scholarly journals Pharmacologic activation of peroxisome proliferator-activating receptor-α accelerates hepatic fatty acid oxidation in neonatal pigs

Oncotarget ◽  
2018 ◽  
Vol 9 (35) ◽  
pp. 23900-23914 ◽  
Author(s):  
Kwanseob Shim ◽  
Sheila Jacobi ◽  
Jack Odle ◽  
Xi Lin
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Neonatal Pigs ◽  
Hepatic Fatty Acid ◽  
Hepatic Fatty Acid Oxidation ◽  
Activating Receptor

scholarly journals Neddylation inhibition ameliorates steatosis in NAFLD by boosting hepatic fatty acid oxidation via DEPTOR-mTOR axis

2021 ◽  
pp. 101275
Author(s):  
Marina Serrano-Maciá ◽  
Jorge Simón ◽  
Maria J. González-Rellan ◽  
Mikel Azkargorta ◽  
Naroa Goikoetxea-Usandizaga ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Hepatic Fatty Acid ◽  
Hepatic Fatty Acid Oxidation

scholarly journals Agmatine Stimulates Hepatic Fatty Acid Oxidation

2006 ◽  
Vol 281 (13) ◽  
pp. 8486-8496 ◽  
Author(s):  
Itzhak Nissim ◽  
Yevgeny Daikhin ◽  
Ilana Nissim ◽  
Bohdan Luhovyy ◽  
Oksana Horyn ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Hepatic Fatty Acid ◽  
Hepatic Fatty Acid Oxidation

RS4-type resistant starch prevents high-fat diet-induced obesity via increased hepatic fatty acid oxidation and decreased postprandial GIP in C57BL/6J mice

2010 ◽  
Vol 298 (3) ◽  
pp. E652-E662 ◽  
Author(s):  
Akira Shimotoyodome ◽  
Junko Suzuki ◽  
Daisuke Fukuoka ◽  
Ichiro Tokimitsu ◽  
Tadashi Hase
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Resistant Starch ◽  
High Fat Diet ◽  
Acid Oxidation ◽  
High Fat ◽  
Fat Utilization ◽  
Hepatic Fatty Acid ◽  
Diet Induced Obesity ◽  
Hepatic Fatty Acid Oxidation

Chemically modified starches (CMS) are RS4-type resistant starch, which shows a reduced availability, as well as high-amylose corn starch (HACS, RS2 type), compared with the corresponding unmodified starch. Previous studies have shown that RS4 increases fecal excretion of bile acids and reduces zinc and iron absorption in rats. The aim of this study was to investigate the effects of dietary RS4 supplementation on the development of diet-induced obesity in mice. Weight- and age-matched male C57BL/6J mice were fed for 24 wk on a high-fat diet containing unmodified starch, hydroxypropylated distarch phosphate (RS4), or HACS (RS2). Those fed the RS4 diet had significantly lower body weight and visceral fat weight than those fed either unmodified starch or the RS2 diet. Those fed the RS4 diet for 4 wk had a significantly higher hepatic fatty acid oxidation capacity and related gene expression and lower blood insulin than those fed either unmodified starch or the RS2 diet. Indirect calorimetry showed that the RS4 group exhibited higher energy expenditure and fat utilization compared with the RS2 group. When gavaged with fat (trioleate), RS4 stimulated a lower postprandial glucose-dependent insulinotropic polypeptide (GIP; incretin) response than RS2. Higher blood GIP levels induced by chronic GIP administration reduced fat utilization in high-fat diet-fed mice. In conclusion, dietary supplementation with RS4-type resistant starch attenuates high-fat diet-induced obesity more effectively than RS2 in C57BL/6J mice, which may be attributable to lower postprandial GIP and increased fat catabolism in the liver.

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