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Brain insulin controls adipose tissue lipolysis and lipogenesis.

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Brain insulin controls adipose tissue lipolysis and lipogenesis. / Scherer, Thomas; O'Hare, James; Diggs-Andrews, Kelly; Schweiger, Martina; Cheng, Bob; Lindtner, Claudia; Zielinski, Elizabeth; Vempati, Prashant; Su, Kai; Dighe, Shveta; Milsom, Thomas; Puchowicz, Michelle; Scheja, Ludger; Zechner, Rudolf; Fisher, Simon J; Previs, Stephen F; Buettner, Christoph.

in: CELL METAB, Jahrgang 13, Nr. 2, 2, 2011, S. 183-194.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Scherer, T, O'Hare, J, Diggs-Andrews, K, Schweiger, M, Cheng, B, Lindtner, C, Zielinski, E, Vempati, P, Su, K, Dighe, S, Milsom, T, Puchowicz, M, Scheja, L, Zechner, R, Fisher, SJ, Previs, SF & Buettner, C 2011, 'Brain insulin controls adipose tissue lipolysis and lipogenesis.', CELL METAB, Jg. 13, Nr. 2, 2, S. 183-194. <http://www.ncbi.nlm.nih.gov/pubmed/21284985?dopt=Citation>

APA

Scherer, T., O'Hare, J., Diggs-Andrews, K., Schweiger, M., Cheng, B., Lindtner, C., Zielinski, E., Vempati, P., Su, K., Dighe, S., Milsom, T., Puchowicz, M., Scheja, L., Zechner, R., Fisher, S. J., Previs, S. F., & Buettner, C. (2011). Brain insulin controls adipose tissue lipolysis and lipogenesis. CELL METAB, 13(2), 183-194. [2]. http://www.ncbi.nlm.nih.gov/pubmed/21284985?dopt=Citation

Vancouver

Scherer T, O'Hare J, Diggs-Andrews K, Schweiger M, Cheng B, Lindtner C et al. Brain insulin controls adipose tissue lipolysis and lipogenesis. CELL METAB. 2011;13(2):183-194. 2.

Bibtex

@article{cff5e5899efc44b69e7308e6febbf58d,
title = "Brain insulin controls adipose tissue lipolysis and lipogenesis.",
abstract = "White adipose tissue (WAT) dysfunction plays a key role in the pathogenesis of type 2 diabetes (DM2). Unrestrained WAT lipolysis results in increased fatty acid release, leading to insulin resistance and lipotoxicity, while impaired de novo lipogenesis in WAT decreases the synthesis of insulin-sensitizing fatty acid species like palmitoleate. Here, we show that insulin infused into the mediobasal hypothalamus (MBH) of Sprague-Dawley rats increases WAT lipogenic protein expression, inactivates hormone-sensitive lipase (Hsl), and suppresses lipolysis. Conversely, mice that lack the neuronal insulin receptor exhibit unrestrained lipolysis and decreased de novo lipogenesis in WAT. Thus, brain and, in particular, hypothalamic insulin action play a pivotal role in WAT functionality.",
keywords = "Animals, Male, Mice, Rats, Rats, Sprague-Dawley, Signal Transduction, Adipose Tissue, White/*metabolism, Brain/*metabolism, Glucose/metabolism, Insulin/*metabolism, Lipogenesis, Lipolysis, Receptor, Insulin/metabolism, Animals, Male, Mice, Rats, Rats, Sprague-Dawley, Signal Transduction, Adipose Tissue, White/*metabolism, Brain/*metabolism, Glucose/metabolism, Insulin/*metabolism, Lipogenesis, Lipolysis, Receptor, Insulin/metabolism",
author = "Thomas Scherer and James O'Hare and Kelly Diggs-Andrews and Martina Schweiger and Bob Cheng and Claudia Lindtner and Elizabeth Zielinski and Prashant Vempati and Kai Su and Shveta Dighe and Thomas Milsom and Michelle Puchowicz and Ludger Scheja and Rudolf Zechner and Fisher, {Simon J} and Previs, {Stephen F} and Christoph Buettner",
year = "2011",
language = "English",
volume = "13",
pages = "183--194",
journal = "CELL METAB",
issn = "1550-4131",
publisher = "Cell Press",
number = "2",

}

RIS

TY - JOUR

T1 - Brain insulin controls adipose tissue lipolysis and lipogenesis.

AU - Scherer, Thomas

AU - O'Hare, James

AU - Diggs-Andrews, Kelly

AU - Schweiger, Martina

AU - Cheng, Bob

AU - Lindtner, Claudia

AU - Zielinski, Elizabeth

AU - Vempati, Prashant

AU - Su, Kai

AU - Dighe, Shveta

AU - Milsom, Thomas

AU - Puchowicz, Michelle

AU - Scheja, Ludger

AU - Zechner, Rudolf

AU - Fisher, Simon J

AU - Previs, Stephen F

AU - Buettner, Christoph

PY - 2011

Y1 - 2011

N2 - White adipose tissue (WAT) dysfunction plays a key role in the pathogenesis of type 2 diabetes (DM2). Unrestrained WAT lipolysis results in increased fatty acid release, leading to insulin resistance and lipotoxicity, while impaired de novo lipogenesis in WAT decreases the synthesis of insulin-sensitizing fatty acid species like palmitoleate. Here, we show that insulin infused into the mediobasal hypothalamus (MBH) of Sprague-Dawley rats increases WAT lipogenic protein expression, inactivates hormone-sensitive lipase (Hsl), and suppresses lipolysis. Conversely, mice that lack the neuronal insulin receptor exhibit unrestrained lipolysis and decreased de novo lipogenesis in WAT. Thus, brain and, in particular, hypothalamic insulin action play a pivotal role in WAT functionality.

AB - White adipose tissue (WAT) dysfunction plays a key role in the pathogenesis of type 2 diabetes (DM2). Unrestrained WAT lipolysis results in increased fatty acid release, leading to insulin resistance and lipotoxicity, while impaired de novo lipogenesis in WAT decreases the synthesis of insulin-sensitizing fatty acid species like palmitoleate. Here, we show that insulin infused into the mediobasal hypothalamus (MBH) of Sprague-Dawley rats increases WAT lipogenic protein expression, inactivates hormone-sensitive lipase (Hsl), and suppresses lipolysis. Conversely, mice that lack the neuronal insulin receptor exhibit unrestrained lipolysis and decreased de novo lipogenesis in WAT. Thus, brain and, in particular, hypothalamic insulin action play a pivotal role in WAT functionality.

KW - Animals

KW - Male

KW - Mice

KW - Rats

KW - Rats, Sprague-Dawley

KW - Signal Transduction

KW - Adipose Tissue, White/metabolism

KW - Brain/metabolism

KW - Glucose/metabolism

KW - Insulin/metabolism

KW - Lipogenesis

KW - Lipolysis

KW - Receptor, Insulin/metabolism

KW - Animals

KW - Male

KW - Mice

KW - Rats

KW - Rats, Sprague-Dawley

KW - Signal Transduction

KW - Adipose Tissue, White/metabolism

KW - Brain/metabolism

KW - Glucose/metabolism

KW - Insulin/metabolism

KW - Lipogenesis

KW - Lipolysis

KW - Receptor, Insulin/metabolism

M3 - SCORING: Journal article

VL - 13

SP - 183

EP - 194

JO - CELL METAB

JF - CELL METAB

SN - 1550-4131

IS - 2

M1 - 2

ER -