The relationship between pancreas steatosis and the risk of metabolic syndrome and insulin resistance in Chinese adolescents with concurrent obesity and non‐alcoholic fatty liver disease

Abstract

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.

Association between Visceral Adipose Tissue and Non-Alcoholic Steatohepatitis Histology in Patients with Known or Suspected Non-Alcoholic Fatty Liver Disease

“…There are conflicting studies in the literature about the association between abdominal fat and hepatic fat content [22,[25][26][27]. Sharma et al observed statistically significant correlations among liver fat fraction, BMI and SAT [22].…”

Pancreas Optical Clearing and 3-D Microscopy in Health and Diabetes

“…Unlike the fatty liver, in which lipid droplets accumulate in the cytoplasm in the hepatocytes, pancreatic fatty infiltration involves the fat cells (adipocytes) ectopically developing and accumulating in and around the pancreatic lobules alongside the exocrine and endocrine tissues. The fat content in the pancreas increases with age ( 90 ) and is detectable as early as in adolescence ( 91 ), and the degree is linked with obesity ( 92 – 94 ). In the progression from obesity to type 2 diabetes, the state of hyperinsulinemia is likely to accelerate the pancreatic fat accumulation due to the organ’s high insulin concentration.…”

Parallels between non-alcoholic fatty liver disease and non-alcoholic fatty pancreatic disease: looking for points of contact or regard through the lens of metabolic syndrome

“…Тесную взаимосвязь между НАЖБП, НАЖБПЖ, МС и ИР подчеркивают китайские ученые [14]. Обследовав 52 подростка с ожирением и НАЖБП в возрасте 14-18 лет, исследователи распределили детей на две в группы в зависимости от наличия/ отсутствия МРТ-признаков НАЖБПЖ (протонная плотность жировой фракции ≥5%).…”

“…Развитие стеатоза ПЖ на фоне ожирения ассоциировано с ИР (OШ 1,58; 95% ДИ 0,39-6,4) и МС (OШ 1,70; 95% ДИ 0, 5). Авторы этой работы предлагают рассматривать стеатоз ПЖ не как доброкачественную находку, обнаруженную в ходе визуализирующего исследования, а считать его биомаркером прогрессирующей метаболической и эндокринной дисфункции ПЖ [14].…”