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02-Aug-2017 06:51

In contrast to these adverse effects, recent studies have also shown that -Glc NAc levels and cellular function is complex and not well-understood, it is clear that these pathways play a critical role in the regulation of cell function and survival in the cardiovascular system and may be implicated in the adverse effects of metabolic disease on the heart.

The association of metabolic diseases with increased risk for heart failure raises the distinct possibility that alterations in myocardial metabolic pathways play a critical role in the development and progression of the disease.

Glucose metabolism via the HBP leads to the formation of uridine 5′-diphosphate--linkage to specific serine and threonine residues on numerous nuclear and cytoplasmic proteins [3].

There is growing evidence that the impact of increased HBP flux on cell function is mediated via elevated levels of -Glc NAc levels can have diverse effects on cell function and survival [3,4].

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University of Alabama at Birmingham, Department of Medicine, 1530 3rd Avenue South, MCLM 684, Birmingham, AL 35294-0005, United States. Email address: [email protected] NAc) on serine and threonine residues of nuclear and cytoplasmic proteins is a highly dynamic post-translational modification that plays a key role in signal transduction pathways.

Numerous proteins have been identified as targets of -Glc NAc is regulated in part by the metabolism of glucose via the hexosamine biosynthesis pathway (HBP), and the metabolic abnormalities associated with insulin resistance and diabetes, such as hyperglycemia, hyperlipidemia, and hyperinsulinemia, are all associated with increased flux through the HBP and elevated -Glc NAc levels have been implicated in the impaired relaxation of isolated cardiomyocytes, blunted response to angiotensin II and phenylephrine, hyperglycemia-induced cardiomyocyte apoptosis, and endothelial and vascular cell dysfunction.

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The role of the HBP in the development of insulin resistance was first described by Marshall et al. Transgenic mice overexpressing GFAT in skeletal muscle and adipose tissue develop insulin resistance and hyperleptinaemia [8,9].

In vivo glucosamine infusion also resulted in skeletal muscle insulin resistance [10–12].

These data support the notion that increased flux through the hexosamine biosynthesis pathway plays an important role in the development of insulin resistance and glucose toxicity.

However, a causal relationship between metabolic dysfunction and increased risk of heart failure has been hard to establish.

Even in animal models of metabolic disease, where there is evidence of specific cardiomyocyte dysfunction, there is no consensus as to the specific metabolic or nutrient signaling pathways that contribute to this dysfunction [1]. 1) has been proposed as a nutrient sensor, and excess glucose flux into the HBP has been implicated in the development of insulin resistance as well as the vascular complications of diabetes [2].

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