Pancreatic Lipomatosis Is a Structural Marker in Nondiabetic Children With Mutations in Carboxyl-Ester Lipase

Pancreatic Lipomatosis Is a Structural Marker in Nondiabetic Children With Mutations in Carboxyl-Ester Lipase Helge Ræder 1 , Ingfrid S. Haldorsen 2 , Lars Ersland 3 , Renate Grüner 4 , Torfinn Taxt 4 , Oddmund Søvik 1 , Anders Molven 5 6 and Pål R. Njølstad 1 7 1 Section for Pediatrics, Department...

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Published inDiabetes (New York, N.Y.) Vol. 56; no. 2; pp. 444 - 449
Main Authors RAEDER, Helge, HALDORSEN, Ingfrid S, ERSLAND, Lars, GRFÜNER, Renate, TAXT, Torfinn, SØVIK, Oddmund, MOLVEN, Anders, NJØLSTAD, Pal R
Format Journal Article
LanguageEnglish
Published Alexandria, VA American Diabetes Association 01.02.2007
Subjects
Online AccessGet full text
ISSN0012-1797
1939-327X
1939-327X
DOI10.2337/db06-0859

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Abstract Pancreatic Lipomatosis Is a Structural Marker in Nondiabetic Children With Mutations in Carboxyl-Ester Lipase Helge Ræder 1 , Ingfrid S. Haldorsen 2 , Lars Ersland 3 , Renate Grüner 4 , Torfinn Taxt 4 , Oddmund Søvik 1 , Anders Molven 5 6 and Pål R. Njølstad 1 7 1 Section for Pediatrics, Department of Clinical Medicine, University of Bergen, Bergen, Norway 2 Section for Radiology, Department of Surgery, University of Bergen, Bergen, Norway 3 Department of Clinical Engineering, Haukeland University Hospital, Bergen, Norway 4 Department of Biomedicine, University of Bergen, Bergen, Norway 5 Section for Pathology, the Gade Institute, University of Bergen, Norway 6 Department of Pathology, Haukeland University Hospital, Bergen, Norway 7 Department of Pediatrics, Haukeland University Hospital, Bergen, Norway Address correspondence and reprint requests to Prof. Pål Rasmus Njølstad, MD PhD, Section for Pediatrics, Department of Clinical Medicine, University of Bergen, N-5020 Bergen, Norway. E-mail: pal.njolstad{at}uib.no Abstract Both pancreatic volume reduction and lipomatosis have been observed in subjects with diabetes. The underlying molecular and pathological mechanisms are, however, poorly known, and it has been speculated that both features are secondary to diabetes. We have recently described pancreatic atrophy and lipomatosis in diabetic subjects of two Norwegian families with a novel syndrome of diabetes and exocrine pancreatic dysfunction caused by heterozygous carboxyl-ester lipase ( CEL ) mutations. To explore the early pathological events in this syndrome, we performed radiological examinations of the pancreas in nondiabetic mutation carriers with signs of exocrine dysfunction. In a case series study at a tertiary hospital, we evaluated 11 nondiabetic and mutation-positive children with fecal elastase deficiency and 11 age- and sex-matched control subjects using ultrasound and magnetic resonance imaging (MRI) to estimate pancreatic fat content. The pancreata of nondiabetic mutation carriers exhibited increased reflectivity on ultrasound and had MRI findings indicative of lipomatosis. Apparently, carriers of heterozygous CEL mutations accumulate fat in their pancreas before the anticipated development of diabetes. Our findings suggest that lipomatosis of the pancreas reflects early events involved in the pathogenesis of diabetes and exocrine pancreatic dysfunction syndrome. MRI, magnetic resonance imaging VIBE, volume interpolated breath-hold examination Footnotes Additional information can be found in an online appendix at http://dx.doi.org/10.2337/db06-0859 . The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Accepted October 26, 2006. Received June 23, 2006. DIABETES
AbstractList Both pancreatic volume reduction and lipomatosis have been observed in subjects with diabetes. The underlying molecular and pathological mechanisms are, however, poorly known, and it has been speculated that both features are secondary to diabetes. We have recently described pancreatic atrophy and lipomatosis in diabetic subjects of two Norwegian families with a novel syndrome of diabetes and exocrine pancreatic dysfunction caused by heterozygous carboxyl-ester lipase (CEL) mutations. To explore the early pathological events in this syndrome, we performed radiological examinations of the pancreas in nondiabetic mutation carriers with signs of exocrine dysfunction. In a case series study at a tertiary hospital, we evaluated 11 nondiabetic and mutation-positive children with fecal elastase deficiency and 11 age- and sex-matched control subjects using ultrasound and magnetic resonance imaging (MRI) to estimate pancreatic fat content. The pancreata of nondiabetic mutation carriers exhibited increased reflectivity on ultrasound and had MRI findings indicative of lipomatosis. Apparently, carriers of heterozygous CEL mutations accumulate fat in their pancreas before the anticipated development of diabetes. Our findings suggest that lipomatosis of the pancreas reflects early events involved in the pathogenesis of diabetes and exocrine pancreatic dysfunction syndrome. Diabetes 56: 444-449, 2007
Both pancreatic volume reduction and lipomatosis have been observed in subjects with diabetes. The underlying molecular and pathological mechanisms are, however, poorly known, and it has been speculated that both features are secondary to diabetes. We have recently described pancreatic atrophy and lipomatosis in diabetic subjects of two Norwegian families with a novel syndrome of diabetes and exocrine pancreatic dysfunction caused by heterozygous carboxyl-ester lipase (CEL) mutations. To explore the early pathological events in this syndrome, we performed radiological examinations of the pancreas in nondiabetic mutation carriers with signs of exocrine dysfunction. In a case series study at a tertiary hospital, we evaluated 11 nondiabetic and mutation-positive children with fecal elastase deficiency and 11 age- and sex-matched control subjects using ultrasound and magnetic resonance imaging (MRI) to estimate pancreatic fat content. The pancreata of nondiabetic mutation carriers exhibited increased reflectivity on ultrasound and had MRI findings indicative of lipomatosis. Apparently, carriers of heterozygous CEL mutations accumulate fat in their pancreas before the anticipated development of diabetes. Our findings suggest that lipomatosis of the pancreas reflects early events involved in the pathogenesis of diabetes and exocrine pancreatic dysfunction syndrome.
