scholarly journals Folic acid supplementation during high-fat diet feeding restores AMPK activation via an AMP-LKB1-dependent mechanism

2015 ◽  
Vol 309 (10) ◽  
pp. R1215-R1225 ◽  
Author(s):  
Victoria Sid ◽  
Nan Wu ◽  
Lindsei K. Sarna ◽  
Yaw L. Siow ◽  
James D. House ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
Folic Acid Supplementation ◽  
Ampk Activation ◽  
Hepatic Cholesterol ◽  
High Fat ◽  
Acid Supplementation ◽  
Ampk Phosphorylation

AMPK is an endogenous energy sensor that regulates lipid and carbohydrate metabolism. Nonalcoholic fatty liver disease (NAFLD) is regarded as a hepatic manifestation of metabolic syndrome with impaired lipid and glucose metabolism and increased oxidative stress. Our recent study showed that folic acid supplementation attenuated hepatic oxidative stress and lipid accumulation in high-fat diet-fed mice. The aim of the present study was to investigate the effect of folic acid on hepatic AMPK during high-fat diet feeding and the mechanisms involved. Male C57BL/6J mice were fed a control diet (10% kcal fat), a high-fat diet (60% kcal fat), or a high-fat diet supplemented with folic acid (26 mg/kg diet) for 5 wk. Mice fed a high-fat diet exhibited hyperglycemia, hepatic cholesterol accumulation, and reduced hepatic AMPK phosphorylation. Folic acid supplementation restored AMPK phosphorylation (activation) and reduced blood glucose and hepatic cholesterol levels. Activation of AMPK by folic acid was mediated through an elevation of its allosteric activator AMP and activation of its upstream kinase, namely, liver kinase B1 (LKB1) in the liver. Consistent with in vivo findings, 5-methyltetrahydrofolate (bioactive form of folate) restored phosphorylation (activation) of both AMPK and LKB1 in palmitic acid-treated HepG2 cells. Activation of AMPK by folic acid might be responsible for AMPK-dependent phosphorylation of HMG-CoA reductase, leading to reduced hepatic cholesterol synthesis during high-fat diet feeding. These results suggest that folic acid supplementation may improve cholesterol and glucose metabolism by restoration of AMPK activation in the liver.

Folic acid supplementation attenuates high fat diet induced hepatic oxidative stress via regulation of NADPH oxidase

2012 ◽  
Vol 90 (2) ◽  
pp. 155-165 ◽  
Author(s):  
Lindsei K. Sarna ◽  
Nan Wu ◽  
Pengqi Wang ◽  
Sun-Young Hwang ◽  
Yaw L. Siow ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Liver Injury ◽  
Nadph Oxidase ◽  
High Fat Diet ◽  
Folic Acid Supplementation ◽  
High Fat ◽  
Acid Supplementation ◽  
Hepatic Oxidative Stress ◽  
Enhanced Expression

Diets high in saturated fat and cholesterol facilitate weight gain, a predisposing factor that contributes to the onset of obesity and metabolic disorders. Hepatic oxidative stress is commonly reported in various animal models of obesity and has been associated with enhanced expression of NADPH oxidase. We have previously reported several antioxidant mechanisms through which folic acid confers protection during hyperhomocysteinemia-induced oxidative stress. The objective of the present study was to investigate whether folic acid supplementation ameliorates high-fat diet induced oxidative stress in the liver, and to identify the underlying mechanisms. Male C57BL/6J mice were fed a control diet, a high-fat diet, or a high-fat diet supplemented with folic acid for 12 weeks. A high-fat diet led to increased body mass, hepatic lipid peroxidation, and liver injury. There was a significant increase in hepatic NADPH oxidase activity, which was associated with enhanced expression of several NADPH-oxidase subunits. Folic acid supplementation had a protective effect against high-fat diet induced hepatic oxidative stress and liver injury. Further analysis revealed that the antioxidant effect of folic acid was attributed, in part, to transcriptional regulation of NADPH oxidase. These results suggested that folic acid supplementation may be hepatoprotective from liver injury associated with a high-fat diet.

