Inhibition by orthophosphate esters of glucose-6-phosphatase

Abstract

Inhibition of rat liver microsomal glucose-6-phosphatase (D-glucose-6-phosphate phosphohydrolase, EC 3.1.3.9) by orthophosphate and organophosphate esters was examined at pH 6.0 and 7.5 with and without enzyme pretreatment with 0.2% (w/v) deoxycholate. Inhibition by orthophosphate and monoethyl phosphate was competitive with respect to glucose-6-P while inhibition by mono- and di-phenyl phosphate was of the mixed type. Monoalkyl phosphates were more effective inhibitors than the analogous di- and tri-alkyl phosphates and deoxycholate potentiated the inhibitory effects. Mono- and di-phenyl phosphates were more effective inhibitors than triphenyl phosphate, and deoxycholate decreased these inhibitory effects. The results are interpreted in terms of inhibitor and deoxycholate interactions with the enzyme.

Calcium Transport in Synaptosomes and Subcellular Membrane Fractions of Brain Tissue in Spontaneously Hypertensive Rats

“…Data obtained in this study for identification of fractions F2 and F4 are in accordance with the results of other authors [16]. It should be noted that the maximum glucose 6-phosphatase activity [20] was observed in fraction F6, together with hgh activity of both S'hucleotidase and acetylcholinesterase (Table 1). Taking into consideration the data on the distribution of glucose 6-phosphatase activity in membrane fractions of liver and kidney, for which this enzyme was found to be a marker of endoplasmic reticulum [20], it may be suggested that our fraction F6 consisted mostly of endoplasmic reticulum, which contains the enzymes commonly acting as markers for plasma membranes, or non-synaptosomal plasma membranes enriched by glucose 6-phosphatase.…”

Applying a modified systematic review and integrated assessment framework (SYRINA) – a case study on triphenyl phosphate

“…On the endocrine activity side, increased lipid accumulation, 38,65 increased cholesterol and triglycerides, increased adipogenic differentiation in cells 66 as well as effects on glucose homeostasis, including increased insulin resistance, increased glucose levels and increased glucose uptake have been reported for TPP. 48,50,66,70,71…”

“…50 On the endocrine activity side, increased lipid accumulation, 38,65 increased cholesterol and triglycerides, increased adipogenic differentiation in cells 66 as well as effects on glucose homeostasis, including increased insulin resistance, increased glucose levels and increased glucose uptake have been reported for TPP. 48,50,66,70,71 Obesity is commonly a major risk factor for T2 diabetes 72 and lipid accumulation and/or increased adipogenic differentiation in cells can lead to increased fat deposits, as shown in Green et al 50 and Cano-Sancho et al 66 A high triglyceride level could be a risk factor for T2 diabetes as well 73,74 and there is a strong correlation between increased plasma free fatty acids, leptin levels, lipid accumulation and insulin resistance. [75][76][77][78][79] Also, large fat cells and the resulting increased plasma non-esteried fatty acid concentration are risk factors for the development of noninsulin-dependent diabetes mellitus.…”