scholarly journals Dietary Effects of Oxidized Eicosapentaenoic Acid (EPA) and Intact EPA on Hepatic Steatosis Induced by a High-sucrose Diet and Liver-X-receptor α Agonist in Mice

2016 ◽  
Vol 65 (3) ◽  
pp. 233-240
Author(s):  
Hidehiro Furumoto ◽  
Tharnath Nanthirudjanar ◽  
Takashi Hirata ◽  
Tatsuya Sugawara
Keyword(s):  
Eicosapentaenoic Acid ◽  
Hepatic Steatosis ◽  
Liver X Receptor ◽  
Dietary Effects ◽  
Liver X Receptor Α ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
High Sucrose

Hepatic steatosis and plasma dyslipidemia induced by a high-sucrose diet are corrected by an acute leptin infusion

2007 ◽  
Vol 102 (6) ◽  
pp. 2260-2265 ◽  
Author(s):  
Wan Huang ◽  
Nikolas Dedousis ◽  
Robert M. O'Doherty
Keyword(s):  
Hepatic Steatosis ◽  
Model Assessment ◽  
Phosphatidylinositol 3 Kinase ◽  
Homeostasis Model Assessment ◽  
Hepatic Lipid Metabolism ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
Tg 29 ◽  
Plasma Leptin ◽  
High Sucrose

High sucrose (HS) feeding in rats induces hepatic steatosis and plasma dyslipidemia. In previous reports (Huang W, Dedousis N, Bhatt BA, O'Doherty RM. J Biol Chem 279: 21695–21700, 2004; and Huang W, Dedousis N, Bandi A, Lopaschuk GD, O'Doherty RM. Endocrinology 147: 1480–1487, 2006), our laboratory demonstrated a rapid (∼100 min) leptin-induced decrease in liver and plasma VLDL triglycerides (TG) in lean rats, effects that were abolished in obese rats fed a high-fat diet, a model that also presents with hepatic steatosis and plasma dyslipidemia. To further examine the capacity of acute leptin treatment to improve metabolic abnormalities induced by nutrient excess, hepatic leptin action was studied in rats after 5 wk of HS feeding. HS feeding induced hepatic steatosis (TG +80 ± 8%; P = 0.001), plasma hyperlipidemia (VLDL-TG +102 ± 14%; P = 0.001), hyperinsulinemia (plasma insulin +67 ± 12%; P = 0.04), and insulin resistance as measured by homeostasis model assessment (+125 ± 20%; P = 0.02), without increases in adiposity or plasma leptin concentration compared with standard chow-fed controls. A 120-min infusion of leptin (plasma leptin 13.6 ± 0.7 ng/ml) corrected hepatic steatosis (liver TG −29 ± 3%; P = 0.003) and plasma hyperlipidemia in HS (VLDL-TG −42 ± 4%; P = 0.001) and increased plasma ketones (+45 ± 3%; P = 0.006), without altering plasma glucose, insulin, or homeostasis model assessment compared with saline-infused HS controls. In addition, leptin activated liver phosphatidylinositol 3-kinase (+70 ± 18%; P = 0.01) and protein kinase B (Akt; +90 ± 29%; P = 0.02), and inhibited acetyl-CoA carboxylase (40 ± 7%; P = 0.04) in HS, further demonstrating that hepatic leptin action was intact in these animals. We conclude that 1) leptin action on hepatic lipid metabolism remains intact in HS-fed rats, 2) leptin rapidly reverses hepatic steatosis and plasma dyslipidemia induced by sucrose, and 3) the preservation of hepatic leptin action after a HS diet is associated with the maintenance of low adiposity and plasma leptin concentrations.

scholarly journals Involvement of AMP-activated protein kinase in beneficial effects of betaine on high-sucrose diet-induced hepatic steatosis

2007 ◽  
Vol 293 (4) ◽  
pp. G894-G902 ◽  
Author(s):  
Zhenyuan Song ◽  
Ion Deaciuc ◽  
Zhanxiang Zhou ◽  
Ming Song ◽  
Theresa Chen ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Hepatic Steatosis ◽  
Critical Role ◽  
Standard Diet ◽  
Fat Accumulation ◽  
Beneficial Effects ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
Amp Activated Protein Kinase ◽  
High Sucrose

Although simple steatosis was originally thought to be a pathologically inert histological change, fat accumulation in the liver may play a critical role not only in disease initiation, but also in the progression to nonalcoholic steatohepatitis and cirrhosis. Therefore, prevention of fat accumulation in the liver may be an effective therapy for multiple stages of nonalcoholic fatty liver disease (NAFLD). Promising beneficial effects of betaine supplementation on human NAFLD have been reported in some pilot clinical studies; however, data related to betaine therapy in NAFLD are limited. In this study, we examined the effects of betaine on fat accumulation in the liver induced by high-sucrose diet and evaluated mechanisms by which betaine could attenuate or prevent hepatic steatosis in this model. Male C57BL/6 mice weighing 20 ± 0.5 g (means ± SE) were divided into four groups (8 mice per group) and started on one of four treatments: standard diet (SD), SD+betaine, high-sucrose diet (HS), and HS + betaine. Betaine was supplemented in the drinking water at a concentration of 1% (wt/vol) (anhydrous). Long-term feeding of high-sucrose diet to mice caused significant hepatic steatosis accompanied by markedly increased lipogenic activity. Betaine significantly attenuated hepatic steatosis in this animal model, and this change was associated with increased activation of hepatic AMP-activated protein kinase (AMPK) and attenuated lipogenic capability (enzyme activities and gene expression) in the liver. Our findings are the first to suggest that betaine might serve as a therapeutic tool to attenuate hepatic steatosis by targeting the hepatic AMPK system.

scholarly journals Antiobesity Effect of Eicosapentaenoic Acid in High-Fat/High-Sucrose Diet–Induced Obesity

Diabetes ◽  
2010 ◽  
Vol 59 (10) ◽  
pp. 2495-2504 ◽  
Author(s):  
Ayumi Sato ◽  
Hiroyuki Kawano ◽  
Tatsuto Notsu ◽  
Masahiko Ohta ◽  
Masanori Nakakuki ◽  
...  
Keyword(s):  
Eicosapentaenoic Acid ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
High Sucrose
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