In Vitro Effects of Aqueous Extracts of Turkish Coffee and Instant Coffee on Glucose Metabolism in Cow Liver Tissue

2014 ◽  
Vol 03 (02) ◽  
Author(s):  
Zahide Esra Durak
1984 ◽  
Vol 16 (01) ◽  
pp. 27-31 ◽  
Author(s):  
M. Matsumura ◽  
T. Fukushima ◽  
H. Saito ◽  
Shiro Saito

Proceedings ◽  
2020 ◽  
Vol 61 (1) ◽  
pp. 20
Author(s):  
Miguel Rebollo-Hernanz ◽  
Yolanda Aguilera ◽  
Maria A. Martin-Cabrejas ◽  
Elvira Gonzalez de Mejia

This study aimed to assess the effect of the primary phytochemicals from coffee by-products and two aqueous extracts from the coffee husk and silverskin on lipid and glucose metabolism regulation in hepatocytes using an in vitro model of non-alcoholic fatty liver disease. Coffee husk and silverskin were used to prepare two aqueous extracts (CHE and CSE, respectively) using water. The phytochemical composition was determined using UPLC-MS/MS analysis. HepG2 cells were co-treated with 10–50 µmol L‒1 of either pure caffeine, chlorogenic acid, caffeic acid, protocatechuic acid, or gallic acid, and kaempferol, CHE, or CSE (20–100 µg mL‒1) in the presence or absence of palmitic acid (PA, 500 µmol L‒1). Different biomarkers of cell metabolism were assessed 24 h after the co-treatment in cell supernatants and lysates using chemical, biochemical, and immunochemical techniques. Phytochemicals from coffee by-products decreased PA-triggered lipid accumulation (16–94%, p < 0.05) by reducing fatty acid synthase activity and stimulating lipolysis (8–83%, p < 0.05). CHE, CSE, and therein-bioactive compounds promoted glucose uptake (13–45%) via the increase in the phosphorylation of the insulin receptor (1.9- to 2.7-fold), protein kinase B (AKT) (1.4- to 3.1-fold), AMPKα (1.6- to 2.4-fold), and PTEN (2.0- to 4.2-fold). In conclusion, our results proved that phytochemicals from coffee by-products, mainly caffeine and chlorogenic acid, could regulate hepatic lipid and glucose metabolism. Overall, our results generate new insights into the use of coffee by-products as a sustainable food ingredient to encounter non-alcoholic fatty liver disease.


2011 ◽  
Vol 110 (6) ◽  
pp. 2221-2227 ◽  
Author(s):  
Xiaoyan Yang ◽  
Bo Huang ◽  
Jianping Chen ◽  
Shiguang Huang ◽  
Huanqin Zheng ◽  
...  

1976 ◽  
Vol 10 (5) ◽  
pp. 733-741 ◽  
Author(s):  
Hiromu Shoji ◽  
Joseph F. Nicastro ◽  
George D. Rovere ◽  
Anthony G. Gristina

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
HM Lee ◽  
TG Ahn ◽  
CW Kim ◽  
HJ An
Keyword(s):  

1990 ◽  
Vol 64 (03) ◽  
pp. 402-406 ◽  
Author(s):  
M D Oethinger ◽  
E Seifried

SummaryThe present in vitro study investigated dose-, time- and temperature-dependent effects of two-chain urokinase plasminogen activato(u-PA, urokinase) on normal citrated plasma. When 10 μg/ml u-PA wereadded to pooled normal plasma and incubated for 30 min at an ambient temperature (25° C), α2-antiplas-min decreased to 8% of the control value. Incubation on ice yielded a decrease to 45% of control,whereas α2-antiplasmin was fully consumed at 37° C. Fibrinogen and plasminogen fell to 46% and 39%, respectively, after a 30 min incubation at 25° C. Thrombin time prolonged to 190% of control.Various inhibitors were studied with respect to their suitability and efficacy to prevent these in vitro effects. Aprotinin exhibited a good protective effect on fibrinogen at concentrations exceeding 500 KlU/ml plasma. Its use, however, was limited due to interferences with some haemostatic assays. We could demonstrate that L-Glutamyl-L-Glycyl-L-Arginyl chloromethyl ketone (GGACK) and a specific polyclonal anti-u-PA-antibody (anti-u-PA-IgG) effectively inhibited urokinase-induced plasmin generation without interfering with haemostatic assays. The anti-u-PA-antibody afforded full protection ofα2-antiplasmin at therapeutic levels of u-PA.It is concluded that u-PA in plasma samples from patients during thrombolytic therapy may induce in vitro effects which should be prevented by the use of a suitable inhibitor such as GGACK or specific anti-u-PA-antibody.


1989 ◽  
Vol 61 (02) ◽  
pp. 254-258 ◽  
Author(s):  
Margaret L Rand ◽  
Peter L Gross ◽  
Donna M Jakowec ◽  
Marian A Packham ◽  
J Fraser Mustard

SummaryEthanol, at physiologically tolerable concentrations, inhibits platelet responses to low concentrations of collagen or thrombin, but does not inhibit responses of washed rabbit platelets stimulated with high concentrations of ADP, collagen, or thrombin. However, when platelet responses to high concentrations of collagen or thrombin had been partially inhibited by prostacyclin (PGI2), ethanol had additional inhibitory effects on aggregation and secretion. These effects were also observed with aspirin- treated platelets stimulated with thrombin. Ethanol had no further inhibitory effect on aggregation of platelets stimulated with ADP, or the combination of ADP and epinephrine. Thus, the inhibitory effects of ethanol on platelet responses in the presence of PGI2 were very similar to its inhibitory effects in the absence of PGI2, when platelets were stimulated with lower concentrations of collagen or thrombin. Ethanol did not appear to exert its inhibitory effects by increasing cyclic AMP above basal levels and the additional inhibitory effects of ethanol in the presence of PGI2 did not appear to be brought about by further increases in platelet cyclic AMP levels.


Sign in / Sign up

Export Citation Format

Share Document