Global deletion of lipocalin 2 does not reverse high-fat diet-induced obesity resistance in stearoyl-CoA desaturase-1 skin-specific knockout mice

Nicholas J. Friedlander; Maggie S. Burhans; Lacmbouh Ade; Lucas M. O'Neill; Xiaoli Chen; James M. Ntambi

doi:10.1016/j.bbrc.2014.02.035

Global deletion of lipocalin 2 does not reverse high-fat diet-induced obesity resistance in stearoyl-CoA desaturase-1 skin-specific knockout mice

Nicholas J. Friedlander, Maggie S. Burhans, Lacmbouh Ade, Lucas M. O'Neill, Xiaoli Chen, James M. Ntambi

Food Science and Nutrition

Research output: Contribution to journal › Article › peer-review

3 Scopus citations

Abstract

Over the past century, obesity has developed into a paramount health issue that affects millions of people worldwide. Obese individuals have an increased risk to develop other metabolic disorders, such as insulin resistance and atherosclerosis, among others. Previously we determined that mice lacking stearoyl-CoA desaturase-1 (SCD1) enzyme specifically in the skin (SKO) were lean and protected from high-fat diet induced adiposity. Additionally, lipocalin 2 (Lcn2) mRNA was found to be 27-fold higher in the skin of SKO mice compared to control mice. Given reports suggesting that Lcn2 plays a role in protection against diet-induced weight gain, adiposity and insulin resistance, we hypothesized that deletion of Lcn2 alongside the skin-specific SCD1 deficiency would diminish the obesity resistance observed in SKO mice. To test this, we developed mice lacking SCD1 expression in the skin and also lacking Lcn2 expression globally and surprisingly, these mice did not gain significantly more weight than the SKO mice under high-fat diet conditions. Therefore, we conclude that Lcn2 does not mediate the protection against high-fat diet-induced adiposity observed in SKO mice.

Original language	English (US)
Pages (from-to)	578-583
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	445
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2014.02.035
State	Published - Mar 14 2014

Bibliographical note

Funding Information:
We thank Peter Crump of the CALS Statistical Consulting Group at the University of Wisconsin-Madison. We thank Dr. Matt Flowers for assistance in development of the Lcn2−/−;SCD1 SKO mouse line. This work was supported by NIH grant R01-DK-062388 and USDA Hatch W2005 grant (to J.M.N.), NIH Predoctoral Training grant T32-DK-007665 (to M.S.B.) and NIH National Research Service Award T32 GM07215 and Advanced Opportunity Fellowship through SciMed Graduate Research Scholars at University of Wisconsin-Madison (to L.M.O.).

Keywords

Lipocalin 2
Metabolism
Obesity
Stearoyl-CoA desaturase

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Global deletion of lipocalin 2 does not reverse high-fat diet-induced obesity resistance in stearoyl-CoA desaturase-1 skin-specific knockout mice. / Friedlander, Nicholas J.; Burhans, Maggie S.; Ade, Lacmbouh et al.
In: Biochemical and Biophysical Research Communications, Vol. 445, No. 3, 14.03.2014, p. 578-583.

Research output: Contribution to journal › Article › peer-review

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abstract = "Over the past century, obesity has developed into a paramount health issue that affects millions of people worldwide. Obese individuals have an increased risk to develop other metabolic disorders, such as insulin resistance and atherosclerosis, among others. Previously we determined that mice lacking stearoyl-CoA desaturase-1 (SCD1) enzyme specifically in the skin (SKO) were lean and protected from high-fat diet induced adiposity. Additionally, lipocalin 2 (Lcn2) mRNA was found to be 27-fold higher in the skin of SKO mice compared to control mice. Given reports suggesting that Lcn2 plays a role in protection against diet-induced weight gain, adiposity and insulin resistance, we hypothesized that deletion of Lcn2 alongside the skin-specific SCD1 deficiency would diminish the obesity resistance observed in SKO mice. To test this, we developed mice lacking SCD1 expression in the skin and also lacking Lcn2 expression globally and surprisingly, these mice did not gain significantly more weight than the SKO mice under high-fat diet conditions. Therefore, we conclude that Lcn2 does not mediate the protection against high-fat diet-induced adiposity observed in SKO mice.",

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note = "Funding Information: We thank Peter Crump of the CALS Statistical Consulting Group at the University of Wisconsin-Madison. We thank Dr. Matt Flowers for assistance in development of the Lcn2−/−;SCD1 SKO mouse line. This work was supported by NIH grant R01-DK-062388 and USDA Hatch W2005 grant (to J.M.N.), NIH Predoctoral Training grant T32-DK-007665 (to M.S.B.) and NIH National Research Service Award T32 GM07215 and Advanced Opportunity Fellowship through SciMed Graduate Research Scholars at University of Wisconsin-Madison (to L.M.O.).",

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Global deletion of lipocalin 2 does not reverse high-fat diet-induced obesity resistance in stearoyl-CoA desaturase-1 skin-specific knockout mice

Abstract

Bibliographical note

Keywords

UN SDGs

Access

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