Selenium significantly inhibits adipocyte hypertrophy and abdominal fat accumulation in OLETF rats via induction of fatty acid β-oxidation.
A combination of selenium (Se) with other trace element is associated with partially modulate fatty acid distribution as well as reduction of the body weight and feed efficiency. To investigate whether or not Se treatment has an impact on lipid metabolism, we examined the levels of lipid metabolism-related factors, including abdominal fat, adiponectin, cholesterol, very long chain dehydrogenase (VLCAD), and medium chain acyl-CoA dehydrogenase (MCAD) in 20-week-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats following sodium selenite treatment for 2 weeks. Herein, we observed that (a) Se treatment induced insulin-like effects by lowering the serum glucose level in rats; (b) Se-treated rats showed significance values decreases in abdominal fat mass, adipocyte size, and adiponectin, which are associated with lipid metabolism; (c) Se treatment led to reduced levels of cholesterol, triglycerides, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol; (d) fat tissue in Se-treated rats displayed significantly lower expression of adipocyte marker genes along with increased expression of VLCAD and MCAD; and (e) fatty liver formation and β-oxidation gene expression were both significantly reduced in liver tissue of Se-treated rats. Therefore, our results suggest that Se may induce inhibition of adipocyte hypertrophy and abdominal fat accumulation along with suppression of fatty liver formation by the differential regulation of the gene expression for fatty acid β-oxidation in the OLETF model.
College of Natural Resources & Life Science, Pusan National University, Miryang, 627-706, Republic of Korea.
Ji Eun
JE
Kim
Sun Il
SI
Choi
Hye Ryun
HR
Lee
In Sik
IS
Hwang
Young Ju
YJ
Lee
Beum Soo
BS
An
Sang Hak
SH
Lee
Hak Jin
HJ
Kim
Byeong Cheol
BC
Kang
Dae Youn
DY
Hwang
D050153:Abdominal Fat / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D042964:Acyl-CoA Dehydrogenase / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D044942:Acyl-CoA Dehydrogenase, Long-Chain / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D050154:Adiposity; D000818:Animals; D019440:Anti-Obesity Agents / Q000627:therapeutic use*; D048909:Diabetes Complications / Q000097:blood / Q000178:diet therapy / Q000378:metabolism / Q000473:pathology; D019587:Dietary Supplements; D004790:Enzyme Induction; D005234:Fatty Liver / Q000209:etiology / Q000517:prevention & control; D006984:Hypertrophy; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D050356:Lipid Metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D009765:Obesity / Q000150:complications / Q000178:diet therapy* / Q000378:metabolism / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D020334:Rats, Inbred OLETF; D011919:Rats, Inbred Strains; D012643:Selenium / Q000627:therapeutic use*; D018038:Sodium Selenite / Q000008:administration & dosage
D019440:Anti-Obesity Agents; D007004:Hypoglycemic Agents; D000960:Hypolipidemic Agents; D042964:Acyl-CoA Dehydrogenase; D044942:Acyl-CoA Dehydrogenase, Long-Chain; D012643:Selenium; D018038:Sodium Selenite