Obesity and NK cells affect the expression of the long form of the leptin receptor Ob-Rb in liver of F344 rats.

Christiane D Wrann; Ursula Ehmer; Anne Lautenbach; Susanne Kuhlmann; Heike Nave

Obesity and NK cells affect the expression of the long form of the leptin receptor Ob-Rb in liver of F344 rats.

Standard

Obesity and NK cells affect the expression of the long form of the leptin receptor Ob-Rb in liver of F344 rats. / Wrann, Christiane D; Ehmer, Ursula; Lautenbach, Anne; Kuhlmann, Susanne; Nave, Heike.

In: EXP TOXICOL PATHOL, Vol. 62, No. 1, 1, 2010, p. 1-8.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Wrann, CD, Ehmer, U, Lautenbach, A, Kuhlmann, S & Nave, H 2010, 'Obesity and NK cells affect the expression of the long form of the leptin receptor Ob-Rb in liver of F344 rats.', EXP TOXICOL PATHOL, vol. 62, no. 1, 1, pp. 1-8. <http://www.ncbi.nlm.nih.gov/pubmed/19186040?dopt=Citation>

APA

Wrann, C. D., Ehmer, U., Lautenbach, A., Kuhlmann, S., & Nave, H. (2010). Obesity and NK cells affect the expression of the long form of the leptin receptor Ob-Rb in liver of F344 rats. EXP TOXICOL PATHOL, 62(1), 1-8. [1]. http://www.ncbi.nlm.nih.gov/pubmed/19186040?dopt=Citation

Vancouver

Wrann CD, Ehmer U, Lautenbach A, Kuhlmann S, Nave H. Obesity and NK cells affect the expression of the long form of the leptin receptor Ob-Rb in liver of F344 rats. EXP TOXICOL PATHOL. 2010;62(1):1-8. 1.

Bibtex

@article{755aa140d9b44f939fe92d90fc093bf8,

title = "Obesity and NK cells affect the expression of the long form of the leptin receptor Ob-Rb in liver of F344 rats.",

abstract = "In obesity, the regulatory effects of leptin, a primarily adipocyte-derived hormone, are severely disturbed affecting the control of energy homeostasis and immune functions. In addition, recent studies indicate that specific immune cells can affect glucose and lipid metabolism of liver. However, the contribution of body weight and immune cells, such as Natural Killer (NK) cells, to the regulation of the leptin-receptor expression remains elusive. Therefore, we investigated the expression of the signal-transducing long form of the leptin receptor (Ob-Rb) in diet-induced obesity and after adoptive cross-over NK cell transfer between normal weight and obese male F344 rats. Expression of Ob-Rb was significantly increased in liver in diet-induced obese rats as compared to normal weight littermates. Similarly, the expression of Ob-Rb was higher in liver of obese animals that received NK cells from either obese or normal weight donors as compared to normal weight animals that received NK cells from normal weight donors. Interestingly, normal weight animals that were transferred with NK cells from obese donors also showed a tendency towards a higher Ob-Rb expression. In contrast to the findings in liver, the expression of Ob-Rb in spleen or lung remained unaffected by changes in body weight or cross-over NK cell transfer. Our results suggest that the expression of Ob-Rb mRNA in liver, but not in spleen or lung, is dependent on the body weight but can also be influenced by NK cells, thereby indicating a bidirectional cross-talk between the metabolic and the immune system.",

keywords = "Animals, Male, Rats, Reverse Transcriptase Polymerase Chain Reaction, Flow Cytometry, Gene Expression Regulation/physiology, Signal Transduction/physiology, RNA, Messenger/genetics, Adoptive Transfer, Rats, Inbred F344, Body Weight/physiology, Killer Cells, Natural/*physiology, Liver/*physiology, Lung/physiology, Obesity/*physiopathology, Receptors, Leptin/biosynthesis/genetics/*physiology, Spleen/physiology, Animals, Male, Rats, Reverse Transcriptase Polymerase Chain Reaction, Flow Cytometry, Gene Expression Regulation/physiology, Signal Transduction/physiology, RNA, Messenger/genetics, Adoptive Transfer, Rats, Inbred F344, Body Weight/physiology, Killer Cells, Natural/*physiology, Liver/*physiology, Lung/physiology, Obesity/*physiopathology, Receptors, Leptin/biosynthesis/genetics/*physiology, Spleen/physiology",

