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Enterostatin decreases postprandial pancreatic UCP2 mRNA levels and increases plasma insulin and amylin

Arsenijevic, D; Gallmann, E; Moses, W; Lutz, T; Erlanson-Albertsson, Charlotte LU and Langhans, W (2005) In American Journal of Physiology: Endocrinology and Metabolism 289(1). p.40-45
Abstract
This study investigated the chronic effect of enterostatin on body weight and some of the associated changes in postprandial metabolism. Rats were adapted to 6 h of food access/day and a choice of low-fat and high-fat (HF) food and then given enterostatin or vehicle by an intraperitoneally implanted minipump delivering 160 nmol enterostatin/h continuously over a 5-day infusion period. Enterostatin resulted in a slight but significant reduction of HF intake and body weight. After the last 6-h food access period, enterostatin-treated animals had lower plasma triglyceride and free fatty acid but higher plasma glucose and lactate levels than control animals. Enterostatin infusion resulted in increased uncoupling protein-2 (UCP2) expression in... (More)
This study investigated the chronic effect of enterostatin on body weight and some of the associated changes in postprandial metabolism. Rats were adapted to 6 h of food access/day and a choice of low-fat and high-fat (HF) food and then given enterostatin or vehicle by an intraperitoneally implanted minipump delivering 160 nmol enterostatin/h continuously over a 5-day infusion period. Enterostatin resulted in a slight but significant reduction of HF intake and body weight. After the last 6-h food access period, enterostatin-treated animals had lower plasma triglyceride and free fatty acid but higher plasma glucose and lactate levels than control animals. Enterostatin infusion resulted in increased uncoupling protein-2 (UCP2) expression in various tissues, including epididymal fat and liver. UCP2 was reduced in the pancreas of enterostatin-treated animals, and this was associated with increased plasma levels of insulin and amylin. Whether these two hormones are involved in the observed decreased food intake due to enterostatin remains to be determined. As lipid metabolism appeared to be altered by enterostatin, we measured peroxisome proliferator-activated receptor (PPAR) expression in tissues and observed that PPAR alpha, -beta, -gamma 1, and -gamma 2 expression were modified by enterostatin in epididymal fat, pancreas, and liver. This further links altered lipid metabolism with body weight loss. Our data suggest that alterations in UCP2 and PPAR gamma 2 play a role in the control of insulin and amylin release from the pancreas. This implies that enterostatin changes lipid and carbohydrate metabolic pathways in addition to its effects on food intake and energy expenditure. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
peroxisome proliferator-activated, glutathione, body weight, appetite, receptors, uncoupling protein-2
in
American Journal of Physiology: Endocrinology and Metabolism
volume
289
issue
1
pages
40 - 45
publisher
American Physiological Society
external identifiers
  • pmid:15713687
  • wos:000230113600007
  • scopus:21044459394
ISSN
1522-1555
DOI
10.1152/ajpendo.00367.2004
language
English
LU publication?
yes
id
ca8d080d-3116-434c-907e-f8bb87d62234 (old id 234015)
date added to LUP
2007-08-10 10:33:02
date last changed
2017-01-01 06:39:33
@article{ca8d080d-3116-434c-907e-f8bb87d62234,
  abstract     = {This study investigated the chronic effect of enterostatin on body weight and some of the associated changes in postprandial metabolism. Rats were adapted to 6 h of food access/day and a choice of low-fat and high-fat (HF) food and then given enterostatin or vehicle by an intraperitoneally implanted minipump delivering 160 nmol enterostatin/h continuously over a 5-day infusion period. Enterostatin resulted in a slight but significant reduction of HF intake and body weight. After the last 6-h food access period, enterostatin-treated animals had lower plasma triglyceride and free fatty acid but higher plasma glucose and lactate levels than control animals. Enterostatin infusion resulted in increased uncoupling protein-2 (UCP2) expression in various tissues, including epididymal fat and liver. UCP2 was reduced in the pancreas of enterostatin-treated animals, and this was associated with increased plasma levels of insulin and amylin. Whether these two hormones are involved in the observed decreased food intake due to enterostatin remains to be determined. As lipid metabolism appeared to be altered by enterostatin, we measured peroxisome proliferator-activated receptor (PPAR) expression in tissues and observed that PPAR alpha, -beta, -gamma 1, and -gamma 2 expression were modified by enterostatin in epididymal fat, pancreas, and liver. This further links altered lipid metabolism with body weight loss. Our data suggest that alterations in UCP2 and PPAR gamma 2 play a role in the control of insulin and amylin release from the pancreas. This implies that enterostatin changes lipid and carbohydrate metabolic pathways in addition to its effects on food intake and energy expenditure.},
  author       = {Arsenijevic, D and Gallmann, E and Moses, W and Lutz, T and Erlanson-Albertsson, Charlotte and Langhans, W},
  issn         = {1522-1555},
  keyword      = {peroxisome proliferator-activated,glutathione,body weight,appetite,receptors,uncoupling protein-2},
  language     = {eng},
  number       = {1},
  pages        = {40--45},
  publisher    = {American Physiological Society},
  series       = {American Journal of Physiology: Endocrinology and Metabolism},
  title        = {Enterostatin decreases postprandial pancreatic UCP2 mRNA levels and increases plasma insulin and amylin},
  url          = {http://dx.doi.org/10.1152/ajpendo.00367.2004},
  volume       = {289},
  year         = {2005},
}