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Adipose‐specific deletion of SCD1 does not protect mice from obesity
Author(s) -
Flowers Matthew,
Strable Maggie,
Ade Lacmbouh,
Zhao Minghui,
Ntambi James
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.851.1
Subject(s) - adipose tissue , lipogenesis , white adipose tissue , cre recombinase , medicine , transgene , endocrinology , obesity , biology , genetically modified mouse , fatty acid , leptin , gene , biochemistry
A critical regulator of lipogenesis is stearoyl‐CoA desaturase 1 (SCD1), which catalyzes the synthesis of monounsaturated fatty acids (MUFA) from saturated fatty acids. To explore the role of SCD1 in the adipose tissue, we used the Cre‐lox system to delete SCD1 from white and brown adipose tissue (AKO) using the aP2‐Cre recombinase transgene. We also generated mice with simultaneous deletion of SCD1 from both adipose and liver (LAKO) or from liver alone (LKO) using the albumin‐Cre transgene. Mice were subjected to high‐fat diet‐induced obesity (DIO; Research Diets 12492) or genetically‐induced obesity using the leptin‐resistant yellow agouti (Ay/a) allele and compared to control mice not expressing Cre recombinase (LOX). Food intakes and changes in body weights were similar amongst the LOX, AKO, LKO and LAKO mice in both models of obesity. Additionally, fat pad mass (epididymal and subcutaneous) was unaffected by adipose and/or liver deletion of SCD1. Immunoblot analysis confirmed deletion of SCD1 and fatty acid composition analysis by gas chromatography revealed reduced MUFA content in the targeted tissues. In light of our previous observations that mice with a whole‐body or skin‐specific deletion of SCD1 are resistant to obesity, the current study suggest that SCD1 deletion from adipose and/or liver is insufficient to elicit protection from obesity. Research supported by funding from NIH‐NIDDK and AHA.