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Nonalcoholic fatty pancreas disease and Nonalcoholic fatty liver disease: more than ectopic fat
C Della Corte1, A Mosca1, F Majo2
1Hepato-Metabolic Department, 'Bambino Gesù' Children's Hospital, IRCCS, Rome, Italy.
Insights
Fatty pancreas (NAFPD) is common in obese children with fatty liver disease (NAFLD). Pancreatic fat impacts glucose metabolism and liver disease severity, increasing metabolic syndrome risk.
Area of Science:
- Pediatric Endocrinology
- Hepatology
- Metabolic Disorders
Background:
- Nonalcoholic fatty liver disease (NAFLD) is prevalent in obese children.
- The metabolic implications of nonalcoholic fatty pancreas disease (NAFPD) in this population are not well understood.
- NAFPD is characterized by fat accumulation in the pancreas.
Purpose of the Study:
- To investigate the metabolic effects of NAFPD in obese pediatric patients with NAFLD.
- To assess the association between NAFPD and the severity of liver disease.
- To determine if NAFPD contributes to metabolic syndrome risk.
Main Methods:
- 121 obese children with hepatic steatosis were included.
- Abdominal ultrasound assessed pancreatic echogenicity to identify NAFPD.
- Patients underwent liver function tests, lipid profiles, and gluco-insulinemic assessments; a subset had liver biopsies.
Main Results:
- 58 of 121 patients had NAFPD.
- NAFPD patients had higher z-BMI, fasting insulin, HOMA-IR, and lower ISI compared to controls.
- NAFPD was associated with more advanced liver disease, including higher fibrosis, ballooning, and NAS scores.
Conclusions:
- NAFPD is a frequent finding in obese pediatric NAFLD patients.
- Pancreatic fat accumulation negatively impacts glucose metabolism.
- NAFPD is linked to increased liver disease severity and metabolic syndrome risk.
Objective:
The aim of this study was to evaluate the metabolic effects of fatty pancreas (nonalcoholic fatty pancreas disease - NAFPD) in a group of obese paediatric patients with nonalcoholic fatty liver disease (NAFLD).
Methods:
We included 121 consecutive children with echographic evidence of hepatic steatosis. All patients underwent to abdominal ultrasound to evaluate pancreatic echogenic pattern. We divided the patients into two groups on the basis of the presence of fatty pancreas. In all patients liver function tests, lipid and gluco-insulinemic profile were evaluated. A selected subset of patients (67) underwent to liver biopsy.
Results:
Of these 121 patients, 58 showed NAFPD and 63 patients exhibited a normal pancreatic echogenic pattern. No differences were found in age, transaminases serum levels, lipid profile and pancreatic enzymes between the two groups. The patients with NAFPD had a significantly higher z-BMI, fasting insulin, insulin resistance (HOMA-IR) and lower ISI respect to the group without fatty pancreas. The patients with fatty pancreas showed a more advanced form of liver disease, with higher values of fibrosis, ballooning and NAS score with respect to the group without NAFPD.
Conclusions:
Our study demonstrated that NAFPD is a frequent condition in obese paediatric patients affected by NAFLD. Our data suggest that pancreatic fat should not be considered an inert accumulation of fat, but as an additional factor able to affect glucose metabolism and severity of liver disease, increasing the risk of develop metabolic syndrome.
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