Kaempferol reduces hepatic triglyceride accumulation by inhibiting Akt

2019 ◽  
Vol 43 (11) ◽  
Author(s):  
Minh‐Hien Hoang ◽  
Yaoyao Jia ◽  
Ji Hae Lee ◽  
Yeonji Kim ◽  
Sung‐Joon Lee
Keyword(s):  
Hepatic Triglyceride ◽  
Triglyceride Accumulation

scholarly journals Hydroethanolic Extract of Defatted Buchholzia coriacea Seeds Alleviates Tamoxifen-Induced Hepatic Triglyceride Accumulation, Inflammation and Oxidative Distress in Rat

Medicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 1
Author(s):  
Ayokanmi Ore ◽  
Abideen Idowu Adeogun ◽  
Oluseyi Adeboye Akinloye
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Liver Injury ◽  
Hepatic Function ◽  
Protein Carbonyls ◽  
Control Group ◽  
Hepatic Triglyceride ◽  
Triglyceride Accumulation ◽  
Group I ◽  
Hydroethanolic Extract

Background: Tamoxifen (TMX) has proven to be effective in the prevention and treatment of breast cancer. However, long-term use of TMX is associated with hepatic steatosis, oxidative liver injury and hepatocarcinoma. Buchholzia coriacea seeds (BCS) have been widely applied in traditional medicine due to their nutritional and therapeutic potentials. This study investigates the protective effect of hydroethanolic extract of (defatted) B. coriacea seeds (HEBCS) against TMX–induced hepatotoxicity in rats. Methods: Thirty-six (36) male albino rats were divided into six groups (n = 6/group). Group I served as control. Group II received 50 mg/kg/day TMX orally (p.o.) (TMX) for 21 days, group III received TMX plus 125 mg/kg/d HEBCS p.o. (HEBCS 125) for 21 days, group IV received TMX plus 250 mg/kg/d HEBCS p.o. (HEBCS 250) for 21 days and rats in group V and VI received HEBCS 125 and HEBCS 250 respectively for 21 days. Results: Compared with the control, TMX caused a significant increase (p < 0.05) in serum hepatic function biomarkers: alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase by 57%, 60% and 68% respectively. TMX also caused a significant increase in hepatic triglycerides level by 166% when compared with control and a significant decrease in serum HDL-cholesterol level by 37%. Compared with control, hepatic marker of inflammation, tumour necrosis factor alpha (TNF-α) increased significantly by 220%, coupled with significant increase in expression of interleukin 6 and cyclooxygenase 2. There was also significant increase in levels of Biomarkers of oxidative stress, nitric oxide, malondialdehyde and protein carbonyls in the TMX group by 89%, 175% and 114% respectively when compared with the control. Hepatic antioxidants, reduced glutathione (GSH) level and activities of superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST) and glutathione peroxidase (GSH-Px) decreased significantly in the TMX group by 35%, 67%, 41%, 59% and 53% respectively when compared with the control. However, HEBCS at 250 mg/kg significantly protected against TMX–induced hepatotoxicity by decreasing hepatic triglyceride content, serum hepatic function biomarkers, hepatic inflammation and oxidative stress with significant improvement in hepatic antioxidant system. Histopathological findings show that HEBCS alleviate TMX–induced hepatocyte ballooning. Conclusions: Current data suggest that HEBCS protected against TMX–induced hepatotoxicity in rats. HEBCS may be useful in managing TMX–induced toxicities in breast cancer patients. It may also be helpful against other forms of liver injury involving steatosis, inflammation, free radicals, and oxidative damage.

