Nonalcoholic fatty pancreas disease

Abhishek Mathur, Megan Marine, Debao Lu, Deborah A. Swartz-Basile, Romil Saxena, Nicholas J. Zyromski, Henry A. Pitt

Research output: Contribution to journalArticle

Abstract

Background. Obesity leads to fat infiltration of multiple organs including the heart, kidneys, and liver. Under conditions of oxidative stress, fat-derived cytokines are released locally and result in an inflammatory process and organ dysfunction. In the liver, fat infiltration has been termed nonalcoholic fatty liver disease, which may lead to nonalcoholic steatohepatitis. No data are available, however, on the influence of obesity on pancreatic fat and cytokines, and nonalcoholic fatty pancreas disease (NAFPD) has not been described. Therefore, we designed a study to determine whether obesity is associated with increased pancreatic fat and cytokines. Materials and methods. Thirty C57BL/6J lean control and 30 leptin-deficient obese female mice were fed a 15% fat diet for 4 weeks. At 12 weeks of age all animals underwent total pancreatectomy. Pancreata from each strain were pooled for measurement of a) wet and dry weight, b) histologic presence of fat, c) triglycerides, free fatty acids (FFAs), cholesterol, phospholipids, and total fat, and d) interleukin (IL)-1β and tumor necrosis factor-alpha (TNF-α. Data were analyzed by Student's t test and Fisher's exact test. Results. Pancreata from obese mice were heavier (p <0.05) and had more fat histologically (p <0.05). Pancreata from obese mice had more triglycerides, FFAs, cholesterol, and total fat (p <0.05). Triglycerides represented 11% of pancreatic fat in lean mice compared with 67% of pancreatic fat in obese mice (p <0.01). Cytokines IL-1β and TNF-α also were elevated in the pancreata of obese mice (p <0.05). Conclusions. These data suggest that obese mice have 1) heavier pancreata, 2) more pancreatic fat, especially triglycerides and FFAs, and 3) increased cytokines. We conclude that obesity leads to nonalcoholic fatty pancreatic disease.

Original languageEnglish (US)
Pages (from-to)312-318
Number of pages7
JournalHPB
Volume9
Issue number4
DOIs
StatePublished - 2007
Externally publishedYes

Fingerprint

Pancreas
Fats
Obese Mice
Cytokines
Triglycerides
Obesity
Nonesterified Fatty Acids
Interleukin-1
Cholesterol
Pancreatic Diseases
Pancreatectomy
Liver
Leptin
Phospholipids
Oxidative Stress
Tumor Necrosis Factor-alpha
Students
Diet
Kidney
Weights and Measures

Keywords

  • Cytokines
  • Fat
  • Obesity
  • Pancreas

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Mathur, A., Marine, M., Lu, D., Swartz-Basile, D. A., Saxena, R., Zyromski, N. J., & Pitt, H. A. (2007). Nonalcoholic fatty pancreas disease. HPB, 9(4), 312-318. https://doi.org/10.1080/13651820701504157

Nonalcoholic fatty pancreas disease. / Mathur, Abhishek; Marine, Megan; Lu, Debao; Swartz-Basile, Deborah A.; Saxena, Romil; Zyromski, Nicholas J.; Pitt, Henry A.

In: HPB, Vol. 9, No. 4, 2007, p. 312-318.

Research output: Contribution to journalArticle

Mathur, A, Marine, M, Lu, D, Swartz-Basile, DA, Saxena, R, Zyromski, NJ & Pitt, HA 2007, 'Nonalcoholic fatty pancreas disease', HPB, vol. 9, no. 4, pp. 312-318. https://doi.org/10.1080/13651820701504157
Mathur A, Marine M, Lu D, Swartz-Basile DA, Saxena R, Zyromski NJ et al. Nonalcoholic fatty pancreas disease. HPB. 2007;9(4):312-318. https://doi.org/10.1080/13651820701504157
Mathur, Abhishek ; Marine, Megan ; Lu, Debao ; Swartz-Basile, Deborah A. ; Saxena, Romil ; Zyromski, Nicholas J. ; Pitt, Henry A. / Nonalcoholic fatty pancreas disease. In: HPB. 2007 ; Vol. 9, No. 4. pp. 312-318.
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abstract = "Background. Obesity leads to fat infiltration of multiple organs including the heart, kidneys, and liver. Under conditions of oxidative stress, fat-derived cytokines are released locally and result in an inflammatory process and organ dysfunction. In the liver, fat infiltration has been termed nonalcoholic fatty liver disease, which may lead to nonalcoholic steatohepatitis. No data are available, however, on the influence of obesity on pancreatic fat and cytokines, and nonalcoholic fatty pancreas disease (NAFPD) has not been described. Therefore, we designed a study to determine whether obesity is associated with increased pancreatic fat and cytokines. Materials and methods. Thirty C57BL/6J lean control and 30 leptin-deficient obese female mice were fed a 15{\%} fat diet for 4 weeks. At 12 weeks of age all animals underwent total pancreatectomy. Pancreata from each strain were pooled for measurement of a) wet and dry weight, b) histologic presence of fat, c) triglycerides, free fatty acids (FFAs), cholesterol, phospholipids, and total fat, and d) interleukin (IL)-1β and tumor necrosis factor-alpha (TNF-α. Data were analyzed by Student's t test and Fisher's exact test. Results. Pancreata from obese mice were heavier (p <0.05) and had more fat histologically (p <0.05). Pancreata from obese mice had more triglycerides, FFAs, cholesterol, and total fat (p <0.05). Triglycerides represented 11{\%} of pancreatic fat in lean mice compared with 67{\%} of pancreatic fat in obese mice (p <0.01). Cytokines IL-1β and TNF-α also were elevated in the pancreata of obese mice (p <0.05). Conclusions. These data suggest that obese mice have 1) heavier pancreata, 2) more pancreatic fat, especially triglycerides and FFAs, and 3) increased cytokines. We conclude that obesity leads to nonalcoholic fatty pancreatic disease.",
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AU - Mathur, Abhishek