Folic Acid Supplementation Attenuates Chronic Hepatic Inflammation in High-Fat Diet Fed Mice

Lipids ◽  
2018 ◽  
Vol 53 (7) ◽  
pp. 709-716 ◽  
Author(s):  
Victoria Sid ◽  
Yue Shang ◽  
Yaw L. Siow ◽  
Susara Madduma Hewage ◽  
James D. House ◽  
...  
Keyword(s):  
Folic Acid ◽  
High Fat Diet ◽  
Folic Acid Supplementation ◽  
Hepatic Inflammation ◽  
High Fat ◽  
Acid Supplementation

Impact of iron and folic acid supplementation on oxidative stress during pregnancy

2015 ◽  
Vol 35 (8) ◽  
pp. 803-806 ◽  
Author(s):  
E. Lymperaki ◽  
A. Tsikopoulos ◽  
K. Makedou ◽  
E. Paliogianni ◽  
L. Kiriazi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Folic Acid Supplementation ◽  
Acid Supplementation ◽  
Iron And Folic Acid

Folic acid attenuates homocysteine and enhances antioxidative capacity in atherosclerotic rats

2017 ◽  
Vol 42 (10) ◽  
pp. 1015-1022 ◽  
Author(s):  
Shanshan Cui ◽  
Wen Li ◽  
Xin Lv ◽  
Pengyan Wang ◽  
Guowei Huang ◽  
...  
Keyword(s):  
Folic Acid ◽  
Antioxidant Capacity ◽  
Wistar Rats ◽  
Folic Acid Supplementation ◽  
Plasma Homocysteine ◽  
Serum Folate ◽  
Antioxidative Capacity ◽  
High Fat ◽  
Acid Supplementation ◽  
Atherosclerotic Lesions

Atherosclerosis is a chronic disease that can seriously endanger human life. Folic acid supplementation modulates several disorders, including atherosclerosis, via its antiapoptotic and antioxidative properties. This study investigated whether folic acid alleviates atherogenesis by restoring homocysteine levels and antioxidative capacity in atherosclerosis Wistar rats. To this end, 28 Wistar rats were randomly divided into 4 groups (7 rats/group) as follows: (i) wild-type group, fed only the AIN-93 semi-purified rodent diet (folic acid: 2.1 mg/kg); (ii) high-fat + folic acid-deficient group (HF+DEF) (folic acid: 0.2 mg/kg); (iii) high-fat + normal folic acid group (folic acid: 2.1 mg/kg); and (iv) high-fat + folic acid-supplemented group (folic acid: 4.2 mg/kg). After 12 weeks, histopathological changes in the atherosclerotic lesions of the aortic arch were determined. In addition, serum folate levels, plasma homocysteine levels, plasma S-adenosyl-homocysteine levels, antioxidant status, oxidant status, and lipid profiles were evaluated. The results show aggravated atherosclerotic lesions in the HF+DEF group. Folic acid supplementation increased concentrations of serum folate. Further, folic acid supplementation increased high-density lipoprotein-cholesterol, decreased plasma homocysteine levels, and improved antioxidant capacity in atherogenic rats. These findings are consistent with the hypothesis that folic acid alleviates atherogenesis by reducing plasma homocysteine levels and improving antioxidant capacity in rats fed a high-fat diet.

scholarly journals Ganoderma lucidum Extract Reduces Insulin Resistance by Enhancing AMPK Activation in High-Fat Diet-Induced Obese Mice

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3338
Author(s):  
Hyeon A Lee ◽  
Jae-Han Cho ◽  
Qonita Afinanisa ◽  
Gi-Hong An ◽  
Jae-Gu Han ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Protein Kinase ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
Ganoderma Lucidum ◽  
Fatty Acid Synthase ◽  
Metabolic Diseases ◽  
Ampk Activation ◽  
High Fat ◽  
Amp Activated Protein Kinase