author = "Wrann, {Christiane D} and Ursula Ehmer and Anne Lautenbach and Susanne Kuhlmann and Heike Nave",

year = "2010",

language = "English",

volume = "62",

pages = "1--8",

number = "1",

}

RIS

TY - JOUR

T1 - Obesity and NK cells affect the expression of the long form of the leptin receptor Ob-Rb in liver of F344 rats.

AU - Wrann, Christiane D

AU - Ehmer, Ursula

AU - Lautenbach, Anne

AU - Kuhlmann, Susanne

AU - Nave, Heike

PY - 2010

Y1 - 2010

N2 - In obesity, the regulatory effects of leptin, a primarily adipocyte-derived hormone, are severely disturbed affecting the control of energy homeostasis and immune functions. In addition, recent studies indicate that specific immune cells can affect glucose and lipid metabolism of liver. However, the contribution of body weight and immune cells, such as Natural Killer (NK) cells, to the regulation of the leptin-receptor expression remains elusive. Therefore, we investigated the expression of the signal-transducing long form of the leptin receptor (Ob-Rb) in diet-induced obesity and after adoptive cross-over NK cell transfer between normal weight and obese male F344 rats. Expression of Ob-Rb was significantly increased in liver in diet-induced obese rats as compared to normal weight littermates. Similarly, the expression of Ob-Rb was higher in liver of obese animals that received NK cells from either obese or normal weight donors as compared to normal weight animals that received NK cells from normal weight donors. Interestingly, normal weight animals that were transferred with NK cells from obese donors also showed a tendency towards a higher Ob-Rb expression. In contrast to the findings in liver, the expression of Ob-Rb in spleen or lung remained unaffected by changes in body weight or cross-over NK cell transfer. Our results suggest that the expression of Ob-Rb mRNA in liver, but not in spleen or lung, is dependent on the body weight but can also be influenced by NK cells, thereby indicating a bidirectional cross-talk between the metabolic and the immune system.

AB - In obesity, the regulatory effects of leptin, a primarily adipocyte-derived hormone, are severely disturbed affecting the control of energy homeostasis and immune functions. In addition, recent studies indicate that specific immune cells can affect glucose and lipid metabolism of liver. However, the contribution of body weight and immune cells, such as Natural Killer (NK) cells, to the regulation of the leptin-receptor expression remains elusive. Therefore, we investigated the expression of the signal-transducing long form of the leptin receptor (Ob-Rb) in diet-induced obesity and after adoptive cross-over NK cell transfer between normal weight and obese male F344 rats. Expression of Ob-Rb was significantly increased in liver in diet-induced obese rats as compared to normal weight littermates. Similarly, the expression of Ob-Rb was higher in liver of obese animals that received NK cells from either obese or normal weight donors as compared to normal weight animals that received NK cells from normal weight donors. Interestingly, normal weight animals that were transferred with NK cells from obese donors also showed a tendency towards a higher Ob-Rb expression. In contrast to the findings in liver, the expression of Ob-Rb in spleen or lung remained unaffected by changes in body weight or cross-over NK cell transfer. Our results suggest that the expression of Ob-Rb mRNA in liver, but not in spleen or lung, is dependent on the body weight but can also be influenced by NK cells, thereby indicating a bidirectional cross-talk between the metabolic and the immune system.

KW - Animals

KW - Male

KW - Rats

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Flow Cytometry

KW - Gene Expression Regulation/physiology

KW - Signal Transduction/physiology

KW - RNA, Messenger/genetics

KW - Adoptive Transfer

KW - Rats, Inbred F344

KW - Body Weight/physiology

KW - Killer Cells, Natural/physiology

KW - Liver/physiology

KW - Lung/physiology

KW - Obesity/physiopathology

KW - Receptors, Leptin/biosynthesis/genetics/physiology

KW - Spleen/physiology