Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.

Obesity and related metabolic disorders have become leading causes of adult morbidity and mortality. KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule, however, its physiolog...

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Autores principales:	Takahiro Fujimoto, Kyoko Miyasaka, Midori Koyanagi, Toshiyuki Tsunoda, Iwai Baba, Keiko Doi, Minoru Ohta, Norihiro Kato, Takehiko Sasazuki, Senji Shirasawa
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2009
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b4778bdc2ee3424facb1ca4f37c4ad5e
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spelling	oai:doaj.org-article:b4778bdc2ee3424facb1ca4f37c4ad5e2021-11-25T06:17:41ZAltered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.1932-620310.1371/journal.pone.0004240https://doaj.org/article/b4778bdc2ee3424facb1ca4f37c4ad5e2009-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19156225/?tool=EBIhttps://doaj.org/toc/1932-6203Obesity and related metabolic disorders have become leading causes of adult morbidity and mortality. KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule, however, its physiological roles remain unknown. Here we demonstrate that KRAP-deficient (KRAP(-/-)) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP(-/-) mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. Notably, glucose uptake in the brown adipose tissue (BAT) in KRAP(-/-) mice is enhanced in an insulin-independent manner, suggesting that BAT is involved in altered energy homeostasis in KRAP(-/-) mice, although UCP (Uncoupling protein) expressions are not altered. Of interest is the down-regulation of fatty acid metabolism-related molecules, including acetyl-CoA carboxylase (ACC)-1, ACC-2 and fatty acid synthase in the liver of KRAP(-/-) mice, which could in part account for the metabolic phenotype in KRAP(-/-) mice. Thus, KRAP is a novel regulator in whole-body energy homeostasis and may be a therapeutic target in obesity and related diseases.Takahiro FujimotoKyoko MiyasakaMidori KoyanagiToshiyuki TsunodaIwai BabaKeiko DoiMinoru OhtaNorihiro KatoTakehiko SasazukiSenji ShirasawaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 4, Iss 1, p e4240 (2009)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Takahiro Fujimoto Kyoko Miyasaka Midori Koyanagi Toshiyuki Tsunoda Iwai Baba Keiko Doi Minoru Ohta Norihiro Kato Takehiko Sasazuki Senji Shirasawa Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.
description	Obesity and related metabolic disorders have become leading causes of adult morbidity and mortality. KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule, however, its physiological roles remain unknown. Here we demonstrate that KRAP-deficient (KRAP(-/-)) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP(-/-) mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. Notably, glucose uptake in the brown adipose tissue (BAT) in KRAP(-/-) mice is enhanced in an insulin-independent manner, suggesting that BAT is involved in altered energy homeostasis in KRAP(-/-) mice, although UCP (Uncoupling protein) expressions are not altered. Of interest is the down-regulation of fatty acid metabolism-related molecules, including acetyl-CoA carboxylase (ACC)-1, ACC-2 and fatty acid synthase in the liver of KRAP(-/-) mice, which could in part account for the metabolic phenotype in KRAP(-/-) mice. Thus, KRAP is a novel regulator in whole-body energy homeostasis and may be a therapeutic target in obesity and related diseases.
format	article
author	Takahiro Fujimoto Kyoko Miyasaka Midori Koyanagi Toshiyuki Tsunoda Iwai Baba Keiko Doi Minoru Ohta Norihiro Kato Takehiko Sasazuki Senji Shirasawa
author_facet	Takahiro Fujimoto Kyoko Miyasaka Midori Koyanagi Toshiyuki Tsunoda Iwai Baba Keiko Doi Minoru Ohta Norihiro Kato Takehiko Sasazuki Senji Shirasawa
author_sort	Takahiro Fujimoto
title	Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.
title_short	Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.
title_full	Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.
title_fullStr	Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.
title_full_unstemmed	Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.
title_sort	altered energy homeostasis and resistance to diet-induced obesity in krap-deficient mice.
publisher	Public Library of Science (PLoS)
publishDate	2009
url	https://doaj.org/article/b4778bdc2ee3424facb1ca4f37c4ad5e
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Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.

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