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Role of brain stearoyl‐CoA desaturase‐1 in metabolism, obesity, and glucose homeostasis (605.2)
Author(s) -
Harrington Kristin,
Burhans Maggie,
Ntambi James
Publication year - 2014
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.28.1_supplement.605.2
Subject(s) - insulin resistance , medicine , endocrinology , adipose tissue , steatosis , obesity , glucose homeostasis , triglyceride , type 2 diabetes , homeostasis , biology , chemistry , diabetes mellitus , cholesterol
The high prevalence of obesity, coupled with its potential to develop into serious health issues including type II diabetes, insulin resistance and coronary artery disease, reveals it is a significant health problem. To investigate how excess adipose tissue manifests into these health issues, we have observed the effects of a disruption in stearoyl‐CoA desaturase 1 (SCD1), which is involved in the synthesis of endogenous monounsaturated fatty acids from saturated fatty acids. We have previously demonstrated that whole‐body deficiency of SCD1 in mice protects from high‐fat diet‐induced obesity, hepatic steatosis and insulin resistance. However, the tissue‐specific contribution of SCD1 to these phenotypes remains to be fully elucidated. In the current study, we investigated the role of brain SCD1 in mediating the metabolic consequences of a high‐fat diet (HFD). We fed nestin‐cre+;SCD1 flox/flox brain‐specific SCD1 knockout (BKO) mice a HFD for 18 weeks. We observed that both male and female BKO mice weighed significantly less than Lox controls. In addition, male BKO mice had lower hepatic triglyceride levels than Lox mice, and enhanced glucose tolerance relative to Lox mice. Overall, these results indicate brain SCD1 plays a role in HFD‐induced adiposity and glucose homeostasis.