Circulatory Adipokines and Incretins in Adolescent Idiopathic Scoliosis: A Pilot Study

Abstract

Adolescent idiopathic scoliosis (AIS) is a three-dimensional malformation of the spine of unknown cause that develops between 10 and 18 years old and affects 2–3% of adolescents, mostly girls. It has been reported that girls with AIS have a taller stature, lower body mass index (BMI), and bone mineral density (BMD) than their peers, but the causes remain unexplained. Energy metabolism discrepancies, including alterations in adipokine and incretin circulatory levels, could influence these parameters and contribute to disease pathophysiology. This pilot study aims to compare the anthropometry, BMD, and metabolic profile of 19 AIS girls to 19 age-matched healthy controls. Collected data include participants' fasting metabolic profile, anthropometry (measurements and DXA scan), nutritional intake, and physical activity level. AIS girls (14.8 ± 1.7 years, Cobb angle 27 ± 10°), compared to controls (14.8 ± 2.1 years), were leaner (BMI-for-age z-score ± SD: −0.59 ± 0.81 vs. 0.09 ± 1.11, p = 0.016; fat percentage: 24.4 ± 5.9 vs. 29.2 ± 7.2%, p = 0.036), had lower BMD (total body without head z-score ± SD: −0.6 ± 0.83 vs. 0.23 ± 0.98, p = 0.038; femoral neck z-score: −0.54 ± 1.20 vs. 0.59 ± 1.59, p = 0.043), but their height was similar. AIS girls had higher adiponectin levels [56 (9–287) vs. 32 (7–74) ug/mL, p = 0.005] and lower leptin/adiponectin ratio [0.042 (0.005–0.320) vs. 0.258 (0.024–1.053), p = 0.005]. AIS participants with a Cobb angle superior to 25° had higher resistin levels compared to controls [98.2 (12.8–287.2) vs. 32.1 (6.6–73.8), p = 0.0013]. This pilot study suggests that adipokines are implicated in AIS development and/or progression, but more work is needed to confirm their role in the disease.

Investigating the Differential Circulating microRNA Expression in Adolescent Females with Severe Idiopathic Scoliosis: A Proof-of-Concept Observational Clinical Study

“…In mice, the high production of hepatic serum amyloid A1 promoted chronic inflammation and caused bone loss [ 97 ]. Regarding cofilin-1, a recent pilot study reported adipokines were implicated also in AIS development and progression [ 98 ]. Bisphosphonates disrupts actin organization and decreases in vitro cofilin levels, an actin regulatory protein that severs actin filaments [ 99 ].…”

Metabolic Imbalances and Bone Remodeling Agents in Adolescent Idiopathic Scoliosis: A Study in Postmenarcheal Girls

“…Disturbance in the lipid profile has also been suggested as a marker of AIS [15]. In addition, the literature data indicate that abnormal levels of many hormones, including estrogen, melatonin, growth hormone, leptin, adiponectin, calmodulin, and ghrelin, may be related to the development and progression of AIS [10,[16][17][18][19][20]. Furthermore, recently published studies have highlighted body composition as an essential factor in the onset and development of AIS [21,22].…”