scholarly journals Presence, induction and possible role of glucose 6-phosphatase in mammalian pancreatic islets

1969 ◽  
Vol 114 (2) ◽  
pp. 387-394 ◽  
Author(s):  
I.-B. Täljedal

1. Pancreatic islets from several mammalian species were investigated for hydrolytic activity towards glucose 6-phosphate. Both the total phosphatase activity towards this substrate and the proportion cleaving glucose 6-phosphate in preference to β-glycerophosphate varied widely between species. In pancreatic-islet homogenates prepared from mice and guinea pigs there was a higher rate of liberation of Pi at pH6·7 from glucose 6-phosphate than from β-glycerophosphate. In these two species cortisone treatment enhanced the enzyme activity towards glucose 6-phosphate but not that towards β-glycerophosphate. Simultaneous injections of ethionine or puromycin blocked this stimulating effect of cortisone. 2. With whole homogenates of mouse pancreatic islets, inverse plots of the relationship between glucose 6-phosphate concentration and enzyme activity suggested the simultaneous action of two enzymes with different Km values. After fractionation of islets from obese–hyperglycaemic mice by differential centrifugation, one of these enzymes could be shown to be localized in the microsome fraction. It had Km for glucose 6-phosphate about 0·5mm and optimum pH6·7. It split glucose 6-phosphate in preference to β-glycerophosphate, glucose 1-phosphate, fructose 6-phosphate and fructose 1,6-diphosphate. Incubation of the microsomes at pH5·0 and 37° for 15min. decreased the enzyme activity by about 80%. Glucose was a potent inhibitor, the type of inhibition being neither strictly competitive nor non-competitive. It is suggested that the results indicate the presence of glucose 6-phosphatase in mammalian endocrine pancreas, and that this enzyme may play a role in the metabolic regulation of release of insulin.

Author(s):  
Barbara K. Stepien ◽  
Samir Vaid ◽  
Wieland B. Huttner

The neocortex, a six-layer neuronal brain structure that arose during the evolution of, and is unique to, mammals, is the seat of higher order brain functions responsible for human cognitive abilities. Despite its recent evolutionary origin, it shows a striking variability in size and folding complexity even among closely related mammalian species. In most mammals, cortical neurogenesis occurs prenatally, and its length correlates with the length of gestation. The evolutionary expansion of the neocortex, notably in human, is associated with an increase in the number of neurons, particularly within its upper layers. Various mechanisms have been proposed and investigated to explain the evolutionary enlargement of the human neocortex, focussing in particular on changes pertaining to neural progenitor types and their division modes, driven in part by the emergence of human-specific genes with novel functions. These led to an amplification of the progenitor pool size, which affects the rate and timing of neuron production. In addition, in early theoretical studies, another mechanism of neocortex expansion was proposed—the lengthening of the neurogenic period. A critical role of neurogenic period length in determining neocortical neuron number was subsequently supported by mathematical modeling studies. Recently, we have provided experimental evidence in rodents directly supporting the mechanism of extending neurogenesis to specifically increase the number of upper-layer cortical neurons. Moreover, our study examined the relationship between cortical neurogenesis and gestation, linking the extension of the neurogenic period to the maternal environment. As the exact nature of factors promoting neurogenic period prolongation, as well as the generalization of this mechanism for evolutionary distinct lineages, remain elusive, the directions for future studies are outlined and discussed.


Author(s):  
Hamideh Abotalebi ◽  
Babak Ebrahimi ◽  
Raziyeh Shahriyari ◽  
Reyhaneh Shafieian

Abstract Adult neurogenesis is the production of new nerve cells in the adult brain. Neurogenesis is a clear example of the neuroplasticity phenomenon which can be observed in most of mammalian species, including human beings. This phenomenon occurs, at least, in two regions of the brain: the subgranular zone of the dentate gyrus in hippocampus and the ventricular zone of lateral ventricles. Numerous studies have investigated the relationship between sex steroid hormones and neurogenesis of adult brain; of which, mostly concentrated on the role of estradiol. It has been shown that estrogen plays a significant role in this process through both classic and non-classic mechanisms, including a variety of different growth factors. Therefore, the objective of this review is to investigate the role of female sex steroids with an emphasis on estradiol and also its potential implications for regulating the neurogenesis in the adult brain.


