Nonalcoholic fatty liver disease is related to nonalcoholic fatty pancreas disease.
ABSTRACT Obesity and insulin resistance cause fatty infiltration of many organs, including the pancreas (pancreatic steatosis [PS]) and the liver (nonalcoholic fatty liver disease [NAFLD]). In contrast to NAFLD, pathophysiological mechanisms and clinical relevance of PS remain unknown. This study aimed to identify a possible relation between PS and NAFLD.
In this study including postmortem collected material of 80 patients, clinical and histological data were collected and revised. Patients with hepatic or pancreatic disease and alcohol abuse were excluded. Nonalcoholic fatty liver disease activity score was used for grading the histology of the liver, whereas pancreatic lipomatosis score assessed PS. Ordinal logistic regression was used to analyze correlations.
Interlobular and total pancreatic fat were both related to NAFLD activity score in patients without steatogenic medication (P = 0.02 and P = 0.03, respectively). When corrected for body mass index, no relation could be found. Total pancreatic fat was a significant predictor for the presence of NAFLD (P = 0.02). Presence of intralobular pancreatic fat was related to nonalcoholic steatohepatitis; however, total fat was not.
This study demonstrates that NAFLD and PS are related. This relationship seems to be mediated by general obesity. Intralobular pancreatic fat is associated with nonalcoholic steatohepatitis.
Article: Pancreatic fat accumulation and its relationship with liver fat content and other fat depots in obese individuals.[show abstract] [hide abstract]
ABSTRACT: We assessed the associations between pancreatic fat accumulation and other fat compartments, including liver fat and visceral adipose tissue as well as insulin resistance and other metabolic abnormalities in obese individuals. We studied 42 Caucasian adults with obesity [20 men and 22 women; mean body mass index (BMI) 35.2±4 kg/m2], who had no history of liver diseases or excessive alcohol consumption, in which subcutaneous, visceral, liver, and pancreatic fat contents were quantified by an in-opposed-phase magnetic resonance imaging (MRI) technique. Compared with patients in the lower tertile (<5.6%, no.=15), those in the upper tertile of liver fat content had more visceral adipose tissue, greater insulin resistance and had higher values of BMI, blood pressure, triglycerides and lower HDL-cholesterol and adiponectin. Notably, pancreatic fat accumulation also significantly increased across tertiles of liver fat content. In univariate analysis, the strongest correlates of pancreatic fat were visceral and liver fat contents (r=0.80 and r=0.54, p<0.001- 0.0001, respectively). Pancreatic fat accumulation was also moderately associated with insulin resistance and other metabolic syndrome features. However, when adjusted for age, gender and visceral adipose tissue, the associations of pancreatic fat accumulation with liver fat and other metabolic abnormalities were no longer significant. There are significant associations between pancreatic fat accumulation and liver fat content as well as insulin resistance and other metabolic abnormalities in obese, but otherwise healthy, individuals. However, these associations are largely mediated by the amount of visceral adipose tissue.Journal of endocrinological investigation 10/2011; 35(8):748-53. · 1.57 Impact Factor
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ABSTRACT: Little is known about pancreatic fat accumulation and its possible associations with metabolic syndrome (MetS) and glucose metabolism. The aim of the present study was to quantify pancreatic fat fraction (PFF) in lean and obese adolescents and explore its relation to metabolic parameters. We recruited 25 lean and 24 obese adolescents. PFF and visceral adipose tissue (VAT) were determined using magnetic resonance imaging. We measured blood pressure, fasting glucose, insulin, liver enzymes, leptin, and lipid levels. Obese subjects underwent an oral glucose tolerance test. PFF was significantly higher in obese than in lean subjects (4.8±1.2 vs 3.6±0.9; P<0.001) and was associated with VAT, γ-glutamyltransferase, triglycerides, high-density lipoprotein cholesterol, leptin concentrations, and MetS (P<0.05 for all). None of the obese subjects had glucose intolerance, but when adjusted for VAT, the following 3 parameters correlated negatively with PFF: fasting and 30- minute and 120-minute insulin levels. We divided subjects into 3 groups: group I, lean without MetS; group II, obese without MetS; and group III, obese with MetS, and observed that PFF increased gradually among groups (I: 3.56%±0.88%; II: 4.70%±1.06%; III: 5.34%±1.49%; P<0.001). Obese adolescents accumulate fat in the pancreas. PFF correlates with the presence of MetS. Even in the absence of glucose intolerance, pancreatic fat deposition is associated with impaired insulin response to glucose overload. This suggests that β-cell dysfunction may already be present in nondiabetic obese adolescents, mirroring what has been shown in adults, and that pancreatic fat accumulation may participate in obesity-associated pancreatic endocrine dysfunction.Journal of pediatric gastroenterology and nutrition 12/2011; 54(6):720-6. · 2.18 Impact Factor