Insulin resistance: metabolic mechanisms and consequences in the heart.
Authors Abel ED, O'Shea KM, Ramasamy R
Submitted By E. Dale Abel on 10/31/2012
Status Published
Journal Arteriosclerosis, thrombosis, and vascular biology
Year 2012
Date Published 9/1/2012
Volume : Pages 32 : 2068 - 2076
PubMed Reference 22895668
Abstract Insulin resistance is a characteristic feature of obesity and type 2 diabetes
mellitus and impacts the heart in various ways. Impaired insulin-mediated
glucose uptake is a uniformly observed characteristic of the heart in these
states, although changes in upstream kinase signaling are variable and dependent
on the severity and duration of the associated obesity or diabetes mellitus. The
understanding of the physiological and pathophysiological role of insulin
resistance in the heart is evolving. To maintain its high energy demands, the
heart is capable of using many metabolic substrates. Although insulin signaling
may directly regulate cardiac metabolism, its main role is likely the regulation
of substrate delivery from the periphery to the heart. In addition to promoting
glucose uptake, insulin regulates long-chain fatty acid uptake, protein
synthesis, and vascular function in the normal cardiovascular system. Recent
advances in understanding the role of metabolic, signaling, and inflammatory
pathways in obesity have provided opportunities to better understand the
pathophysiology of insulin resistance in the heart. This review will summarize
our current understanding of metabolic mechanisms for and consequences of
insulin resistance in the heart and will discuss potential new areas for
investigating novel mechanisms that contribute to insulin resistance in the
heart.


Investigators with authorship
NameInstitution
E. Dale AbelUniversity of Iowa

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