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Increased expression of transthyretin in leptin-deficient ob/ob mice is not causative for their major phenotypic abnormalities.

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Increased expression of transthyretin in leptin-deficient ob/ob mice is not causative for their major phenotypic abnormalities. / Rendenbach, C; Ganswindt, Stefanie; Seitz, S; Barvencik, F; Hübner, Antje K.; Baranowsky, A; Streichert, T; Niemeier, A; Heeren, J; Amling, M; Bartelt, A; Schinke, T.

In: J NEUROENDOCRINOL, Vol. 25, No. 1, 1, 2013, p. 14-22.

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

Harvard

Rendenbach, C, Ganswindt, S, Seitz, S, Barvencik, F, Hübner, AK, Baranowsky, A, Streichert, T, Niemeier, A, Heeren, J, Amling, M, Bartelt, A & Schinke, T 2013, 'Increased expression of transthyretin in leptin-deficient ob/ob mice is not causative for their major phenotypic abnormalities.', J NEUROENDOCRINOL, vol. 25, no. 1, 1, pp. 14-22. https://doi.org/10.1111/j.1365-2826.2012.02366.x

APA

Rendenbach, C., Ganswindt, S., Seitz, S., Barvencik, F., Hübner, A. K., Baranowsky, A., Streichert, T., Niemeier, A., Heeren, J., Amling, M., Bartelt, A., & Schinke, T. (2013). Increased expression of transthyretin in leptin-deficient ob/ob mice is not causative for their major phenotypic abnormalities. J NEUROENDOCRINOL, 25(1), 14-22. [1]. https://doi.org/10.1111/j.1365-2826.2012.02366.x

Vancouver

Rendenbach C, Ganswindt S, Seitz S, Barvencik F, Hübner AK, Baranowsky A et al. Increased expression of transthyretin in leptin-deficient ob/ob mice is not causative for their major phenotypic abnormalities. J NEUROENDOCRINOL. 2013;25(1):14-22. 1. https://doi.org/10.1111/j.1365-2826.2012.02366.x

Bibtex

@article{a8eabb1f7a0344c8a11115c6f4e68ad7,
title = "Increased expression of transthyretin in leptin-deficient ob/ob mice is not causative for their major phenotypic abnormalities.",
abstract = "The hormone leptin is a critical regulator of adipogenesis and energy metabolism. Similarly, leptin-deficient ob/ob mice display various metabolic abnormalities, including not only obesity and insulin resistance, but also hypogonadism and high bone mass. By genome-wide expression analysis using hypothalamus RNA from wild-type and ob/ob mice, we observed the increased expression of the gene for transthyretin (Ttr) in the latter, as confirmed by quantitative real-time-polymerase chain reaction. Because Ttr encodes a carrier protein for retinol transport, and because we further found increased retinol levels in the serum of ob/ob mice, we investigated whether the additional absence of Ttr would influence the ob/ob phenotype. It was found that Ttr-deficient ob/ob mice were indistinguishable from ob/ob littermates in terms of body weight, as well as serum glucose, insulin and cholesterol levels. Although all of these parameters were identical to wild-type controls in Ttr-deficient mice, we found that the sole deletion of Ttr caused a significant increase of trabecular bone mass, bone marrow adiposity and mean adipocyte area in white adipose tissue. Interestingly, all these latter parameters were highest in Ttr-deficient ob/ob mice, and only in these mice did we observe a full penetrance of liver steatosis at 24 weeks of age. Taken together, our data demonstrate that the increased expression of Ttr in ob/ob mice does not cause (but rather attenuates) their phenotypic abnormalities.",
keywords = "Animals, Male, Female, Mice, Mice, Knockout, Mutation, Body Weight, Insulin Resistance, *Phenotype, RNA, Messenger/genetics/metabolism, Blood Glucose/metabolism, Insulin/blood, Adipose Tissue/metabolism, Bone and Bones/metabolism, Fatty Liver/genetics/metabolism, Hypothalamus/*metabolism, Leptin/genetics/*metabolism, Mice, Obese, Obesity/genetics/*metabolism, Prealbumin/genetics/*metabolism, Animals, Male, Female, Mice, Mice, Knockout, Mutation, Body Weight, Insulin Resistance, *Phenotype, RNA, Messenger/genetics/metabolism, Blood Glucose/metabolism, Insulin/blood, Adipose Tissue/metabolism, Bone and Bones/metabolism, Fatty Liver/genetics/metabolism, Hypothalamus/*metabolism, Leptin/genetics/*metabolism, Mice, Obese, Obesity/genetics/*metabolism, Prealbumin/genetics/*metabolism",
author = "C Rendenbach and Stefanie Ganswindt and S Seitz and F Barvencik and H{\"u}bner, {Antje K.} and A Baranowsky and T Streichert and A Niemeier and J Heeren and M Amling and A Bartelt and T Schinke",
note = "{\textcopyright} 2012 British Society for Neuroendocrinology.",
year = "2013",
doi = "10.1111/j.1365-2826.2012.02366.x",
language = "English",
volume = "25",
pages = "14--22",
journal = "J NEUROENDOCRINOL",
issn = "0953-8194",
publisher = "Wiley-Blackwell",
number = "1",

}

RIS

TY - JOUR

T1 - Increased expression of transthyretin in leptin-deficient ob/ob mice is not causative for their major phenotypic abnormalities.

