Role of TPNH in fatty acid synthesis from acetate by normal and diabetic rat-liver homogenate fractions

Abraham, S.; Matthes, K.J.; Chaikoff, I.L.

doi:10.1016/0006-3002(59)90207-0

Cited by 48 publications

(10 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The liver were cut from other attached organs gently and transferred to liquid nitrogen tank (–80°C) for further use. The liver homogenate was primed with proper method with slight modification as defined earlier . The liver tissue was cut with sterilized scissor and homogenized in 10 volume of 0.2 M cold phosphate buffer at 4°C for 2 minutes at pH 7.4 mixed with 2 mM mercaptoethanol and 2 Nm EDTA.…”

Section: Methodsmentioning

confidence: 99%

Molecular mechanisms of action of styrene toxicity in blood plasma and liver

Niaz

Mabqool

Khan

et al. 2017

Environmental Toxicology

View full text Add to dashboard Cite

Styrene is an aromatic colorless hydrocarbon available in liquid form and highly volatile. In its pure form, it gives a sweet smell. The primary source of exposure in the environment is from plastic materials, rubber industries, packaging materials, insulations, and fiber glass and carpet industry. Natural sources of styrene include: few metabolites in plants which are transferred through food chain. The current study was designed to evaluate styrene toxicity, including: superoxide dismutase (SOD) and protein carbonyl, oxidative stress, glucose-6-phosphatase (G6Pase), glycogen phosphorylase (GP), and phosphoenolpyruvate carboxykinase (PEPCK) activities, adenosine triphosphate (ATP) to adenosine diphosphate (ADP) ratio, and changes in gene expressions such as glutamate dehydrogenase 1 (GLUD1), glucose transporter 2 (GLUT2), and glucokinase (GCK) in the rat liver tissue. For this purpose, styrene was dissolved in corn oil and was administered via gavage, at doses 250, 500, 1000, 1500, 2000, mg/kg/day per mL and control (corn oil) to each rat with one day off in a week, for 42 days. Plasma SOD and protein carbonyl of plasma were significantly up-regulated in 1000, 1500, and 2000 mg/kg/day styrene administrated groups (P < .001). In addition, styrene caused an increase in lipid peroxidation (LPO) and reactive oxygen species (ROS) in the dose-dependent manners in liver tissue (P < .001). Furthermore, the ferrous reducing antioxidant power (FRAP) and total thiol molecules (TTM) in styrene-treated groups were significantly decreased in liver tissue (P < .001) with increasing doses. In treated rats, styrene significantly increased G6Pase activity (P < .001) and down-regulated GP activity (P < .001) as compared to the control group. The PEPCK activity was significantly raised in a dose-dependent manner (P < .001). The ATP/ADP ratio of live cells was significantly raised by increasing the dose (P < .001). There was significantly an up-regulation of GLUD1 and GCK at 2000 mg/kg group (P < .01) and a down-regulation for GLUT2 at the same dose. While in the rest of group, GLUT2 showed up-regulation of relative fold change. By targeting genes such as GLUD1, GLUT2, and GCK, disruption of hepatic gluconeogenesis, glycogenolysis, and insulin secretory functions are obvious. The present study illustrates that induction of oxidative stress followed by changes in G6Pase, GP, and PEPCK activities and the genes responsible for glucose metabolism are the mechanisms of styrene's action in the liver.

show abstract

Section: Methodsmentioning

confidence: 99%

Molecular mechanisms of action of styrene toxicity in blood plasma and liver

Niaz

Mabqool

Khan

et al. 2017

Environmental Toxicology

View full text Add to dashboard Cite

show abstract

“…The stimulatory effects of these compounds may be a consequence of the aconitase activity present in the particlefree supernatant fractions of the human and rat liver homogenates, which converts these acids to citrate, or of the action of isocitric dehydrogenase, which produces a-ketoglutarate, bicarbonate, and TPNH. As previously noted for rat liver (11) and lactating rat mammary gland (29) preparations, a-ketoglutarate plus bicarbonate in the presence of TPNH will not completely substitute for citrate in the human liver system.…”

Section: Resultsmentioning

confidence: 63%

“…Because glucose-6-phosphate did not stimulate lipogenesis from acetate in human or rat liver systems, it might be concluded that the amount of glucose-6-phosphate dehydrogenase (G-6-PD) present in these systems was limiting the pro- 6 Previous experiments with the rat liver system have shown that glucose-6-phosphate in concentrations from 8 x 10^to 1.6 X 10V M will not stimulate fatty acid synthesis (11). 7 The extinction coefficient of TPNH at 340 m/y is 6.22 X 10 cm' per mole (33).…”

Section: Resultsmentioning

confidence: 99%

“…Early observations with liver slices demonstrated the superiority of a bicarbonate incubation medium for the synthesis of fatty acids (38), and the more recent studies with liver homogenate fractions have left no doubt that bicarbonate is an active participant in the reaction sequence (10,11). Although an absolute requirement during the reaction, bicarbonate is not incorporated into the final free fatty acid molecule (6,39).…”

Section: Resultsmentioning

confidence: 99%

“…Lipogenesis has also been demonstrated in several isolated human tissues, such as placenta (19) and aorta (20). However, most of the details on the mechanism of fatty acid synthesis have been obtained from studies with liver homogenates prepared from lower animals: rat (11), pigeon (3), pig (21), and chicken (22). In order to study the pathway of fatty acid synthesis in a human tissue, we used biopsy specimens of human liver.…”

mentioning

confidence: 99%

See 2 more Smart Citations