The relationship between the postprandial lipemic response and lipid composition in persons with spinal cord injury

Abstract

Objective: To determine the influence of lipid concentration, lipid particle size, and total abdominal fat (TAF) on postprandial lipemic response (PPLr) in persons with spinal cord injury (SCI). Methods: Thirty-five persons with SCI (17 paraplegia, 18 tetraplegia) and 18 able-bodied (AB) individuals participated. Following a 10-hour fast, blood was drawn for lipids, apolipoprotein (apo) A1 and B concentrations, and low-density (LSP) and high-density (HSP) lipoprotein particle sizes. A high-fat milkshake was consumed (∼1.3 g fat/kg). Blood was drawn at 2, 4, and 6 hours to determine PPLr, (triglyceride (TG) area under the curve). TAF and visceral (VF) fat were measured by ultrasonography; total body fat (TBF) by dual-energy X-ray absorptiometry. Differences between the groups were determined by independent sample t-tests. Pearson correlation coefficients determined the relationship among PPLr and lipids, and TAF. Results: There were no significant differences in fasting TG, low-density lipoprotein (LDL), apoB, TAF, or PPLr values between the groups. In SCI, PPLr significantly correlated with: apoB (r = 0.63, P < 0.01, LSP (r = 0.57, P < 0.01), and TAF (r = 0.36, P < 0.01). After controlling for age and duration of injury, PPLr significantly correlated with apoB (r = 0.66, P = 0.001), TBF (r = 0.45, P = 0.03), VF (r = 0.66, P = 0.02), and TAF (r = 0.56, P = 0.007). Conclusions: Although concentrations of LDL cholesterol and apoB were not different between SCI and AB groups, LSP, apoB, and TAF correlated with PPLr in persons with SCI. ApoB was associated with a greater PPLr in those with motor complete SCI, after controlling for age and duration of injury.

Effect of Paraplegia on the Time Course of Exogenous Fatty Acid Incorporation Into the Plasma Triacylglycerol Pool in the Postprandial State

“…Clinical practice guidelines for CMD in this population acknowledge SCI’s pronounced effect on obesity and dyslipidemia ( Nash et al, 2019 ), and impaired postprandial fat metabolism has been described ( Nash et al, 2005 ; Emmons et al, 2010 , 2014 ; Ellenbroek et al, 2014 ). However, the mechanisms of impaired postprandial fat metabolism have yet to be understood.…”

“…The Consortium for Spinal Cord Medicine’s recent Clinical Practice Guidelines for diagnosis and management of CMD in SCI ( Nash et al, 2019 ) note a high prevalence of obesity and unique clustering of CMD risk factors related to fat metabolism ( Libin et al, 2013 ). Unique dyslipidemia following SCI includes an increased adiposity per unit body mass index (BMI) ( Spungen et al, 2000 ; Clasey and Gater, 2005 ; Gorgey and Gater, 2011 ; Gorgey et al, 2011 ; Yarar-Fisher et al, 2013 ; Beck et al, 2014 ; Cirnigliaro et al, 2015 ), reduced high-density lipoproteins (HDL) ( Bauman et al, 1999 ; Myers et al, 2007 ; Groah et al, 2009 ; Wahman et al, 2010 ), elevated fasted triglyceride (TAG) ( Bauman et al, 1999 ; Myers et al, 2007 ; Groah et al, 2009 ; Wahman et al, 2010 ), and exaggerated postprandial lipemia ( Nash et al, 2005 ; Emmons et al, 2010 , 2014 ; Ellenbroek et al, 2014 ). Despite the plausible dietary contributions to dyslipidemia in SCI ( Bigford and Nash, 2017 ), little is known about the acute physiological and fat trafficking responses to feeding in SCI persons.…”

The Physiology of Neurogenic Obesity: Lessons from Spinal Cord Injury Research

“…The combined effect of decreased skeletal cross-sectional area and increased intramuscular fat is an independent predictor of plasma glucose responses during an oral glucose tolerance test and has been thought to be a potential contributor to insulin resistance following SCI [84]. Importantly, findings from PwSCI demonstrate that skeletal muscle is the largest body reservoir for nutrient metabolism, including ingested fats [85].…”

Effects of Exercise Mode on Postprandial Metabolism in Humans with Chronic Paraplegia

“…The finding of dysglycemia despite normal fasted glucose levels demonstrates how metabolic changes after SCI seem dormant until the system is presented with a challenge. Similarly, dyslipidemia can occur in SCI despite a “normal” serum triglyceride (TG) concentration (10), whereas laboratory postprandial lipemia (PPL) tests have consistently shown an impaired ability to handle an oral lipid challenge (11–14). When also considering obesity and intermuscular fat accumulation (15) in this population, it seems that disorders of fat metabolism are paramount in the development of CMD in SCI.…”