Essential fatty acid deficiency and plasma triglyceride turnover in rats

1980 ◽  
Vol 238 (5) ◽  
pp. E499-E505 ◽  
Author(s):  
M. T. Huang ◽  
M. A. Williams
Keyword(s):  
Fatty Acid ◽  
Essential Fatty Acid ◽  
Essential Fatty Acid Deficiency ◽  
Plasma Triglyceride ◽  
Hepatic Triglyceride ◽  
Triglyceride Accumulation ◽  
Essential Fatty Acid Deficient ◽  
Triglyceride Secretion ◽  
Acid Deficiency ◽  
Fatty Acid Deficiency

Hepatic triglyceride secretion in essential fatty acid-deficient rats was examined by three separate techniques in an effort to resolve conflicting evidence on the question of whether essential fatty acid deficiency altered hepatic triglyceride secretion in vivo. First, plasma triglyceride turnover was measured by intravenous injection of [2-3H]glycerol trioleate. Equations of the kinetics were formulated based on a single, open pool model. Turnover rates and pool sizes of plasma triglyceride were calculated from these equations. Second, [2-3H]glycerol was injected, and apparent rate constants for plasma triglyceride secretion and clearance were calculated by kinetic analysis. Third, Triton WR-1339 was used to inhibit lipoprotein clearance from blood plasma, and rates of plasma triglyceride accumulation were measured. The results of these studies showed that the rate of hepatic triglyceride secretion was 2-3 times greater in essential fatty acid-deficient rats than in nondeficient controls. The increase in triglyceride secretion, as well as the higher level of liver triglyceride typical of essential fatty acid-deficient rats, could be caused by increased lipogenesis and increased mobilization of fatty acids from adipose tissues.

PKCδ regulates hepatic triglyceride accumulation and insulin signaling in Leprdb/db mice

2014 ◽  
Vol 450 (4) ◽  
pp. 1619-1625 ◽  
Author(s):  
Jian Zhang ◽  
Christine M. Burrington ◽  
Samantha K. Davenport ◽  
Andrew K. Johnson ◽  
Melissa J. Horsman ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Hepatic Triglyceride ◽  
Triglyceride Accumulation

scholarly journals Per-Arnt-Sim Kinase (PASK) Deficiency Increases Cellular Respiration on a Standard Diet and Decreases Liver Triglyceride Accumulation on a Western High-Fat High-Sugar Diet

Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1990 ◽  
Author(s):  
Jenny Pape ◽  
Colleen Newey ◽  
Haley Burrell ◽  
Audrey Workman ◽  
Katelyn Perry ◽  
...  
Keyword(s):  
The United States ◽  
Cellular Respiration ◽  
Standard Diet ◽  
Male Mice ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
High Sugar ◽  
Triglyceride Accumulation ◽  
Pas Kinase

Diabetes and the related disease metabolic syndrome are epidemic in the United States, in part due to a shift in diet and decrease in physical exercise. PAS kinase is a sensory protein kinase associated with many of the phenotypes of these diseases, including hepatic triglyceride accumulation and metabolic dysregulation in male mice placed on a high-fat diet. Herein we provide the first characterization of the effects of western diet (high-fat high-sugar, HFHS) on Per-Arnt-Sim kinase mice (PASK−/−) and the first characterization of both male and female PASK−/− mice. Soleus muscle from the PASK−/− male mice displayed a 2-fold higher oxidative phosphorylation capacity than wild type (WT) on the normal chow diet. PASK−/− male mice were also resistant to hepatic triglyceride accumulation on the HFHS diet, displaying a 2.7-fold reduction in hepatic triglycerides compared to WT mice on the HFHS diet. These effects on male hepatic triglyceride were further explored through mass spectrometry-based lipidomics. The absence of PAS kinase was found to affect many of the 44 triglycerides analyzed, preventing hepatic triglyceride accumulation in response to the HFHS diet. In contrast, the female mice showed resistance to hepatic triglyceride accumulation on the HFHS diet regardless of genotype, suggesting the effects of PAS kinase may be masked.

Glucokinase activation leads to an unsustained hypoglycaemic effect with hepatic triglyceride accumulation in db/db mice

2021 ◽  
Author(s):  
Shinichiro Kawata ◽  
Akinobu Nakamura ◽  
Hideaki Miyoshi ◽  
Kelaier Yang ◽  
Ikumi Shigesawa ◽  
...  
Keyword(s):  
Hypoglycaemic Effect ◽  
Hepatic Triglyceride ◽  
Triglyceride Accumulation
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