In persons with SCI, the usual clinical measures of total body fat, such as weight and body mass index (BMI), underestimate the degree of adiposity (Bauman et al. 1997; Mollinger et al. 1985; Spungen et al. 1993; Spungen et al. 2000; Spungen et al. 2003). The metabolic alterations related to adverse body composition changes, decreased physical activity and other factors in individuals with SCI are considered atherogenic (Maki et al. 1995; National Cholesterol Education Program 2001, 2002). Even a mild decline in glucose tolerance is associated with insulin resistance and hyperinsulinemia, which are also considered atherogenic (Haffner et al. 1990).
Many factors contribute to increased risk of insulin resistance and hyperinsulinemia, glucose intolerance, CVD and obesity in persons with SCI. These factors tend to correlate with the severity and level of the neurological deficit (Javierre et al. 2005). It is hypothesized that the decreased lean muscle mass and increased adipose tissue which follow a SCI lead to impaired glucose uptake and an imbalance in whole body glucose homeostasis (Javierre et al. 2005). Pathogenesis of SCI combined with lifestyle practices impact blood glucose management thereby increasing the risk of morbidity and mortality due to CVDs, a frequent cause of death among persons with SCI (Arrowwood et al. 1987; Javierre et al. 2005; Yekutiel et al. 1989). Abnormalities in lipid metabolism in SCI develop early following injury and tend to progress over time (Brenes et al. 1986; Bauman et al. 1992; Kocina 1997; Szlachcic et al. 2001). Insulin resistance and exaggerated hyperinsulinemia in response to an oral glucose challenge are associated with the development of type II diabetes mellitus, atherosclerosis and ischemic heart disease (Bauman et al. 1992; Defronzo et al. 1991; Duckworth et al. 1983; Mohr et al. 2001). Conventional risk factors for coronary heart disease should be identified and treated aggressively in individuals with SCI according to current standards of care (Bauman & Spungen 2008).
Four studies have examined altered glucose metabolism in individuals after a SCI (Bauman et al. 1999; Bauman & Spungen 1994; Bennegard & Karlsson 2008, Battram et al. 2007). Significantly higher serum glucose concentration and diabetes mellitus was seen in persons with complete tetraplegia than any other classification of SCI (Bauman et al. 1999). Gender had no effect on level of serum glucose; however, men had greater insulin levels than women (p<0.05; Bauman et al. 1999). In the remaining two studies, fasting glucose levels were compared between individuals with and without SCI. Bauman and Spungen (1994) reported that 38% and 50% of individuals with tetraplegia and paraplegia, respectively, had normal oral glucose tolerance compared to 83% of the non-SCI control group. Their findings were supported by Bennegard and Karlsson (2008) who reported a significantly higher glucose uptake in individuals with SCI compared to non-SCI controls. Those with SCI had higher plasma flow rate in their legs compared to the controls; however, lean tissue mass was lower than those without SCI (Bennegard & Karlsson 2008). Battram et al. (2007) found that caffeine ingestion does not impair glucose tolerance in tetraplegics as well.
Recent research has begun to examine the altered glucose response in relation to visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT). Gorgey and Gater (2011) examined 32 males with SCI (mean body mass=74±14 kg; mean BMI=23.5±4.5) after an overnight glucose fast and found that both leg and trunk fat mass were associated with an altered metabolic profile. Further, those with tetraplegia (n=7) had greater leg, trunk and body fat mass than those with paraplegia (n=25). Fasting glucose was higher and the resting metabolic rate was 18% lower in those with tetraplegia than in those with paraplegia (p<0.05). Similarly, Gorgey et al. (2011) assessed VAT and SAT among 13 males with SCI (mean body mass=74±13 kg; mean BMI=23±4) after an overnight glucose fast. The authors reported that individuals with VAT >100 cm2 had higher fasting plasma glucose compared to those with <100 cm2; further, VAT and SAT were associated with an altered metabolic profile. Although Gorgey and Gater (2011) and Gorgey et al. (2011) have presented a connection between fat mass and altered glucose response in individuals with SCI, the findings were conflicted with regard to lipid profile.
Altered lipid metabolism is apparent in the SCI population. In a prospective controlled trial, Ketover et al. (1996), evaluated gallbladder emptying in non-SCI individuals compared to persons with SCI after administering liquid meal (20 g fat). Both groups demonstrated similar gallbladder emptying and volumes post interventions; however, diabetic and obese subjects with SCI showed poor gallbladder emptying (Ketover et al. 1996).
There are a significant number of other biochemical changes in serum concentrations that occur after a SCI. Studies that examine these trends without specific regard to nutritional status or intervention have been placed in either the Aging Chapter or Cardiovascular Chapter. Please review those chapters for further exploration of resting glucose, insulin, lipid and other blood levels post SCI.
There is level 2 evidence (from one prospective controlled trial and one cohort study: Bennegard & Karlsson 2008; Bauman & Spungen 1994) that glucose uptake is higher in paralyzed, spastic legs of SCI subjects than in able-bodied controls. There is a regional difference in glucose uptake in able-bodied with a lower uptake in legs than in arms.
There is level 2 evidence (from one cohort study and one pre-post study: Bauman & Spungen 1994; Bauman et al. 1999) that SCI individuals with tetraplegia have higher rates of altered glucose metabolism than other SCI individuals.
There is level 2 evidence (from one prospective controlled trial: Ketover et al. 1996) that diabetic and obese SCI individuals show impaired gallbladder emptying in response to a high fat meal compared to healthy SCI individuals.