AIMS/HYPOTHESIS: This study aimed to perform a comprehensive analysis of interlobular, intralobular and parenchymal pancreatic fat in order to assess their respective effects on beta cell function. METHODS: Fifty-six participants (normal glucose tolerance [NGT] (n = 28), impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) (n = 14) and patients with type 2 diabetes (n = 14)) underwent a frequent-sampling OGTT and non-invasive magnetic resonance imaging (MRI; whole-body and pancreatic) and proton magnetic resonance spectroscopy ((1)H-MRS; liver and pancreatic fat). Total pancreatic fat was assessed by a standard 2 cm(3) (1)H-MRS method, intralobular fat by 1 cm(3) (1)H-MRS that avoided interlobular fat within modified DIXON (mDIXON) water images, and parenchymal fat by a validated mDIXON-MRI fat-fraction method. RESULTS: Comparison of (1)H-MRS techniques revealed an inhomogeneous distribution of interlobular and intralobular adipose tissue, which increased with decreasing glucose tolerance. mDIXON-MRI measurements provided evidence against uniform steatosis, revealing regions of parenchymal tissue void of lipid accumulation in all participants. Total (r = 0.385, p < 0.01) and intralobular pancreas adipose tissue infiltration (r = 0.310, p < 0.05) positively associated with age, but not with fasting or 2 h glucose levels, BMI or visceral fat content (all p > 0.5). Furthermore, no associations were found between total and intralobular pancreatic adipose tissue infiltration and insulin secretion or beta cell function within NGT, IFG/IGT or patients with type 2 diabetes (all p > 0.2). CONCLUSIONS/ INTERPRETATION: The pancreas does not appear to be another target organ for abnormal endocrine function because of ectopic parenchymal fat storage. No relationship was found between pancreatic adipose tissue infiltration and beta cell function, regardless of glucose tolerance status.
AIMS/HYPOTHESIS: This study aimed to perform a comprehensive analysis of interlobular, intralobular and parenchymal pancreatic fat in order to assess their respective effects on beta cell function. METHODS: Fifty-six participants (normal glucose tolerance [NGT] (n = 28), impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) (n = 14) and patients with type 2 diabetes (n = 14)) underwent a frequent-sampling OGTT and non-invasive magnetic resonance imaging (MRI; whole-body and pancreatic) and proton magnetic resonance spectroscopy ((1)H-MRS; liver and pancreatic fat). Total pancreatic fat was assessed by a standard 2 cm(3) (1)H-MRS method, intralobular fat by 1 cm(3) (1)H-MRS that avoided interlobular fat within modified DIXON (mDIXON) water images, and parenchymal fat by a validated mDIXON-MRI fat-fraction method. RESULTS: Comparison of (1)H-MRS techniques revealed an inhomogeneous distribution of interlobular and intralobular adipose tissue, which increased with decreasing glucose tolerance. mDIXON-MRI measurements provided evidence against uniform steatosis, revealing regions of parenchymal tissue void of lipid accumulation in all participants. Total (r = 0.385, p < 0.01) and intralobular pancreas adipose tissue infiltration (r = 0.310, p < 0.05) positively associated with age, but not with fasting or 2 h glucose levels, BMI or visceral fat content (all p > 0.5). Furthermore, no associations were found between total and intralobular pancreatic adipose tissue infiltration and insulin secretion or beta cell function within NGT, IFG/IGT or patients with type 2 diabetes (all p > 0.2). CONCLUSIONS/ INTERPRETATION: The pancreas does not appear to be another target organ for abnormal endocrine function because of ectopic parenchymal fat storage. No relationship was found between pancreatic adipose tissue infiltration and beta cell function, regardless of glucose tolerance status.
Authors: Lidia S Szczepaniak; Robert L Dobbins; Gregory J Metzger; Greta Sartoni-D'Ambrosia; Debbie Arbique; Wanpen Vongpatanasin; Roger Unger; Ronald G Victor Journal: Magn Reson Med Date: 2003-03 Impact factor: 4.668
Authors: M Krssak; K Falk Petersen; A Dresner; L DiPietro; S M Vogel; D L Rothman; M Roden; G I Shulman Journal: Diabetologia Date: 1999-01 Impact factor: 10.122
Authors: K M Utzschneider; R L Prigeon; J Tong; F Gerchman; D B Carr; S Zraika; J Udayasankar; B Montgomery; A Mari; S E Kahn Journal: Diabetologia Date: 2007-10-11 Impact factor: 10.122
Authors: Maarten E Tushuizen; Mathijs C Bunck; Petra J Pouwels; Saskia Bontemps; Jan Hein T van Waesberghe; Roger K Schindhelm; Andrea Mari; Robert J Heine; Michaela Diamant Journal: Diabetes Care Date: 2007-07-31 Impact factor: 19.112
Authors: Alexandra Kautzky-Willer; Martin Krssak; Christine Winzer; Giovanni Pacini; Andrea Tura; Serdar Farhan; Oswald Wagner; Georg Brabant; Rüdiger Horn; Harald Stingl; Barbara Schneider; Werner Waldhäusl; Michael Roden Journal: Diabetes Date: 2003-02 Impact factor: 9.461
Authors: Kristina M Utzschneider; Ronald L Prigeon; Mirjam V Faulenbach; Jenny Tong; Darcy B Carr; Edward J Boyko; Donna L Leonetti; Marguerite J McNeely; Wilfred Y Fujimoto; Steven E Kahn Journal: Diabetes Care Date: 2008-10-28 Impact factor: 19.112
Authors: Mads J Skytte; Amirsalar Samkani; Amy D Petersen; Mads N Thomsen; Arne Astrup; Elizaveta Chabanova; Jan Frystyk; Jens J Holst; Henrik S Thomsen; Sten Madsbad; Thomas M Larsen; Steen B Haugaard; Thure Krarup Journal: Diabetologia Date: 2019-07-23 Impact factor: 10.122
Authors: Daniel M Tremmel; Austin K Feeney; Samantha A Mitchell; Peter J Chlebeck; Sierra A Raglin; Luis A Fernandez; Jon S Odorico; Sara D Sackett Journal: Am J Transplant Date: 2019-12-16 Impact factor: 8.086