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Conference Paper: Selective inactivation of c-Jun NH2 terminal kinase (JNK) in the adipose tissue is sufficient to protect against diet-induced-obesity and its associated metabolic disorders in mice

TitleSelective inactivation of c-Jun NH2 terminal kinase (JNK) in the adipose tissue is sufficient to protect against diet-induced-obesity and its associated metabolic disorders in mice
Authors
KeywordsMedical sciences
Endocrinology
Issue Date2010
PublisherThe Endocrine Society. The Journal's web site is located at http://edrv.endojournals.org
Citation
The 92nd Annual Meeting & Expo of the Endocrine Society (ENDO 2010), San Diego, CA., 19-22 June 2010. In Endocrine Reviews, 2010, v. 31 n. 3, suppl. 1, p. S481, abstract no. P1-414 How to Cite?
AbstractINTRODUCTION: Obesity caused by feeding a high fat diet is associated with increased activation of c-Jun NH2-terminal kinase (JNK), which has been implicated in the development of obesity-related insulin resistance and type 2 diabetes. However, the relative tissue-specific contribution and the underlying mechanisms remain to be defined. METHOD: In this study, we generated a transgenic mouse model with adipose tissue-specific over-expression of dominant negative (DN) JNK. Their phenotypic changes on a high fat diet were comprehensively characterized. Adipose tissues, liver, muscle and serum were collected for further biochemical and morphological analysis. RESULTS: On the standard chow diet, the transgenic mice showed no significant difference in body weight gain, insulin sensitivity, glucose or lipid profiles, from their wild-type littermates. However, on a high fat diet, the DN-JNK transgenic mice were protected against diet-induced obesity, with reduced weight gain, fat mass and size of adipocytes in the adipose tissues. Significantly, the DN-JNK transgenic mice were resistant to the deleterious impact of high-fat diet on systemic insulin sensitivity and glucose tolerance. They also demonstrated a lower level of hepatic gluconeogenesis in vivo, and greater insulin-induced glucose uptake in skeletal muscles ex vivo. These metabolic changes were accompanied by a markedly decreased macrophage infiltration in the adipose tissue, reduced production of pro-inflammatory adipokines, increased expression of adiponectin and reduced circulating levels of adipocyte fatty acid binding protein. As a secondary effect, the DN-JNK transgenic mice also exhibited a resistance to the hepatosteatosis induced by high fat diet. The DN-JNK mice, when on a high fat diet, had significant increases in 24-hour oxygen consumption and reductions in respiration exchange rates, compared with their wild-type littermates. CONCLUSION: Selective suppression of JNK activation in the adipose tissue alone was sufficient to counteract high fat diet-induced obesity and its associated metabolic dysregulations in mice, in part through an increase in energy expenditure and a decrease in systemic inflammation.
DescriptionOpen URL - http://www.endojournals.org/site/abstracts/P1-1_to_P1-729.pdf
Persistent Identifierhttp://hdl.handle.net/10722/132194
ISSN
2015 Impact Factor: 14.898
2015 SCImago Journal Rankings: 7.086

 

DC FieldValueLanguage
dc.contributor.authorLam, KSLen_US
dc.contributor.authorZhang, Xen_US
dc.contributor.authorWong, RLCen_US
dc.contributor.authorXu, Aen_US
dc.date.accessioned2011-03-21T09:00:40Z-
dc.date.available2011-03-21T09:00:40Z-
dc.date.issued2010en_US
dc.identifier.citationThe 92nd Annual Meeting & Expo of the Endocrine Society (ENDO 2010), San Diego, CA., 19-22 June 2010. In Endocrine Reviews, 2010, v. 31 n. 3, suppl. 1, p. S481, abstract no. P1-414en_US
dc.identifier.issn0163-769X-
dc.identifier.urihttp://hdl.handle.net/10722/132194-
dc.descriptionOpen URL - http://www.endojournals.org/site/abstracts/P1-1_to_P1-729.pdf-
dc.description.abstractINTRODUCTION: Obesity caused by feeding a high fat diet is associated with increased activation of c-Jun NH2-terminal kinase (JNK), which has been implicated in the development of obesity-related insulin resistance and type 2 diabetes. However, the relative tissue-specific contribution and the underlying mechanisms remain to be defined. METHOD: In this study, we generated a transgenic mouse model with adipose tissue-specific over-expression of dominant negative (DN) JNK. Their phenotypic changes on a high fat diet were comprehensively characterized. Adipose tissues, liver, muscle and serum were collected for further biochemical and morphological analysis. RESULTS: On the standard chow diet, the transgenic mice showed no significant difference in body weight gain, insulin sensitivity, glucose or lipid profiles, from their wild-type littermates. However, on a high fat diet, the DN-JNK transgenic mice were protected against diet-induced obesity, with reduced weight gain, fat mass and size of adipocytes in the adipose tissues. Significantly, the DN-JNK transgenic mice were resistant to the deleterious impact of high-fat diet on systemic insulin sensitivity and glucose tolerance. They also demonstrated a lower level of hepatic gluconeogenesis in vivo, and greater insulin-induced glucose uptake in skeletal muscles ex vivo. These metabolic changes were accompanied by a markedly decreased macrophage infiltration in the adipose tissue, reduced production of pro-inflammatory adipokines, increased expression of adiponectin and reduced circulating levels of adipocyte fatty acid binding protein. As a secondary effect, the DN-JNK transgenic mice also exhibited a resistance to the hepatosteatosis induced by high fat diet. The DN-JNK mice, when on a high fat diet, had significant increases in 24-hour oxygen consumption and reductions in respiration exchange rates, compared with their wild-type littermates. CONCLUSION: Selective suppression of JNK activation in the adipose tissue alone was sufficient to counteract high fat diet-induced obesity and its associated metabolic dysregulations in mice, in part through an increase in energy expenditure and a decrease in systemic inflammation.-
dc.languageengen_US
dc.publisherThe Endocrine Society. The Journal's web site is located at http://edrv.endojournals.org-
dc.relation.ispartofEndocrine Reviewsen_US
dc.subjectMedical sciences-
dc.subjectEndocrinology-
dc.titleSelective inactivation of c-Jun NH2 terminal kinase (JNK) in the adipose tissue is sufficient to protect against diet-induced-obesity and its associated metabolic disorders in miceen_US
dc.typeConference_Paperen_US
dc.identifier.emailLam, KSL: ksllam@hku.hken_US
dc.identifier.emailZhang, X: xinmei_zhang@yahoo.comen_US
dc.identifier.emailWong, RLC: lcwong@hkucc.hku.hken_US
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_US
dc.identifier.authorityLam, KSL=rp00343en_US
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.hkuros178125en_US
dc.identifier.volume31-
dc.identifier.issue3, suppl. 1-
dc.identifier.spageS481-
dc.identifier.epageS481-
dc.publisher.placeUnited States-
dc.description.otherThe 92nd Annual Meeting & Expo of the Endocrine Society (ENDO 2010), San Diego, CA., 19-22 June 2010. In Endocrine Reviews, 2010, v. 31 n. 3, suppl. 1, p. S481, abstract no. P1-414-

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