Diabetes-induced bradycardia is an intrinsic metabolic defect reversed by carnitine

Michael A. Malone, Douglas D. Schocken, Suzan K. Hanna, Xiaomei Liang, John I. Malone

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Rats with streptozotocin-induced diabetes (STZ-D) have reduced serum carnitine levels and bradycardia. Heart rates (HRs) of 24nondiabetic rats (NRs) and 24 STZ-D rats were compared. l-Carnitine (C) was added to the drinking water of rats (12 STZ-D + C) to raise their serum carnitine level. The intrinsic HR for each animal was determined after parasympathetic and sympathetic blockade. The HRs of STZ-D rats (278 ± 15 beats per minute) were less than those of NRs (348 ± 8 beats per minute) (P < .01). STZ-D rats had low serum carnitine compared with control and STZ-D + C rats. The difference in HR of STZ-D rats and NRs continued after blockade, indicating that the bradycardia ofdiabetes is intrinsic to the heart. The metabolic milieu reflected in the rats' urinary organic acid profiles differed between the control and STZ-D rats. The HR of STZ-D + C rats (326 ± 5 beats per minute) did not differ from those of NRs. Increasing either the insulin dose or the serum free carnitine reduced urinary organic acids, but normal HRs were associated only with elevated serum carnitine levels. When glucose is compromised as a myocardial energy source (diabetes mellitus), we propose that elevated levels of serum carnitine may increase myocardial fatty acid metabolism sufficiently to correct the bradycardia of STZ-D rats.

Original languageEnglish (US)
Pages (from-to)1118-1123
Number of pages6
JournalMetabolism: Clinical and Experimental
Volume56
Issue number8
DOIs
StatePublished - Aug 1 2007

Fingerprint

Carnitine
Bradycardia
Experimental Diabetes Mellitus
Heart Rate
Serum
Acids
Drinking Water
Diabetes Mellitus
Fatty Acids
Insulin

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Malone, Michael A. ; Schocken, Douglas D. ; Hanna, Suzan K. ; Liang, Xiaomei ; Malone, John I. / Diabetes-induced bradycardia is an intrinsic metabolic defect reversed by carnitine. In: Metabolism: Clinical and Experimental. 2007 ; Vol. 56, No. 8. pp. 1118-1123.
@article{e9eb8967ef5c41c9bdbd7b2daa2f84e6,
title = "Diabetes-induced bradycardia is an intrinsic metabolic defect reversed by carnitine",
abstract = "Rats with streptozotocin-induced diabetes (STZ-D) have reduced serum carnitine levels and bradycardia. Heart rates (HRs) of 24nondiabetic rats (NRs) and 24 STZ-D rats were compared. l-Carnitine (C) was added to the drinking water of rats (12 STZ-D + C) to raise their serum carnitine level. The intrinsic HR for each animal was determined after parasympathetic and sympathetic blockade. The HRs of STZ-D rats (278 ± 15 beats per minute) were less than those of NRs (348 ± 8 beats per minute) (P < .01). STZ-D rats had low serum carnitine compared with control and STZ-D + C rats. The difference in HR of STZ-D rats and NRs continued after blockade, indicating that the bradycardia ofdiabetes is intrinsic to the heart. The metabolic milieu reflected in the rats' urinary organic acid profiles differed between the control and STZ-D rats. The HR of STZ-D + C rats (326 ± 5 beats per minute) did not differ from those of NRs. Increasing either the insulin dose or the serum free carnitine reduced urinary organic acids, but normal HRs were associated only with elevated serum carnitine levels. When glucose is compromised as a myocardial energy source (diabetes mellitus), we propose that elevated levels of serum carnitine may increase myocardial fatty acid metabolism sufficiently to correct the bradycardia of STZ-D rats.",
author = "Malone, {Michael A.} and Schocken, {Douglas D.} and Hanna, {Suzan K.} and Xiaomei Liang and Malone, {John I.}",
year = "2007",
month = "8",
day = "1",
doi = "10.1016/j.metabol.2007.04.005",
language = "English (US)",
volume = "56",
pages = "1118--1123",
journal = "Metabolism: Clinical and Experimental",
issn = "0026-0495",
publisher = "W.B. Saunders Ltd",
number = "8",

}

Diabetes-induced bradycardia is an intrinsic metabolic defect reversed by carnitine. / Malone, Michael A.; Schocken, Douglas D.; Hanna, Suzan K.; Liang, Xiaomei; Malone, John I.

