Chronic heart failure selectively induces regional heterogeneity of insulin-responsive glucose transporters

Ware, Bruce; Bevier, Marie; Nishijima, Yoshinori; Rogers, Sue; Carnes, Cynthia A.; Lacombe, Véronique A.

doi:10.1152/ajpregu.00822.2010

Cited by 20 publications

(37 citation statements)

References 37 publications

(65 reference statements)

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“…Studies using a canine model for chronic heart failure showed that the expression of both GLUT4 and GLUT12 is affected in specific myocardial structures (Ware et al 2011). Transcriptomic profile of glut12-deficient larvae.…”

Section: Discussionmentioning

confidence: 99%

GLUT12 deficiency during early development results in heart failure and a diabetic phenotype in zebrafish

Jiménez-Amilburu¹,

Jong-Raadsen²,

Bakkers³

et al. 2014

Journal of Endocrinology

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Cardiomyopathies-associated metabolic pathologies (e.g., type 2 diabetes and insulin resistance) are a leading cause of mortality. It is known that the association between these pathologies works in both directions, for which heart failure can lead to metabolic derangements such as insulin resistance. This intricate crosstalk exemplifies the importance of a fine coordination between one of the most energy-demanding organs and an equilibrated carbohydrate metabolism. In this light, to assist in the understanding of the role of insulinregulated glucose transporters (GLUTs) and the development of cardiomyopathies, we have developed a model for glut12 deficiency in zebrafish. GLUT12 is a novel insulin-regulated GLUT expressed in the main insulin-sensitive tissues, such as cardiac muscle, skeletal muscle, and adipose tissue. In this study, we show that glut12 knockdown impacts the development of the embryonic heart resulting in abnormal valve formation. Moreover, glut12-deficient embryos also exhibited poor glycemic control. Glucose measurements showed that these larvae were hyperglycemic and resistant to insulin administration. Transcriptome analysis demonstrated that a number of genes known to be important in cardiac development and function as well as metabolic mediators were dysregulated in these larvae. These results indicate that glut12 is an essential GLUT in the heart where the reduction in glucose uptake due to glut12 deficiency leads to heart failure presumably due to the lack of glucose as energy substrate. In addition, the diabetic phenotype displayed by these larvae after glut12 abrogation highlights the importance of this GLUT during early developmental stages.

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Section: Discussionmentioning

confidence: 99%

GLUT12 deficiency during early development results in heart failure and a diabetic phenotype in zebrafish

Jiménez-Amilburu¹,

Jong-Raadsen²,

Bakkers³

et al. 2014

Journal of Endocrinology

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“…The uptake of both substrates is controlled mostly by plasma membrane protein transporters [1]. It is known that glucose transport is regulated by glucose transporters 1 and 4 (GLUT1 and GLUT4) in the cardiomyocytes [2].…”

Section: Introductionmentioning

confidence: 99%

The Endocannabinoid System Affects Myocardial Glucose Metabolism in the DOCA-Salt Model of Hypertension

Polak

Harasim-Symbor

Malinowska

et al. 2018

Cell Physiol Biochem

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Background/Aims: Recent interest in the use of cannabinoids as therapeutic agents has revealed the involvement of the endogenous cannabinoid system (ECS) in the regulation of the cardiovascular system in hypertension. Abnormalities in glucose metabolism and insulin action are commonly detected in hypertensive animals. Thus, potential antihypertensive drugs should be investigated with respect to modulation of glucose homeostasis. Therefore, the aim of the present study was to evaluate the effects of the ECS activation after chronic fatty acid amide hydrolase inhibitor (URB597) administration on plasma glucose and insulin concentrations as well as parameters of myocardial glucose metabolism in the deoxycorticosterone acetate (DOCA)-salt hypertensive rats, an animal model of secondary hypertension. Methods: Hypertension was induced by DOCA (25mg/kg) injections and addition of 1% NaCl in the drinking water for six weeks. Chronic activation of the ECS was performed by URB597 (1mg/kg) injections for two weeks. We examined fasting plasma levels of insulin (ELISA), glucose and intramyocardial glycogen (colorimetric method). Expressions of glucose transporters (GLUT1, 4) and selected proteins engaged in GLUT translocation as well as glucose metabolism were determined using Western blotting. Results: Hypertension induced hypoinsulinemia with concomitant lack of significant changes in glycemia, reduced intramyocardial glycogen content and increased pyruvate dehydrogenase (PDH) expression in the cardiac muscle. Importantly, chronic URB597 administration in the hypertensive rats increased insulin concentration, elevated plasmalemmal GLUT1 and GLUT4 expression and concomitantly improved myocardial glycogen storage. Conclusion: Chronic administration of fatty acid amide hydrolase (FAAH) inhibitor has potential protective properties on myocardial glucose metabolism in hypertension.

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“…Activity of mTOR signalling pathway has been associated with diabetic kidney nephropathy [42]. Finally, in a canine model of chronic heart failure, increase of GLUT4 and GLUT12 protein and mRNA expression was described in comparison to control heart samples [41].…”

Section: Implication In Cancer and Other Diseasesmentioning

confidence: 98%

“…GLUT12 cDNA has also been cloned from mouse and cow, presenting respectively 83 and 87 % homology with the human isoform [24,49], and expression of GLUT12 has been reported in rat [18], horse [38] and dog [41].…”

Section: Structure and Tissue Distributionmentioning

confidence: 99%

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The facilitative glucose transporter GLUT12: what do we know and what would we like to know?

et al. 2012

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Human GLUT12 was isolated from the breast cancer cell line MCF-7 by its homology with GLUT4.Glucose has been described as its main substrate, but it also can transport other sugars. In humans, GLUT12 protein is expressed mainly in insulin sensitive tissues. Functional analysis has showed that GLUT12 transports sugars down its concentration gradient, but it can also work as a proton-coupled symporter. Studies from our laboratory, performed in Xenopus laevis oocytes expressing GLUT12, show that glucose uptake increases in the presence of Na + and induces inward current. These findings suggest a transport mechanism never described for other GLUTs, which would indicate a distinct functional role for GLUT12. In relation with its physiological and pathophysiological function, GLUT12 has been mainly studied due to its role as a secondary insulin-sensitive glucose transporter and its possible implication in impaired insulin signalling pathologies. Its expression in some tumour tissues has been described and recently, it has been proposed as one of the key proteins in the glucose supply to malignant cells. Overall, even though a lot of information about GLUT12 has been released during the last years, its functional characteristics, physiological role or implication in the development of some diseases is still unclear. Therefore, this review of the literature can help to address further investigations needed to elucidate these issues that, in our view, are of great interest mainly due to the direct GLUT12 relation with cancer and probably with diabetes development.

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Chronic heart failure selectively induces regional heterogeneity of insulin-responsive glucose transporters

Abstract: Ware B, Bevier M, Nishijima Y, Rogers S, Carnes CA, Lacombe VA. Chronic heart failure selectively induces regional heterogeneity of insulin-responsive glucose transporters.

Cited by 20 publications

References 37 publications

GLUT12 deficiency during early development results in heart failure and a diabetic phenotype in zebrafish

GLUT12 deficiency during early development results in heart failure and a diabetic phenotype in zebrafish

The Endocannabinoid System Affects Myocardial Glucose Metabolism in the DOCA-Salt Model of Hypertension

The facilitative glucose transporter GLUT12: what do we know and what would we like to know?

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