Enterostatin deficiency increases serum cholesterol but does not influence growth and food intake in mice
(2009) In American Journal of Physiology: Endocrinology and Metabolism 297(4). p.856-865- Abstract
- Miller R, D'Agostino D, Erlanson-Albertsson C, Lowe ME. Enterostatin deficiency increases serum cholesterol but does not influence growth and food intake in mice. Am J Physiol Endocrinol Metab 297: E856-E865, 2009. First published July 21, 2009; doi:10.1152/ajpendo.91008.2008.-A pentapeptide released from procolipase, enterostatin, selectively attenuates dietary fat intake when administered peripherally or centrally. Enterostatin may act through the afferent vagus nerve and in the hypothalamus and amygdala, primarily in the central nucleus of the amygdala. To investigate the physiological role of endogenous enterostatin, we created an enterostatin-deficient, colipase-sufficient (Ent(-/-)) mouse. Ent(-/-) mice are viable, normally active,... (More)
- Miller R, D'Agostino D, Erlanson-Albertsson C, Lowe ME. Enterostatin deficiency increases serum cholesterol but does not influence growth and food intake in mice. Am J Physiol Endocrinol Metab 297: E856-E865, 2009. First published July 21, 2009; doi:10.1152/ajpendo.91008.2008.-A pentapeptide released from procolipase, enterostatin, selectively attenuates dietary fat intake when administered peripherally or centrally. Enterostatin may act through the afferent vagus nerve and in the hypothalamus and amygdala, primarily in the central nucleus of the amygdala. To investigate the physiological role of endogenous enterostatin, we created an enterostatin-deficient, colipase-sufficient (Ent(-/-)) mouse. Ent(-/-) mice are viable, normally active, and fertile. They exhibit normal growth on low-fat and high-fat diets. Furthermore, Ent(-/-) mice develop diet-induced obesity, as do Ent(-/-) mice, and have normal responses to a two-macronutrient choice diet and to a switch from a high-fat to a low-fat diet. Levels of total serum (P = 0.004) and non-HDL (P = 0.001) cholesterol were higher and levels of HDL cholesterol (P = 0.01) were lower in Ent(-/-) than in wild-type mice. To determine whether enterostatin contributed to the decreased survival or whether colipase deficiency was the sole contributor, we administered enterostatin to procolipase-deficient (Clps(-/-)) mouse pups. Enterostatin significantly improved survival (P <= 0.001). Our results demonstrate that enterostatin is not critically required to regulate food intake or growth, suggesting that other pathways may compensate for the loss of enterostatin. Enterostatin has developmental effects on survival of newborns and alters cholesterol metabolism. (Less)
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https://lup.lub.lu.se/record/1490165
- author
- Miller, Rita ; D'Agostino, Dymphna ; Erlanson-Albertsson, Charlotte LU and Lowe, Mark E.
- organization
- publishing date
- 2009
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- appetite regulation, fat intake, procolipase, satiety
- in
- American Journal of Physiology: Endocrinology and Metabolism
- volume
- 297
- issue
- 4
- pages
- 856 - 865
- publisher
- American Physiological Society
- external identifiers
-
- wos:000270139400004
- scopus:70349624472
- pmid:19622781
- ISSN
- 1522-1555
- DOI
- 10.1152/ajpendo.91008.2008
- language
- English
- LU publication?
- yes
- id
- 8803d39c-06c5-45a7-82b3-9f2688580cc5 (old id 1490165)
- date added to LUP
- 2016-04-01 13:06:54
- date last changed
- 2022-02-26 19:23:09
@article{8803d39c-06c5-45a7-82b3-9f2688580cc5,
abstract = {{Miller R, D'Agostino D, Erlanson-Albertsson C, Lowe ME. Enterostatin deficiency increases serum cholesterol but does not influence growth and food intake in mice. Am J Physiol Endocrinol Metab 297: E856-E865, 2009. First published July 21, 2009; doi:10.1152/ajpendo.91008.2008.-A pentapeptide released from procolipase, enterostatin, selectively attenuates dietary fat intake when administered peripherally or centrally. Enterostatin may act through the afferent vagus nerve and in the hypothalamus and amygdala, primarily in the central nucleus of the amygdala. To investigate the physiological role of endogenous enterostatin, we created an enterostatin-deficient, colipase-sufficient (Ent(-/-)) mouse. Ent(-/-) mice are viable, normally active, and fertile. They exhibit normal growth on low-fat and high-fat diets. Furthermore, Ent(-/-) mice develop diet-induced obesity, as do Ent(-/-) mice, and have normal responses to a two-macronutrient choice diet and to a switch from a high-fat to a low-fat diet. Levels of total serum (P = 0.004) and non-HDL (P = 0.001) cholesterol were higher and levels of HDL cholesterol (P = 0.01) were lower in Ent(-/-) than in wild-type mice. To determine whether enterostatin contributed to the decreased survival or whether colipase deficiency was the sole contributor, we administered enterostatin to procolipase-deficient (Clps(-/-)) mouse pups. Enterostatin significantly improved survival (P <= 0.001). Our results demonstrate that enterostatin is not critically required to regulate food intake or growth, suggesting that other pathways may compensate for the loss of enterostatin. Enterostatin has developmental effects on survival of newborns and alters cholesterol metabolism.}},
author = {{Miller, Rita and D'Agostino, Dymphna and Erlanson-Albertsson, Charlotte and Lowe, Mark E.}},
issn = {{1522-1555}},
keywords = {{appetite regulation; fat intake; procolipase; satiety}},
language = {{eng}},
number = {{4}},
pages = {{856--865}},
publisher = {{American Physiological Society}},
series = {{American Journal of Physiology: Endocrinology and Metabolism}},
title = {{Enterostatin deficiency increases serum cholesterol but does not influence growth and food intake in mice}},
url = {{http://dx.doi.org/10.1152/ajpendo.91008.2008}},
doi = {{10.1152/ajpendo.91008.2008}},
volume = {{297}},
year = {{2009}},
}