Fatty acid metabolism assessed by <sup>125</sup>I‐iodophenyl 9‐methylpentadecanoic acid (9MPA) and expression of fatty acid utilization enzymes in volume‐overloaded hearts

Miyamoto, Takuya; Takeishi, Yasuchika; Tazawa, Shusaku; Inoue, Minoru; Aoyama, Toshifumi; Takahashi, Hitomi; Arimoto, Takanori; Shishido, Tetsuro; Tomoike, Hitonobu

doi:10.1111/j.1365-2362.2004.01312.x

Cited by 17 publications

(13 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…After injection, planar images were obtained followed by single photon emission computed tomography (SPECT) images 3 hours. All images were acquired in the resting state us- ing a dual-head rotating gamma camera (Toshiba, Tokyo, Japan) [15][16][17] . Energy discrimination was provided by a 15% window centered on the 140 keV photopeak.…”

Section: Methodsmentioning

confidence: 99%

Technetium-99m sestamibi retention in skeletal muscles, a potential indicator of mitochondrial function and anaerobic threshold in patients with type 2 diabetes

Sato

Kato

Otsuki

et al. 2015

JPFSM

View full text Add to dashboard Cite

In this study, we investigated the retention of technetium-99m sestamibi (MIBI), a radiopharmaceutical that accumulates in mitochondria, in patients with type 2 diabetes. We hypothesized that patients with type 2 diabetes had lower MIBI counts in their legs than nondiabetic volunteers, and that these abnormalities reflected a low anaerobic threshold (AT) during cardiopulmonary exercise testing (CPX). Eight non-diabetic volunteers (Group N) and 11 patients with type 2 diabetes (Group D) underwent CPX. Mitochondrial function was assessed using MIBI imaging of both legs. The MIBI counts in the legs were significantly lower in Group D than in Group N (D vs. N: 74.1 vs. 94.1 counts/pixel, p < 0.05). Similarly, peak oxygen uptake (peakV ・ O 2 ) and AT were lower in Group D than in Group N (peakV ・ O 2 : 19.8 vs. 26.5 ml/kg/min, p < 0.05; AT: 13.1 vs. 17.2 ml/kg/min, p < 0.05). A strong correlation was observed between MIBI counts and the peakV ・ O 2 and AT (peakV ・ O 2 : r = 0.62, p < 0.01; AT: r = 0.76, p < 0.01). After the exclusion of an outlying subject, the correlation between peakV ・ O 2 and MIBI count in the legs was lost (r = 0.28, p = 0.26); however, the AT correlation was maintained (r = 0.59, p = 0.01). Patients with type 2 diabetes had reduced skeletal muscle MIBI counts, indicating reduced mitochondrial function. This abnormality may be linked to a low AT.

show abstract

Section: Methodsmentioning

confidence: 99%

Technetium-99m sestamibi retention in skeletal muscles, a potential indicator of mitochondrial function and anaerobic threshold in patients with type 2 diabetes

Sato

Kato

Otsuki

et al. 2015

JPFSM

View full text Add to dashboard Cite

show abstract

“…[30][31][32] Miyamoto et al, measured the expression of several enzymes involved in FA metabolism and found that the levels of PPARα, a key transcriptional regulator of metabolic genes were normal in volume-overloaded hypertrophied rabbit hearts. 33 In addition, several studies have reported normal FA uptake, metabolism and carnitine palmitoyltransferase 1 activity, the rate limiting enzyme in mitochondrial beta-oxidation, in cardiac hypertrophy. 30,32 Our findings suggest that the cardiac hypertrophy caused by loss of Cav1 gene expression in cardiac fibroblasts was not severe enough to trigger a switch in myocardial energy metabolism commonly observed in pressure-or volume-overload induced hypertrophy and heart failure.…”

