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. 2005;28(4):320-5.
doi: 10.1080/10790268.2005.11753827.

Evidence for an exaggerated postprandial lipemia in chronic paraplegia

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Evidence for an exaggerated postprandial lipemia in chronic paraplegia

Mark S Nash et al. J Spinal Cord Med. 2005.

Abstract

Background/objective: Excessive delay in triglyceride (TG) metabolism after ingestion of dietary fat represents a significant cardiovascular disease (CVD) risk. The objective of this study was to compare the postprandial lipemic responses of individuals with paraplegia with those of healthy nondisabled individuals.

Methods: The ability of 3 recreationally active individuals with paraplegia having normal fasting TG (mean = 103 mg/dL) to metabolize TG after ingestion of a high-fat test meal was compared with a previously published cohort of 21 recreationally active individuals without paraplegia (TG mean = 86 mg/dL) who underwent identical testing. The subjects with paraplegia had venous blood taken under fasting conditions, and then ingested a milkshake containing premium ice cream blended with heavy whipping cream (approximately 92% of calories from fat). Additional blood samples were obtained at 2, 4, and 6 hours after ingestion. The area under the curve (AUC) for TG clearance for both subject groups was measured with an area planimeter.

Results: TG uptake for both groups was almost identical for the first 2 hours after ingestion. At 4 and 6 hours after ingestion, the TG levels were 50 and 35 mg/dL higher, respectively, in subjects with paraplegia than in nondisabled subjects. When corrected for small baseline differences in TG concentrations (16 mg/dL), the AUC was 46.5% greater for the group with paraplegia than in the nondisabled group. A near mirror association across time was observed between postprandial serum high-density lipoprotein cholesterol (HDL-C) and TG levels in subjects with paraplegia.

Conclusion: This case series finds an exaggerated postprandial lipemia (PPL) in persons with paraplegia with normal fasting TGs. This finding is the first evidence, in a small population, of an unreported potential CVD risk in persons with paraplegia.

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Figures

Figure 1
Figure 1. Responses of subjects with paraplegia and a nondisabled (ND) comparison group to ingestion of a high-fat meal.
Figure 2
Figure 2. Responses of subjects with paraplegia and a nondisabled (ND) comparison group to ingestion of a high-fat meal. Values are corrected to reflect changes from baseline TG concentrations.
Figure 3
Figure 3. Time-dependent effects of fat loading on concentrations of HDL-C and TG concentrations in subjects with paraplegia.

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