Effect of functional sympathetic nervous system impairment of the liver and abdominal visceral adipose tissue on circulating triglyceride-rich lipoproteins

Abstract

BackgroundInterruption of sympathetic innervation to the liver and visceral adipose tissue (VAT) in animal models has been reported to reduce VAT lipolysis and hepatic secretion of very low density lipoprotein (VLDL) and concentrations of triglyceride-rich lipoprotein particles. Whether functional impairment of sympathetic nervous system (SNS) innervation to tissues of the abdominal cavity reduce circulating concentrations of triglyceride (TG) and VLDL particles (VLDL-P) was tested in men with spinal cord injury (SCI).MethodsOne hundred-three non-ambulatory men with SCI [55 subjects with neurologic injury at or proximal to the 4th thoracic vertebrae (↑T4); 48 subjects with SCI at or distal to the 5th thoracic vertebrae (↓T5)] and 53 able-bodied (AB) subjects were studied. Fasting blood samples were obtained for determination of TG, VLDL-P concentration by NMR spectroscopy, serum glucose by autoanalyzer, and plasma insulin by radioimmunoassay. VAT volume was determined by dual energy x-ray absorptiometry imaging with calculation by a validated proprietary software package.ResultsSignificant group main effects for TG and VLDL-P were present; post-hoc tests revealed that serum TG concentrations were significantly higher in ↓T5 group compared to AB and ↑T4 groups [150±9 vs. 101±8 (p<0.01) and 112±8 mg/dl (p<0.05), respectively]. VLDL-P concentration was significantly elevated in ↓T5 group compared to AB and ↑T4 groups [74±4 vs. 58±4 (p<0.05) and 55±4 μmol/l (p<0.05)]. VAT volume was significantly higher in both SCI groups than in the AB group, and HOMA-IR was higher and approached significance in the SCI groups compared to the AB group. A linear relationship between triglyceride rich lipoproteins (i.e., TG or Large VLDL-P) and VAT volume or HOMA-IR was significant only in the ↓T5 group.ConclusionsDespite a similar VAT volume and insulin resistance in both SCI groups, the ↓T5 group had significantly higher serum TG and VLDL-P values than that observed in the ↑T4 and the AB control groups. Thus, level of injury is an important determinate of the concentration of circulating triglyceride rich lipoproteins, which may play a role in the genesis of cardiometabolic dysfunction.

Gender Dimorphism in Central Adiposity May Explain Metabolic Dysfunction After Spinal Cord Injury

“…Using DXA, a recent study confirmed previous findings and showed that VAT volume was not different between persons with SCI above T4 compared to those with SCI below T5 [45]. Those with SCI below T5 experience elevated levels of TG and very-lowÀdensity lipoprotein cholesterol compared to those with SCI above T4 [45]. Contrary to findings in a rat model, an injury at T3 is likely to be accompanied by greater VAT acclamation than SCI at T10 [11].…”

“…In a preliminary study, the level of injury between tetraplegia and paraplegia did not influence distribution of VAT or SAT CSA but did influence the metabolic profile in persons with SCI [10]. Using DXA, a recent study confirmed previous findings and showed that VAT volume was not different between persons with SCI above T4 compared to those with SCI below T5 [45]. Those with SCI below T5 experience elevated levels of TG and very‐low−density lipoprotein cholesterol compared to those with SCI above T4 [45].…”

Liver Adiposity and Metabolic Profile in Individuals with Chronic Spinal Cord Injury

“…In the current study, the association between VLDL-C and liver adiposity is exemplified by the positive relationship between FSF and non-HDL-C, which confirms previous reports in able-bodied individuals [ 47 , 48 ]. Although we did not measure VLDL-C separately from LDL-C, no relationship was observed between FSF and HDL-C or LDL-C, highlighting the importance of VLDL-C related to liver metabolism [ 49 ]. Surprisingly, there was no relationship between FSF and FFA in the current study, which is in contrast to previous studies of persons with NAFLD [ 50 ].…”

Maternal high-fat diet triggers metabolic syndrome disorders that are transferred to first and second offspring generations

“…On the other hand, our present data suggest that the parasympathetic activity is not yet significantly altered because of any change in the sensitivity of the reflex bradycardia. Furthermore, it is well established in the literature that the increase in sympathetic activity induces an increase in plasma leptin (9) , dietary intakes (44,45) , adipose tissue (46,47) and IR (48,49) . In this way, in the present study, the increase in sympathetic activity must be involved in all cardio-metabolic alterations induced by the H diet of the progenitors that were transmitted to female and male F1H and F2H offspring.…”