Impaired Skeletal Muscle Glucose Uptake by [
            <sup>18</sup>
            F]Fluorodeoxyglucose–Positron Emission Tomography in Patients With Peripheral Artery Disease and Intermittent Claudication

Pande, Reena L.; Park, Mi Ae; Perlstein, Todd S.; Desai, Akshay S.; Doyle, Jeanne; Navarrete, Nicole; Copeland‐Halperin, Robert S.; Redline, Whitney; Carli, Marcelo F. Di; Creager, Mark A.

doi:10.1161/atvbaha.110.217687

Cited by 26 publications

(22 citation statements)

References 29 publications

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“…Contrary to the early phase situation, during the later phase of ischemia, we observed a significantly decreased glucose uptake. This result is in accordance with a recent study showing decreased calf muscle glucose uptake in chronic PAD patients with IC compared to healthy control subjects (Pande et al 2011). Interestingly, this metabolic abnormality characterizing later phases of peripheral ischemia in our model relates to impaired walking ability, suggesting that decreased muscle glucose uptake may predict exercise limitation.…”

Section: Discussionsupporting

confidence: 93%

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Experimental peripheral arterial disease: new insights into muscle glucose uptake, macrophage, and T-cell polarization during early and late stages

et al. 2014

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Peripheral arterial disease (PAD) is a common disease with increasing prevalence, presenting with impaired walking ability affecting patient's quality of life. PAD epidemiology is known, however, mechanisms underlying functional muscle impairment remain unclear. Using a mouse PAD model, aim of this study was to assess muscle adaptive responses during early (1 week) and late (5 weeks) disease stages. Unilateral hindlimb ischemia was induced in ApoE−/− mice by iliac artery ligation. Ischemic limb perfusion and oxygenation (Laser Doppler imaging, transcutaneous oxygen pressure assessments) significantly decreased during early and late stage compared to pre‐ischemia, however, values were significantly higher during late versus early phase. Number of arterioles and arteriogenesis‐linked gene expression increased at later stage. Walking ability, evaluated by forced and voluntary walking tests, remained significantly decreased both at early and late phase without any significant improvement. Muscle glucose uptake ([18F]fluorodeoxyglucose positron emission tomography) significantly increased during early ischemia decreasing at later stage. Gene expression analysis showed significant shift in muscle M1/M2 macrophages and Th1/Th2 T cells balance toward pro‐inflammatory phenotype during early ischemia; later, inflammatory state returned to neutrality. Muscular M1/M2 shift inhibition by a statin prevented impaired walking ability in early ischemia. High‐energy phosphate metabolism remained unchanged (31‐Phosphorus magnetic resonance spectroscopy). Results show that rapid transient muscular inflammation contributes to impaired walking capacity while increased glucose uptake may be a compensatory mechanisms preserving immediate limb viability during early ischemia in a mouse PAD model. With time, increased ischemic limb perfusion and oxygenation assure muscle viability although not sufficiently to improve walking impairment. Subsequent decreased muscle glucose uptake may partly contribute to chronic walking impairment. Early inflammation inhibition and/or late muscle glucose impairment prevention are promising strategies for PAD management.

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Section: Discussionsupporting

confidence: 93%

“…Few studies have reported abnormal skeletal muscle metabolism in patients with PAD and IC, including impaired skeletal muscle glucose uptake (Pipinos et al 2007, 2008; Anderson et al 2009; Pande et al 2011), however, this potential mechanistic explanation has not been studied in early and late phases of PAD.…”

Section: Introductionmentioning

confidence: 99%

Experimental peripheral arterial disease: new insights into muscle glucose uptake, macrophage, and T-cell polarization during early and late stages

et al. 2014

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“…96, 97 By evaluating skeletal muscle glucose uptake with PET, it has been shown that PAD patients with intermittent claudication have calf muscle insulin resistance. 98 Additional studies are required to link muscle insulin resistance to functional parameters in PAD and to determine whether interventions to promote insulin sensitivity will reduce limb symptoms.…”