AU - Rendenbach, C

AU - Ganswindt, Stefanie

AU - Seitz, S

AU - Barvencik, F

AU - Hübner, Antje K.

AU - Baranowsky, A

AU - Streichert, T

AU - Niemeier, A

AU - Heeren, J

AU - Amling, M

AU - Bartelt, A

AU - Schinke, T

N1 - © 2012 British Society for Neuroendocrinology.

PY - 2013

Y1 - 2013

N2 - The hormone leptin is a critical regulator of adipogenesis and energy metabolism. Similarly, leptin-deficient ob/ob mice display various metabolic abnormalities, including not only obesity and insulin resistance, but also hypogonadism and high bone mass. By genome-wide expression analysis using hypothalamus RNA from wild-type and ob/ob mice, we observed the increased expression of the gene for transthyretin (Ttr) in the latter, as confirmed by quantitative real-time-polymerase chain reaction. Because Ttr encodes a carrier protein for retinol transport, and because we further found increased retinol levels in the serum of ob/ob mice, we investigated whether the additional absence of Ttr would influence the ob/ob phenotype. It was found that Ttr-deficient ob/ob mice were indistinguishable from ob/ob littermates in terms of body weight, as well as serum glucose, insulin and cholesterol levels. Although all of these parameters were identical to wild-type controls in Ttr-deficient mice, we found that the sole deletion of Ttr caused a significant increase of trabecular bone mass, bone marrow adiposity and mean adipocyte area in white adipose tissue. Interestingly, all these latter parameters were highest in Ttr-deficient ob/ob mice, and only in these mice did we observe a full penetrance of liver steatosis at 24 weeks of age. Taken together, our data demonstrate that the increased expression of Ttr in ob/ob mice does not cause (but rather attenuates) their phenotypic abnormalities.

AB - The hormone leptin is a critical regulator of adipogenesis and energy metabolism. Similarly, leptin-deficient ob/ob mice display various metabolic abnormalities, including not only obesity and insulin resistance, but also hypogonadism and high bone mass. By genome-wide expression analysis using hypothalamus RNA from wild-type and ob/ob mice, we observed the increased expression of the gene for transthyretin (Ttr) in the latter, as confirmed by quantitative real-time-polymerase chain reaction. Because Ttr encodes a carrier protein for retinol transport, and because we further found increased retinol levels in the serum of ob/ob mice, we investigated whether the additional absence of Ttr would influence the ob/ob phenotype. It was found that Ttr-deficient ob/ob mice were indistinguishable from ob/ob littermates in terms of body weight, as well as serum glucose, insulin and cholesterol levels. Although all of these parameters were identical to wild-type controls in Ttr-deficient mice, we found that the sole deletion of Ttr caused a significant increase of trabecular bone mass, bone marrow adiposity and mean adipocyte area in white adipose tissue. Interestingly, all these latter parameters were highest in Ttr-deficient ob/ob mice, and only in these mice did we observe a full penetrance of liver steatosis at 24 weeks of age. Taken together, our data demonstrate that the increased expression of Ttr in ob/ob mice does not cause (but rather attenuates) their phenotypic abnormalities.

KW - Animals

KW - Male

KW - Female

KW - Mice

KW - Mice, Knockout

KW - Mutation

KW - Body Weight

KW - Insulin Resistance

KW - Phenotype

KW - RNA, Messenger/genetics/metabolism

KW - Blood Glucose/metabolism

KW - Insulin/blood

KW - Adipose Tissue/metabolism

KW - Bone and Bones/metabolism

KW - Fatty Liver/genetics/metabolism

KW - Hypothalamus/metabolism

KW - Leptin/genetics/metabolism

KW - Mice, Obese

KW - Obesity/genetics/metabolism

KW - Prealbumin/genetics/metabolism

KW - Animals

KW - Male

KW - Female

KW - Mice

KW - Mice, Knockout

KW - Mutation

KW - Body Weight

KW - Insulin Resistance

KW - Phenotype

KW - RNA, Messenger/genetics/metabolism

KW - Blood Glucose/metabolism

KW - Insulin/blood

KW - Adipose Tissue/metabolism

KW - Bone and Bones/metabolism

KW - Fatty Liver/genetics/metabolism

KW - Hypothalamus/metabolism

KW - Leptin/genetics/metabolism

KW - Mice, Obese

KW - Obesity/genetics/metabolism

KW - Prealbumin/genetics/metabolism

U2 - 10.1111/j.1365-2826.2012.02366.x

DO - 10.1111/j.1365-2826.2012.02366.x

M3 - SCORING: Journal article

C2 - 22849972

VL - 25

SP - 14

EP - 22

JO - J NEUROENDOCRINOL

JF - J NEUROENDOCRINOL

SN - 0953-8194

IS - 1

M1 - 1

ER -