Study Design. A cross-sectional study. Objective. To investigate and compare any morphological differences in paraspinal muscles (PSM) between adolescent idiopathic scoliosis (AIS) patients (with severe or non-severe curves) and healthy controls. Summary of Background Data. Several studies have reported abnormalities in biochemical, electromyographic activity, and histological changes of PSM in AIS. However, these studies only had qualitative data and without comparison with controls. Changes of muscle mass and mean density at the lumbar region have been described for scoliotic spines. All these findings suggested that imbalance of PSM in AIS could be a contributing factor to the development of severe scoliotic curve. Methods. T2-weighted MR images with multi-planar reconstruction were acquired in 41 Chinese AIS girls with a primary right-sided thoracic curve and 23 age-matched controls. In AIS, measurements of PSM were taken on both concavity and convexity of scoliosis starting from two vertebrae above and two below the apex. Morphological assessments of the multifidus (MF) and erector spinae (ES) muscles on both sides were made including signal intensity (SI) and fat deposition using manual tracing and thresholding technique, respectively. Same parameters were measured in controls at matched vertebrae. One-way analysis of variance (ANOVA) and Pearson correlation tests were used for statistical analysis. Results. Abnormalities were found at concavity of muscles between AIS and controls. Significantly higher SI and fatty components was observed in AIS at MF muscles on concavity than controls (P-value <0.001). Additionally, SI at MF muscles was significantly correlated with Cobb angle. Conclusion. Increased SI and fatty components are asymmetrically present in PSM at apex in AIS. Our results showed higher intensity in PSM at concavity in AIS when compared with controls. There was a significant linear correlation between abnormal muscle signal and scoliotic curve. Above features are suggestive of altered muscle composition in concave PSM, possibly due to prolonged compression and reduced muscle activity of PSM caused by the spinal deformity. Level of Evidence: 4

INTRODUCTION: Visceral adipose tissue (VAT) has been found to play a critical role in the development of metabolic syndrome and nonalcoholic fatty liver disease (NAFLD) independent of generalized obesity. METHODS: In this secondary study of prospectively acquired data, 625 participants underwent magnetic resonance spectroscopy and chemical shift fat–water separation MRI (2-point Dixon) of the liver and whole abdomen, respectively, in a 3 Tesla magnet. Whole abdominal VAT and subcutaneous adipose tissue (SAT) were extracted from the 2-point Dixon image series using an automated method. Clinical/anthropometric/blood biochemistry parameters were measured. Using region-specific body mass index, participants were classified into 3 paired subgroups (lean, overweight, and obese) and presence of NAFLD (liver fat content ≥ 5.5%). RESULTS: All relevant clinical/anthropometric/blood biochemistry characteristics and liver enzymes were statistically significant between groups (P < 0.001). NAFLD was found in 12.1%, 43.8%, and 68.3% and metabolic syndrome in 51.1%, 61.9%, and 65% of the lean, overweight, and obese, respectively. Odds ratio for metabolic syndrome and NAFLD was increased by 2.73 (95% confidence interval [CI] 2.18–3.40) and 2.53 (95% CI 2.04–3.12), respectively, for 1SD increase in VAT volume while prevalence of metabolic syndrome was increased by 2.26 (95% CI 1.83–2.79) for 1SD increase in liver fat content (%). VAT/SAT ratio in the lean with fatty liver showed the highest ratio (0.54) among all the subgroups, without a significant difference between the lean and obese with NAFLD (P = 0.127). DISCUSSION: Increased VAT volume/disproportional distribution of VAT/SAT may be vital drivers to the development of metabolic syndrome and NAFLD irrespective of body mass index category.

Summary Background The incidence of childhood obesity and associated comorbidities are on an increasing trend worldwide. More than 340 million children and adolescents aged between 5 and 19 years old were overweight or had obesity in 2016, from which over 124 million children and adolescents (6% of girls and 8% of boys) had obesity. Objective To describe the relationship between pancreas steatosis, body fat and the risk of metabolic syndrome, insulin resistance in Hong Kong Chinese adolescents with both obesity and non‐alcoholic fatty liver disease (NAFLD). Methods Fifty two adolescents with obesity and NAFLD were analysed (14‐18 years), stratified into fatty and non‐fatty pancreas groups using chemical shift encoded MRI‐pancreas proton density fat fraction ≥ 5%. Pancreatic, abdominal subcutaneous adipose tissue (SAT)/visceral adipose tissue (VAT) volumes, biochemical and anthropometric parameters were measured. Mann‐Whitney U test, multiple linear/binary logistic regression analyses and odds ratios were used. Results Fifty percent had fatty pancreas, 38% had metabolic syndrome and 81% had insulin resistance. Liver proton density fat fraction (PDFF) and VAT were independent predictors of insulin resistance ( P = .006, .016). Pancreas and liver PDFF were both independent predictors of beta cells dysfunction ( P = .015, .050) and metabolic syndrome ( P = .021, .041). Presence of fatty pancreas in obesity was associated with insulin resistance (OR = 1.58, 95% CI = 0.39‐6.4) and metabolic syndrome (OR = 1.70, 95% CI = 0.53‐5.5). Conclusion A significant causal relationship exists between fatty pancreas, fatty liver, body fat and the risk of developing metabolic syndrome and insulin resistance. Key Points Fatty pancreas is a common finding in adolescents with obesity, with a prevalence rate of 50% in this study cohort. Liver PDFF and VAT are independent predictors of insulin resistance while pancreas PDFF and liver PDFF are independent predictors of both beta cells dysfunction and metabolic syndrome. Presence of fatty pancreas at imaging should not be considered as a benign finding but rather as an imaging biomarker of emerging pancreatic metabolic and endocrine dysfunction.

Metabolic syndrome and Non-alcoholic fatty liver disease are common findings in obesity. In both conditions, despite many proposed mechanisms to their development, changes in adipose tissue vis-à-vis visceral adipose tissue as a highly metabolically active tissue seem to be a common pathway to their development in both the lean and obese populations.In this review, we detail how the changes that occur in adipose tissue are linked to the development of both metabolic syndrome and non-alcoholic fatty liver disease.