Pancreatic Lipomatosis Is a Structural Marker in Nondiabetic Children With Mutations in Carboxyl-Ester Lipase Helge Ræder 1 , Ingfrid S. Haldorsen 2 , Lars Ersland 3 , Renate Grüner 4 , Torfinn Taxt 4 , Oddmund Søvik 1 , Anders Molven 5 6 and Pål R. Njølstad 1 7 1 Section for Pediatrics, Department of Clinical Medicine, University of Bergen, Bergen, Norway 2 Section for Radiology, Department of Surgery, University of Bergen, Bergen, Norway 3 Department of Clinical Engineering, Haukeland University Hospital, Bergen, Norway 4 Department of Biomedicine, University of Bergen, Bergen, Norway 5 Section for Pathology, the Gade Institute, University of Bergen, Norway 6 Department of Pathology, Haukeland University Hospital, Bergen, Norway 7 Department of Pediatrics, Haukeland University Hospital, Bergen, Norway Address correspondence and reprint requests to Prof. Pål Rasmus Njølstad, MD PhD, Section for Pediatrics, Department of Clinical Medicine, University of Bergen, N-5020 Bergen, Norway. E-mail: pal.njolstad{at}uib.no Abstract Both pancreatic volume reduction and lipomatosis have been observed in subjects with diabetes. The underlying molecular and pathological mechanisms are, however, poorly known, and it has been speculated that both features are secondary to diabetes. We have recently described pancreatic atrophy and lipomatosis in diabetic subjects of two Norwegian families with a novel syndrome of diabetes and exocrine pancreatic dysfunction caused by heterozygous carboxyl-ester lipase ( CEL ) mutations. To explore the early pathological events in this syndrome, we performed radiological examinations of the pancreas in nondiabetic mutation carriers with signs of exocrine dysfunction. In a case series study at a tertiary hospital, we evaluated 11 nondiabetic and mutation-positive children with fecal elastase deficiency and 11 age- and sex-matched control subjects using ultrasound and magnetic resonance imaging (MRI) to estimate pancreatic fat content. The pancreata of nondiabetic mutation carriers exhibited increased reflectivity on ultrasound and had MRI findings indicative of lipomatosis. Apparently, carriers of heterozygous CEL mutations accumulate fat in their pancreas before the anticipated development of diabetes. Our findings suggest that lipomatosis of the pancreas reflects early events involved in the pathogenesis of diabetes and exocrine pancreatic dysfunction syndrome. MRI, magnetic resonance imaging VIBE, volume interpolated breath-hold examination Footnotes Additional information can be found in an online appendix at http://dx.doi.org/10.2337/db06-0859 . The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Accepted October 26, 2006. Received June 23, 2006. DIABETES
Both pancreatic volume reduction and lipomatosis have been observed in subjects with diabetes. The underlying molecular and pathological mechanisms are, however, poorly known, and it has been speculated that both features are secondary to diabetes. We have recently described pancreatic atrophy and lipomatosis in diabetic subjects of two Norwegian families with a novel syndrome of diabetes and exocrine pancreatic dysfunction caused by heterozygous carboxyl-ester lipase (CEL) mutations. To explore the early pathological events in this syndrome, we performed radiological examinations of the pancreas in nondiabetic mutation carriers with signs of exocrine dysfunction. In a case series study at a tertiary hospital, we evaluated 11 nondiabetic and mutation-positive children with fecal elastase deficiency and 11 age- and sex-matched control subjects using ultrasound and magnetic resonance imaging (MRI) to estimate pancreatic fat content. The pancreata of nondiabetic mutation carriers exhibited increased reflectivity on ultrasound and had MRI findings indicative of lipomatosis. Apparently, carriers of heterozygous CEL mutations accumulate fat in their pancreas before the anticipated development of diabetes. Our findings suggest that lipomatosis of the pancreas reflects early events involved in the pathogenesis of diabetes and exocrine pancreatic dysfunction syndrome.Both pancreatic volume reduction and lipomatosis have been observed in subjects with diabetes. The underlying molecular and pathological mechanisms are, however, poorly known, and it has been speculated that both features are secondary to diabetes. We have recently described pancreatic atrophy and lipomatosis in diabetic subjects of two Norwegian families with a novel syndrome of diabetes and exocrine pancreatic dysfunction caused by heterozygous carboxyl-ester lipase (CEL) mutations. To explore the early pathological events in this syndrome, we performed radiological examinations of the pancreas in nondiabetic mutation carriers with signs of exocrine dysfunction. In a case series study at a tertiary hospital, we evaluated 11 nondiabetic and mutation-positive children with fecal elastase deficiency and 11 age- and sex-matched control subjects using ultrasound and magnetic resonance imaging (MRI) to estimate pancreatic fat content. The pancreata of nondiabetic mutation carriers exhibited increased reflectivity on ultrasound and had MRI findings indicative of lipomatosis. Apparently, carriers of heterozygous CEL mutations accumulate fat in their pancreas before the anticipated development of diabetes. Our findings suggest that lipomatosis of the pancreas reflects early events involved in the pathogenesis of diabetes and exocrine pancreatic dysfunction syndrome.