Ganoderma lucidum is used widely in oriental medicine to treat obesity and metabolic diseases. Bioactive substances extracted from G. lucidum have been shown to ameliorate dyslipidemia, insulin resistance, and type 2 diabetes in mice via multiple 5′ AMP-activated protein kinase (AMPK)-mediated mechanisms; however, further studies are required to elucidate the anti-obesity effects of G. lucidum in vivo. In this study, we demonstrated that 3% G. lucidum extract powder (GEP) can be used to prevent obesity and insulin resistance in a mouse model. C57BL/6 mice were provided with a normal diet (ND) or a high-fat diet (HFD) supplemented with 1, 3, or 5% GEP for 12 weeks and the effect of GEP on body weight, liver, adipose tissue, adipokines, insulin and glucose tolerance (ITT and GTT), glucose uptake, glucose-metabolism related proteins, and lipogenesis related genes was examined. GEP administration was found to reduce weight gain in the liver and fat tissues of the mice. In addition, serum parameters were significantly lower in the 3% and 5% GEP mice groups than in those fed a HFD alone, whereas adiponectin levels were significantly higher. We also observed that GEP improved glucose metabolism, reduced lipid accumulation in the liver, and reduced adipocyte size. These effects may have been mediated by enhanced AMPK activation, which attenuated the transcription and translation of lipogenic genes such as fatty acid synthase (FAS), stearoyl-CoA desaturase 1 (SCD1), and sterol regulatory element-binding protein-1c (SREBP1c). Moreover, AMP-activated protein kinase (AMPK) activation increased acetyl-CoA carboxylase (ACC), insulin receptor (IR), IR substrate 1 (IRS1), and Akt protein expression and activation, as well as glucose transporter type 1/4 (GLUT1/4) protein production, thereby improving insulin sensitivity and glucose metabolism. Together, these findings demonstrate that G. lucidum may effectively prevent obesity and suppress obesity-induced insulin resistance via AMPK activation.

Instant White Rice with Pigmented Giant Embryonic Rice Improves Glucose Metabolism and Inhibits Oxidative Stress in High-Fat Diet-Fed Mice

2018 ◽  
Vol 88 (5-6) ◽  
pp. 234-243
Author(s):  
Soo Im Chung ◽  
Catherine W. Rico ◽  
Sang Chul Lee ◽  
Mi Young Kang
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Brown Rice ◽  
Control Group ◽  
Hepatic Glycogen ◽  
High Fat ◽  
White Rice

Abstract. The effects of instant cooked rice made from a combination of white rice and pigmented giant embryonic Keunnunjami rice, in comparison with those of instant regular white or brown rice and instant non-pigmented giant embryonic brown rice, on the glucose metabolism and antioxidant defense status in high-fat diet-fed mice were investigated. 56 male C57BL/6N mice were randomly divided into 7 dietary groups: normal control, high fat (23 %, HF), and HF supplemented with normal white (HF + NW) or brown rice (HF + NB), non-pigmented giant embryonic rice (HF + GB), and white rice with 8 % Keunnunjami (HF + KJ8) and 18 % Keunnunjami (HF + KJ18). After 7 weeks, HF mice showed marked increases in blood glucose (156 mg/dL), plasma insulin (12.1 mg/mL), and lipid peroxidation, and a significant decrease in hepatic glycogen (14.2 mg/g) relative to the control group (p < 0.05). However, addition of instant NB, GB, KJ8, andKJ18) rice suppressed this high-fat diet-induced hyperglycemia and oxidative stress through altering glucose-regulating enzymes (glucokinase, glucose-6-phosphatase, and phosphoenolpyruvate carboxykinase) and activation of antioxidant enzymes (superoxide dismutase, glutathione peroxidase, catalase, glutathione reductase, and paraoxonase). Compared with HF mice, HF + KJ8 and HF + KJ18 groups exhibited significantly lower glucose (139–141 mg/dL), insulin (10.6–10.9 mg/mL), and lipid peroxidation and higher glycogen (15.3–16.4 mg/g) (p < 0.05). The hypoglycemic and antioxidant effects of instant KJ8 and KJ18 rice were generally comparable to those of instant NB and GB rice. These findings illustrate that instant rice made from white rice with 8 % Keunnunjami rice may be useful as a functional food with therapeutic potential against hyperglycemia and oxidative damage.

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