardiac steatosis in diabetes mellitus : A 1H-magnetic resonance spectroscopy study. / McGavock, Jonathan M.; Lingvay, Ildiko; Zib, Ivana; Tillery, Tommy; Salas, Naomi; Unger, Roger H; Levine, Benjamin D; Raskin, Philip; Victor, Ronald G.; Szczepaniak, Lidia S.

In: Circulation, Vol. 116, No. 10, 09.2007, p. 1170-1175.

Research output: Contribution to journalArticle

McGavock, Jonathan M. ; Lingvay, Ildiko ; Zib, Ivana ; Tillery, Tommy ; Salas, Naomi ; Unger, Roger H ; Levine, Benjamin D ; Raskin, Philip ; Victor, Ronald G. ; Szczepaniak, Lidia S. / Cardiac steatosis in diabetes mellitus : A 1H-magnetic resonance spectroscopy study. In: Circulation. 2007 ; Vol. 116, No. 10. pp. 1170-1175.
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AU - Unger, Roger H

AU - Levine, Benjamin D

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N2 - BACKGROUND - The risk of heart failure in type 2 diabetes mellitus is greater than can be accounted for by hypertension and coronary artery disease. Rodent studies indicate that in obesity and type 2 diabetes mellitus, lipid overstorage in cardiac myocytes produces lipotoxic intermediates that cause apoptosis, which leads to heart failure. In humans with diabetes mellitus, cardiac steatosis previously has been demonstrated in explanted hearts of patients with end-stage nonischemic cardiomyopathy. Whether cardiac steatosis precedes the onset of cardiomyopathy in individuals with impaired glucose tolerance or in patients with type 2 diabetes mellitus is unknown. METHODS AND RESULTS - To represent the progressive stages in the natural history of type 2 diabetes mellitus, we stratified 134 individuals (age 45±12 years) into 1 of 4 groups: (1) lean normoglycemic (lean), (2) overweight and obese normoglycemic (obese), (3) impaired glucose tolerance, and (4) type 2 diabetes mellitus. Localized H magnetic resonance spectroscopy and cardiac magnetic resonance imaging were used to quantify myocardial triglyceride content and left ventricular function, respectively. Compared with lean subjects, myocardial triglyceride content was 2.3-fold higher in those with impaired glucose tolerance and 2.1-fold higher in those with type 2 diabetes mellitus (P<0.05). Left ventricular ejection fraction was normal and comparable across all groups. CONCLUSIONS - In humans, impaired glucose tolerance is accompanied by cardiac steatosis, which precedes the onset of type 2 diabetes mellitus and left ventricular systolic dysfunction. Thus, lipid overstorage in human cardiac myocytes is an early manifestation in the pathogenesis of type 2 diabetes mellitus and is evident in the absence of heart failure.

AB - BACKGROUND - The risk of heart failure in type 2 diabetes mellitus is greater than can be accounted for by hypertension and coronary artery disease. Rodent studies indicate that in obesity and type 2 diabetes mellitus, lipid overstorage in cardiac myocytes produces lipotoxic intermediates that cause apoptosis, which leads to heart failure. In humans with diabetes mellitus, cardiac steatosis previously has been demonstrated in explanted hearts of patients with end-stage nonischemic cardiomyopathy. Whether cardiac steatosis precedes the onset of cardiomyopathy in individuals with impaired glucose tolerance or in patients with type 2 diabetes mellitus is unknown. METHODS AND RESULTS - To represent the progressive stages in the natural history of type 2 diabetes mellitus, we stratified 134 individuals (age 45±12 years) into 1 of 4 groups: (1) lean normoglycemic (lean), (2) overweight and obese normoglycemic (obese), (3) impaired glucose tolerance, and (4) type 2 diabetes mellitus. Localized H magnetic resonance spectroscopy and cardiac magnetic resonance imaging were used to quantify myocardial triglyceride content and left ventricular function, respectively. Compared with lean subjects, myocardial triglyceride content was 2.3-fold higher in those with impaired glucose tolerance and 2.1-fold higher in those with type 2 diabetes mellitus (P<0.05). Left ventricular ejection fraction was normal and comparable across all groups. CONCLUSIONS - In humans, impaired glucose tolerance is accompanied by cardiac steatosis, which precedes the onset of type 2 diabetes mellitus and left ventricular systolic dysfunction. Thus, lipid overstorage in human cardiac myocytes is an early manifestation in the pathogenesis of type 2 diabetes mellitus and is evident in the absence of heart failure.

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KW - Obesity

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