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 in | Diabetes (New York, N.Y.) Vol. 56; no. 2; pp. 444 - 449 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Diabetes Association
01.02.2007
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Subjects | |
Online Access | Get full text |
ISSN | 0012-1797 1939-327X 1939-327X |
DOI | 10.2337/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 |
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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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Keywords | Endocrinopathy Human Skin disease Enzyme Diabetes mellitus Triacylglycerol lipase Lipomatosis Esterases Carboxylic ester hydrolases Hydrolases Adipose tissue disorders Benign neoplasm Mutation Pancreas Child |
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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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StartPage | 444 |
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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