Section: Vascular Dysfunction In Padmentioning

confidence: 99%

Pathophysiology of Intermittent Claudication in Peripheral Artery Disease

Hamburg

Creager

2017

Circ J

Self Cite

144

124

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estimates a more than 30% increase in deaths and disability attributable to PAD between 2005 and 2015, which is largely determined by population aging. 3,12 PAD prevalence escalates with advancing age, affecting 1 in 10 adults older than 70 years. In addition to age, smoking and diabetes are the strongest risk factors for PAD across the world. A comprehensive global evaluation of PAD found that its prevalence and risk factors are similar in high-income countries to low-and middle-income countries. 2,13 Lower socioeconomic status is a newly recognized risk factor for PAD. 14 Importantly, there has been a greater increase in PAD prevalence in low-and middle-income countries, rising by 28.7% from 2000 to 2010 as compared with 13.1% in high-income countries. 2, 15 The changing burden of PAD is also greater in women as compared with men.The health implications of PAD derive from both its limb and cardiovascular manifestations. Consistent with the systemic nature of atherosclerosis, polyvascular disease is common in patients with PAD. 16 In the REACH registry, 61% of PAD patients had concomitant coronary artery disease (CAD) and/or cerebrovascular disease. 16 Thus, the presence of PAD portends a high risk for subsequent cardiovascular events. A meta-analysis of over 48,000 participants in population-based cohort studies demonstrated that a low ankle-brachial index (ABI) predicted a 2-fold risk of death, cardiovascular death, and major coronary events at all ranges of the Framingham Risk Score. 4 Further, the elevated risk of cardiovascular events is present in both symptomatic and asymptomatic patients. 17 Patients with atherosclerotic disease in more than 1 vascular territory have particularly poor outcomes. 6 In the over 5,000 Japanese T here is growing recognition of the effect of peripheral artery disease (PAD) on cardiovascular health. 1 Recent studies indicate that, globally, over 200 million adults have PAD, 2,3 which is an expression of systemic atherosclerosis and well-established as heightening the risk for cardiovascular events. 4-6 The limb manifestations of PAD induce considerable suffering. Patients with PAD experience intermittent claudication, characterized as exertional leg pain that limits walking ability, and often times, disability. 7-9 Current medical therapies to reduce the burden of lower extremity symptoms in patients with PAD are limited. Revascularization by endovascular intervention or surgical reconstruction is used to treat lifestyle-limiting claudication if patients do not respond adequately to medical therapy including exercise training. Indeed, lower extremity revascularization with endovascular approaches has undergone a dramatic increase in use. 10 Though endovascular therapy improves blood flow and function, there are significant associated risks, and durability may be limited, especially in infrainguinal disease. Abundant evidence demonstrates the benefits of exercise therapy in claudication, yet the mechanisms underlying the beneficial effects remain incompletely defined. 11 Thus, ...

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“…This decrease is attributed to reduced oxygen and not to deficient oxidative phosphorylation [157–160]. Apart from changes in oxidative metabolism, PAD patients with whole body insulin resistance exhibit decreased glucose uptake in the calf muscle [161]. Due to increased oxidative stress in the muscle, mitochondrial damage has also been reported in PAD muscle.…”

Section: Manifestations Of Peripheral Atherosclerosis In Human Skeletmentioning

confidence: 99%

Crossroads between peripheral atherosclerosis, western-type diet and skeletal muscle pathophysiology: emphasis on apolipoprotein E deficiency and peripheral arterial disease

Sfyri

Matsakas

2017

J Biomed Sci

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Atherosclerosis is a chronic inflammatory process that, in the presence of hyperlipidaemia, promotes the formation of atheromatous plaques in large vessels of the cardiovascular system. It also affects peripheral arteries with major implications for a number of other non-vascular tissues such as the skeletal muscle, the liver and the kidney. The aim of this review is to critically discuss and assimilate current knowledge on the impact of peripheral atherosclerosis and its implications on skeletal muscle homeostasis. Accumulating data suggests that manifestations of peripheral atherosclerosis in skeletal muscle originates in a combination of increased i)-oxidative stress, ii)-inflammation, iii)-mitochondrial deficits, iv)-altered myofibre morphology and fibrosis, v)-chronic ischemia followed by impaired oxygen supply, vi)-reduced capillary density, vii)- proteolysis and viii)-apoptosis. These structural, biochemical and pathophysiological alterations impact on skeletal muscle metabolic and physiologic homeostasis and its capacity to generate force, which further affects the individual’s quality of life. Particular emphasis is given on two major areas representing basic and applied science respectively: a)-the abundant evidence from a well-recognised atherogenic model; the Apolipoprotein E deficient mouse and the role of a western-type diet and b)-on skeletal myopathy and oxidative stress-induced myofibre damage from human studies on peripheral arterial disease. A significant source of reactive oxygen species production and oxidative stress in cardiovascular disease is the family of NADPH oxidases that contribute to several pathologies. Finally, strategies targeting NADPH oxidases in skeletal muscle in an attempt to attenuate cellular oxidative stress are highlighted, providing a better understanding of the crossroads between peripheral atherosclerosis and skeletal muscle pathophysiology.

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Impaired Skeletal Muscle Glucose Uptake by [ ¹⁸ F]Fluorodeoxyglucose–Positron Emission Tomography in Patients With Peripheral Artery Disease and Intermittent Claudication

Cited by 26 publications

References 29 publications

Experimental peripheral arterial disease: new insights into muscle glucose uptake, macrophage, and T-cell polarization during early and late stages

Experimental peripheral arterial disease: new insights into muscle glucose uptake, macrophage, and T-cell polarization during early and late stages

Pathophysiology of Intermittent Claudication in Peripheral Artery Disease

Crossroads between peripheral atherosclerosis, western-type diet and skeletal muscle pathophysiology: emphasis on apolipoprotein E deficiency and peripheral arterial disease

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Impaired Skeletal Muscle Glucose Uptake by [ 18 F]Fluorodeoxyglucose–Positron Emission Tomography in Patients With Peripheral Artery Disease and Intermittent Claudication

Cited by 26 publications

References 29 publications

Experimental peripheral arterial disease: new insights into muscle glucose uptake, macrophage, and T-cell polarization during early and late stages

Experimental peripheral arterial disease: new insights into muscle glucose uptake, macrophage, and T-cell polarization during early and late stages

Pathophysiology of Intermittent Claudication in Peripheral Artery Disease

Crossroads between peripheral atherosclerosis, western-type diet and skeletal muscle pathophysiology: emphasis on apolipoprotein E deficiency and peripheral arterial disease

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Product

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Impaired Skeletal Muscle Glucose Uptake by [ ¹⁸ F]Fluorodeoxyglucose–Positron Emission Tomography in Patients With Peripheral Artery Disease and Intermittent Claudication