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Global deletion of stearoyl‐CoA desaturase‐2 enhances glucose tolerance
Author(s) -
O'Neill Lucas,
Ntambi James
Publication year - 2013
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.27.1_supplement.1017.12
Subject(s) - stearoyl coa desaturase , medicine , endocrinology , biology , insulin , secretion , pancreas , metabolism , chemistry , biochemistry , gene , gene expression
Stearoyl‐CoA desaturase (SCD) catalyzes the rate‐limiting step in the synthesis of monounsaturated fatty acids (MUFAs) from saturated fatty acids. There are four SCD isoforms in mouse (SCD1–4) and two in human (hSCD1 and 5). Here we begin to elucidate the function of stearoyl‐CoA desaturase‐2 (SCD2) in whole body metabolism. SCD2 is highly expressed in the brain, immune cells, and pancreas. Depending on the genetic background, prenatal loss of SCD2 is either embryonic lethal or 70% lethal within 24 hours after birth. Our microarray data comparing SCD2KO embryos to WT embryos showed that ~20% of the genes down regulated are pancreatic. In a follow up study within the pancreas, it was shown that SCD2 is predominately expressed in the alpha and beta cells. We report that global loss of SCD2 in mice confers enhanced glucose tolerance and lowers both fasting and fed plasma glucose levels. We hypothesize this is attributed to enhanced insulin secretion. Moreover, we propose a mechanism where endogenously synthesized MUFAs in beta cells act as antagonists for insulin secretion. This work was funded by NIH.