Adiposity and spinal cord injury

Gorgey, Ashraf S.

doi:10.5312/wjo.v6.i8.567

Cited by 29 publications

(23 citation statements)

References 51 publications

(146 reference statements)

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“…waist circumference) in subjects with SCI [46–48]. More recent advances in in vivo imaging modalities open new possibilities for determining organ specific masses, fat infiltration in non-adipose depots and regional distributions of body fat (subcutaneous versus visceral) which have been shown to differentially influence disease risk and will be important for understanding the changes that occur in subjects following SCI [49–51]. …”

Section: Metabolism-related Alterations Following Spinal Cord Injurymentioning

confidence: 99%

Contributors to Metabolic Disease Risk Following Spinal Cord Injury

Smith

Yarar‐Fisher

2016

Curr Phys Med Rehabil Rep

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Spinal cord injury (SCI) induced changes in neurological function have significant impact on the metabolism and subsequent metabolic-related disease risk in injured individuals. This metabolic-related disease risk relationship is differential depending on the anatomic level and severity of the injury, with high level anatomic injuries contributing a greater risk of glucose and lipid dysregulation resulting in type 2 diabetes and cardiovascular disease risk elevation. Although alterations in body composition, particularly excess adiposity and its anatomical distribution in the visceral depot or ectopic location in non-adipose organs, is known to significantly contribute to metabolic disease risk, changes in fat mass and fat-free mass do not fully account for this elevated disease risk in subjects with SCI. There are other negative adaptations in body composition including reductions in skeletal muscle mass and alterations in muscle fiber type, in addition to significant reduction in physical activity, that contribute to a decline in metabolic rate and increased metabolic disease risk following SCI. Recent studies in adult humans suggest cold- and diet-induced thermogenesis through brown adipose tissue metabolism may be important for energy balance and substrate metabolism, and particularly sensitive to sympathetic nervous signaling. Considering the alterations that occur in the autonomic nervous system (SNS) (sympathetic and parasympathetic) following a SCI, significant dysfunction of brown adipose function is expected. This review will highlight metabolic alterations following SCI and integrate findings from brown adipose tissue studies as potential new areas of research to pursue.

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Section: Metabolism-related Alterations Following Spinal Cord Injurymentioning

confidence: 99%

Contributors to Metabolic Disease Risk Following Spinal Cord Injury

Smith

Yarar‐Fisher

2016

Curr Phys Med Rehabil Rep

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“…Mediators of cellular and subcellular oxidative stress have received considerable attention as potential novel neuroprotective targets in acute SCI, including the involved genes, proteins and factors [2,4,8,12]. PAMM is a promising candidate biomarker for SCI because of its dual independent anti-inflammatory and anti-oxidant properties, and because SCI is characterized by both oxidative stress and inflammatory reaction [13][14][15].…”

Section: Discussionmentioning

confidence: 99%

Circulating PAMM, a novel antioxidant and anti-inflammatory protein, is elevated in acute SCI

Morse

Nguyen

et al. 2020

J Transl Med

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Background: Peroxiredoxin activated in M-CSF stimulated monocytes (PAMM) is a novel protein produced by adipocytes with putative redox regulatory and anti-inflammatory properties. Because acute spinal cord injury (SCI) is associated with oxidative stress and neuroinflammation and because PAMM can be detected in systemic circulation, we hypothesized that acute neuro-trauma might induce changes in circulating PAMM expression. Specifically, we hypothesized that PAMM levels might vary based on the presence or absence of acute, traumatic SCI. We therefore investigated circulating PAMM levels in adults with and without acute traumatic SCI. Methods:We studied 105 men and women (54 with SCI and 51 without SCI). Participants with SCI were admitted for acute rehabilitation within 1 month after injury. Serum samples were obtained during hospitalization and stored at − 80 °C until batch analysis. Total PAMM was quantified by ELISA assay (MyBiosource, Cat. No: MBS9327247) with a detection limit of 0.25 ng/ml. Separate multivariate models including age, BMI, and injury severity were assessed to determine significant clinical predictors of change in PAMM levels.Results: When adjusting for BMI, age, and gender, mean change in PAMM levels were greatest in participants with motor complete SCI compared to able-bodied (1.65 ng/ml versus 0.94 ng/ml, p = 0.003). This model explained 26% of the variation in change in circulating PAMM levels. Conclusions:Our results suggest that PAMM may be a novel biomarker of neurological injury or of native antiinflammatory responses to neurological injury. More work is needed to establish the role of PAMM and other adipocyte-derived factors in the acute response to neurotrauma.

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“…The CSAs of total trunk, VAT, and SAT were analyzed using Win Vessel 2.0 software (Ronald Meyer, PhD, Michigan State University). A detailed description of imaging analysis of SAT and VAT are listed in the (available online) as well as previously published [8,10,11,21].…”

Section: Methodsmentioning

confidence: 99%

“…Studies have shown that increases in central adiposity is negatively associated with altered metabolic profiles in clinical populations, as well as in persons with SCI [7‐9]. Trunk adiposity is an example of regional adiposity that is characterized by an increased accumulation of truncal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) [8,10,11]. VAT has been shown to be 58% greater in persons with SCI compared to waist‐circumference matched able‐bodied controls [7].…”

Section: Introductionmentioning

confidence: 99%