Audience Professional
Author Ingfrid S. Haldorsen
Pål R. Njølstad
Anders Molven
Oddmund Søvik
Renate Grüner
Helge Ræder
Torfinn Taxt
Lars Ersland
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  surname: RAEDER
  fullname: RAEDER, Helge
  organization: Section for Pediatrics, Department of Clinical Medicine, University of Bergen, Bergen, Norway
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  surname: HALDORSEN
  fullname: HALDORSEN, Ingfrid S
  organization: Section for Radiology, Department of Surgery, University of Bergen, Bergen, Norway
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  givenname: Lars
  surname: ERSLAND
  fullname: ERSLAND, Lars
  organization: Department of Clinical Engineering, Haukeland University Hospital, Bergen, Norway
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  givenname: Renate
  surname: GRFÜNER
  fullname: GRFÜNER, Renate
  organization: Department of Biomedicine, University of Bergen, Bergen, Norway
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  givenname: Torfinn
  surname: TAXT
  fullname: TAXT, Torfinn
  organization: Department of Biomedicine, University of Bergen, Bergen, Norway
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  givenname: Oddmund
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  fullname: SØVIK, Oddmund
  organization: Section for Pediatrics, Department of Clinical Medicine, University of Bergen, Bergen, Norway
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  givenname: Anders
  surname: MOLVEN
  fullname: MOLVEN, Anders
  organization: Section for Pathology, the Gade Institute, University of Bergen, Norway
– sequence: 8
  givenname: Pal R
  surname: NJØLSTAD
  fullname: NJØLSTAD, Pal R
  organization: Section for Pediatrics, Department of Clinical Medicine, University of Bergen, Bergen, Norway
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https://www.ncbi.nlm.nih.gov/pubmed/17259390$$D View this record in MEDLINE/PubMed
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Issue 2
Keywords Endocrinopathy
Human
Skin disease
Enzyme
Diabetes mellitus
Triacylglycerol lipase
Lipomatosis
Esterases
Carboxylic ester hydrolases
Hydrolases
Adipose tissue disorders
Benign neoplasm
Mutation
Pancreas
Child
Language English
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PublicationTitle Diabetes (New York, N.Y.)
PublicationTitleAlternate Diabetes
PublicationYear 2007
Publisher American Diabetes Association
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Snippet Pancreatic Lipomatosis Is a Structural Marker in Nondiabetic Children With Mutations in Carboxyl-Ester Lipase Helge Ræder 1 , Ingfrid S. Haldorsen 2 , Lars...
Both pancreatic volume reduction and lipomatosis have been observed in subjects with diabetes. The underlying molecular and pathological mechanisms are,...
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SubjectTerms Adolescent
Adult
Age
Atrophy
Biological and medical sciences
Carboxylesterase - genetics
Care and treatment
Child
Child, Preschool
Dermatology
Diabetes
Diabetes mellitus
Diabetes Mellitus - diagnostic imaging
Diabetes Mellitus - genetics
Diabetes Mellitus - pathology
Diabetes. Impaired glucose tolerance
Disease
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Families & family life
Female
Gene mutation
Gene mutations
Genetic aspects
Glucose
Humans
Insulin
Investigations
Lipomatosis - genetics
Magnetic Resonance Imaging
Male
Medical sciences
Mutation
Pancreas
Pancreas - diagnostic imaging
Pancreas - pathology
Pancreatic beta cells
Pancreatic Diseases - genetics
Pancreatic Elastase - deficiency
Tumors of the skin and soft tissue. Premalignant lesions
Ultrasonic imaging
Ultrasonography
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Title Pancreatic Lipomatosis Is a Structural Marker in Nondiabetic Children With Mutations in Carboxyl-Ester Lipase
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