Section: Discussionmentioning

confidence: 99%

Hearts lacking caveolin-1 develop hypertrophy with normal cardiac substrate metabolism

et al. 2008

View full text Add to dashboard Cite

Cell Cycle 7:16, 2509-2518 15 August 2008]; ©2008 Landes Bioscience Long-chain fatty acids (FA) are the primary energy source utilized by the adult heart. However, during pathological cardiac hypertrophy the fetal gene program is reactivated and glucose becomes the major fuel source metabolized by the heart. Herein we describe the metabolic phenotype associated with caveolin-1(Cav1) gene ablation (Cav1ko) in cardiac fibroblasts. Cav1, the primary protein component of caveolae in non-muscle cells co-localizes with a number of proteins involved in substrate metabolism, including, FA translocase (CD36) and the insulin receptor. We demonstrate that Cav1ko hearts develop cardiac hypertrophy and contractile dysfunction at 5-6mos of age. Surprisingly, we observed an increase in the uptake of Intralipid triglyceride and albumin bound FA by 25% and 47%, respectively, in Cav1ko hearts. Isolated perfused heart studies revealed no significant difference in glucose oxidation and glycolysis, however, we observed a trend toward increased FA oxidation in Cav1ko hearts. Real-time PCR analysis revealed no significant changes in the expression of genes involved in FA and glucose metabolism. We also report myocardial triglyceride, fatty acid and cholesterol levels are significantly reduced in Cav1ko hearts. Microarray gene expression analysis revealed changes in genes that regulate calcium ion and lipid transport as well as a number of genes not previously linked to cardiac hypertrophy. We observed a 4-fold increase in tetraspanin-2 gene expression, a transmembrane protein implicated in regulating intracellular trafficking. Oxysterol binding protein related protein-3, which has been implicated in intracellular lipid synthesis and transport, was increased 3.6-fold.In addition, sarcoplasmic reticulum Ca 2+ -ATPase 3, and calcyclin gene transcripts were significantly increased in Cav1ko hearts. In summary, targeted loss of Cav1 produces a unique model of cardiac hypertrophy with normal substrate utilization and expression of genes involved in energy metabolism.

show abstract

“…It may facilitate switching of substrate utilization. In the rabbit model of volume overload hypertrophic heart failure there was no downregulation in PPAR-␣ protein expression or in the expression of enzymes of fatty acid oxidation, but the uptake and oxidation of fatty acids was increased [61]. In a rat infarction model of heart failure a significant decrease in mRNA expression of PPAR-␣ was …”

Section: Effects On Oxidative Phosphorylationmentioning

confidence: 91%

Metabolic Modulation and Cellular Therapy of Cardiac Dysfunction and Failure

Revenco

Morgan

2009

Journal of Cellular and Molecular Medicine

View full text Add to dashboard Cite

show abstract

Fatty acid metabolism assessed by ¹²⁵I‐iodophenyl 9‐methylpentadecanoic acid (9MPA) and expression of fatty acid utilization enzymes in volume‐overloaded hearts

Cited by 17 publications

References 21 publications

Technetium-99m sestamibi retention in skeletal muscles, a potential indicator of mitochondrial function and anaerobic threshold in patients with type 2 diabetes

Technetium-99m sestamibi retention in skeletal muscles, a potential indicator of mitochondrial function and anaerobic threshold in patients with type 2 diabetes

Hearts lacking caveolin-1 develop hypertrophy with normal cardiac substrate metabolism

Metabolic Modulation and Cellular Therapy of Cardiac Dysfunction and Failure

Contact Info

Product

Resources

About

Fatty acid metabolism assessed by 125I‐iodophenyl 9‐methylpentadecanoic acid (9MPA) and expression of fatty acid utilization enzymes in volume‐overloaded hearts

Cited by 17 publications

References 21 publications

Technetium-99m sestamibi retention in skeletal muscles, a potential indicator of mitochondrial function and anaerobic threshold in patients with type 2 diabetes

Technetium-99m sestamibi retention in skeletal muscles, a potential indicator of mitochondrial function and anaerobic threshold in patients with type 2 diabetes

Hearts lacking caveolin-1 develop hypertrophy with normal cardiac substrate metabolism

Metabolic Modulation and Cellular Therapy of Cardiac Dysfunction and Failure

Contact Info

Product

Resources

About

Fatty acid metabolism assessed by ¹²⁵I‐iodophenyl 9‐methylpentadecanoic acid (9MPA) and expression of fatty acid utilization enzymes in volume‐overloaded hearts