In: Metabolism: Clinical and Experimental, Vol. 56, No. 8, 01.08.2007, p. 1118-1123.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Diabetes-induced bradycardia is an intrinsic metabolic defect reversed by carnitine

AU - Malone, Michael A.

AU - Schocken, Douglas D.

AU - Hanna, Suzan K.

AU - Liang, Xiaomei

AU - Malone, John I.

PY - 2007/8/1

Y1 - 2007/8/1

N2 - Rats with streptozotocin-induced diabetes (STZ-D) have reduced serum carnitine levels and bradycardia. Heart rates (HRs) of 24nondiabetic rats (NRs) and 24 STZ-D rats were compared. l-Carnitine (C) was added to the drinking water of rats (12 STZ-D + C) to raise their serum carnitine level. The intrinsic HR for each animal was determined after parasympathetic and sympathetic blockade. The HRs of STZ-D rats (278 ± 15 beats per minute) were less than those of NRs (348 ± 8 beats per minute) (P < .01). STZ-D rats had low serum carnitine compared with control and STZ-D + C rats. The difference in HR of STZ-D rats and NRs continued after blockade, indicating that the bradycardia ofdiabetes is intrinsic to the heart. The metabolic milieu reflected in the rats' urinary organic acid profiles differed between the control and STZ-D rats. The HR of STZ-D + C rats (326 ± 5 beats per minute) did not differ from those of NRs. Increasing either the insulin dose or the serum free carnitine reduced urinary organic acids, but normal HRs were associated only with elevated serum carnitine levels. When glucose is compromised as a myocardial energy source (diabetes mellitus), we propose that elevated levels of serum carnitine may increase myocardial fatty acid metabolism sufficiently to correct the bradycardia of STZ-D rats.

AB - Rats with streptozotocin-induced diabetes (STZ-D) have reduced serum carnitine levels and bradycardia. Heart rates (HRs) of 24nondiabetic rats (NRs) and 24 STZ-D rats were compared. l-Carnitine (C) was added to the drinking water of rats (12 STZ-D + C) to raise their serum carnitine level. The intrinsic HR for each animal was determined after parasympathetic and sympathetic blockade. The HRs of STZ-D rats (278 ± 15 beats per minute) were less than those of NRs (348 ± 8 beats per minute) (P < .01). STZ-D rats had low serum carnitine compared with control and STZ-D + C rats. The difference in HR of STZ-D rats and NRs continued after blockade, indicating that the bradycardia ofdiabetes is intrinsic to the heart. The metabolic milieu reflected in the rats' urinary organic acid profiles differed between the control and STZ-D rats. The HR of STZ-D + C rats (326 ± 5 beats per minute) did not differ from those of NRs. Increasing either the insulin dose or the serum free carnitine reduced urinary organic acids, but normal HRs were associated only with elevated serum carnitine levels. When glucose is compromised as a myocardial energy source (diabetes mellitus), we propose that elevated levels of serum carnitine may increase myocardial fatty acid metabolism sufficiently to correct the bradycardia of STZ-D rats.

UR - http://www.scopus.com/inward/record.url?scp=34347396956&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34347396956&partnerID=8YFLogxK

U2 - 10.1016/j.metabol.2007.04.005

DO - 10.1016/j.metabol.2007.04.005

M3 - Article

C2 - 17618959

AN - SCOPUS:34347396956

VL - 56

SP - 1118

EP - 1123

JO - Metabolism: Clinical and Experimental

JF - Metabolism: Clinical and Experimental

SN - 0026-0495

IS - 8

ER -