AU - Marine, Megan

AU - Lu, Debao

AU - Swartz-Basile, Deborah A.

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AU - Zyromski, Nicholas J.

AU - Pitt, Henry A.

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N2 - Background. Obesity leads to fat infiltration of multiple organs including the heart, kidneys, and liver. Under conditions of oxidative stress, fat-derived cytokines are released locally and result in an inflammatory process and organ dysfunction. In the liver, fat infiltration has been termed nonalcoholic fatty liver disease, which may lead to nonalcoholic steatohepatitis. No data are available, however, on the influence of obesity on pancreatic fat and cytokines, and nonalcoholic fatty pancreas disease (NAFPD) has not been described. Therefore, we designed a study to determine whether obesity is associated with increased pancreatic fat and cytokines. Materials and methods. Thirty C57BL/6J lean control and 30 leptin-deficient obese female mice were fed a 15% fat diet for 4 weeks. At 12 weeks of age all animals underwent total pancreatectomy. Pancreata from each strain were pooled for measurement of a) wet and dry weight, b) histologic presence of fat, c) triglycerides, free fatty acids (FFAs), cholesterol, phospholipids, and total fat, and d) interleukin (IL)-1β and tumor necrosis factor-alpha (TNF-α. Data were analyzed by Student's t test and Fisher's exact test. Results. Pancreata from obese mice were heavier (p <0.05) and had more fat histologically (p <0.05). Pancreata from obese mice had more triglycerides, FFAs, cholesterol, and total fat (p <0.05). Triglycerides represented 11% of pancreatic fat in lean mice compared with 67% of pancreatic fat in obese mice (p <0.01). Cytokines IL-1β and TNF-α also were elevated in the pancreata of obese mice (p <0.05). Conclusions. These data suggest that obese mice have 1) heavier pancreata, 2) more pancreatic fat, especially triglycerides and FFAs, and 3) increased cytokines. We conclude that obesity leads to nonalcoholic fatty pancreatic disease.

AB - Background. Obesity leads to fat infiltration of multiple organs including the heart, kidneys, and liver. Under conditions of oxidative stress, fat-derived cytokines are released locally and result in an inflammatory process and organ dysfunction. In the liver, fat infiltration has been termed nonalcoholic fatty liver disease, which may lead to nonalcoholic steatohepatitis. No data are available, however, on the influence of obesity on pancreatic fat and cytokines, and nonalcoholic fatty pancreas disease (NAFPD) has not been described. Therefore, we designed a study to determine whether obesity is associated with increased pancreatic fat and cytokines. Materials and methods. Thirty C57BL/6J lean control and 30 leptin-deficient obese female mice were fed a 15% fat diet for 4 weeks. At 12 weeks of age all animals underwent total pancreatectomy. Pancreata from each strain were pooled for measurement of a) wet and dry weight, b) histologic presence of fat, c) triglycerides, free fatty acids (FFAs), cholesterol, phospholipids, and total fat, and d) interleukin (IL)-1β and tumor necrosis factor-alpha (TNF-α. Data were analyzed by Student's t test and Fisher's exact test. Results. Pancreata from obese mice were heavier (p <0.05) and had more fat histologically (p <0.05). Pancreata from obese mice had more triglycerides, FFAs, cholesterol, and total fat (p <0.05). Triglycerides represented 11% of pancreatic fat in lean mice compared with 67% of pancreatic fat in obese mice (p <0.01). Cytokines IL-1β and TNF-α also were elevated in the pancreata of obese mice (p <0.05). Conclusions. These data suggest that obese mice have 1) heavier pancreata, 2) more pancreatic fat, especially triglycerides and FFAs, and 3) increased cytokines. We conclude that obesity leads to nonalcoholic fatty pancreatic disease.

KW - Cytokines

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