1958 ◽  
Vol 195 (2) ◽  
pp. 316-320 ◽  
Author(s):  
Roland W. Richterich ◽  
Leon Goldstein

The distribution of the glutamine metabolizing enzymes was studied in the kidney of four mammalian species (dog, rat, rabbit and guinea pig). Glutaminase I activity of whole kidney was highest in the dog (19.1 µm NH3/gm/min.), intermediate in the rat (8.1 µm NH3/gm/min.), and low in the guinea pig (1.1 µm NH3/ gm/min.) and rabbit (0.6 µm NH3/gm/min.). In all four species, enzyme activity was highest in the cortex and inner medulla. Glutaminase II and glutamine synthetase activity were lower than glutaminase I activity in all four species. Both glutaminase II and glutamine synthetase activity were found only in the cortex and outer medulla. The relationship of the glutamine metabolizing enzymes to the production of urinary ammonia is discussed.


2020 ◽  
Author(s):  
Chuan Yu ◽  
Fuyu Du ◽  
Chunjie Zhang ◽  
Yinju Li ◽  
Chengshui Liao ◽  
...  

Abstract Background: Salmonella enterica serovar Typhimurium ( S. Typhimurium) is an important infectious disease pathogen that can survive and replicate in macrophages. Glycolysis is essential for immune responses against S. Typhimurium infection in macrophages, and is also associated with apoptosis. S. Typhimurium secreted effector K3 (SseK3) was recently identified as a novel translated and secreted protein. However, there is no study about the role of sseK3 in the relationship between apoptosis and glycolysis in cells infected with S. Typhimurium. It is unclear whether this protein exerts a significant role in the progress of apoptosis and glycolysis in S. Typhimurium-infected macrophages. Results: Macrophages were infected with S. Typhimurium SL1344 wild-type (WT), Δ sseK3 mutant or sseK3 -complemented strain, and the effects of sseK3 on apoptosis and glycolysis were determined. The adherence and invasion in the Δ sseK3 mutant group were similar to that in the WT and sseK3 -complemented groups, indicating that SseK3 was not essential for the adherence and invasion of S. Typhimurium in macrophages. However, the percentage of apoptosis in the Δ sseK3 mutant group was much lower than that in the WT and sseK3 -complemented groups. Caspase-3, caspase-8, and caspase-9 enzyme activity in the Δ sseK3 mutant group were significantly lower than in the WT group and sseK3 -complemented groups, indicating that sseK3 could improve the caspase-3, caspase-8, and caspase-9 enzyme activity. We also found that there were no significant differences in pyruvic acid levels between the three groups, but the lactic acid level in the Δ sseK3 mutant group was much lower than that in the WT and sseK3 -complemented groups. The ATP levels in the Δ sseK3 mutant group were remarkably higher than those in the WT and sseK3 -complemented groups. These indicated that the sseK3 enhanced the level of glycolysis in macrophages infected by S. Typhimurium. Conclusions: S. Typhimurium sseK3 is likely involved in promoting macrophage apoptosis and modulating glycolysis in macrophages. Our results could improve our understanding of the relationship between apoptosis and glycolysis in macrophages induced by S. Typhimurium sseK3 .


1986 ◽  
Vol 111 (4) ◽  
pp. 533-538 ◽  
Author(s):  
Kirsten Capito ◽  
Carl Jørgen Hedeskov ◽  
Peter Thams

Abstract. The activity of cyclic AMP phosphodiesterase in mouse pancreatic islets was investigated. 85% of the total activity was found in a 27 000 g supernatant fraction. The phosphodiesterase activity in the supernatant fraction, but not in the particulate fraction, was stimulated approximately 20% by Ca2+ (10−5m) and calmodulin (1 μm). The Km (cyclic AMP) of the unstimulated enzyme in the supernatant fraction was 20 μm, and the Vmax was 2 nmol/min × mg protein−1. The possible influence of a range of phospholipids was investigated. PI* and PS (150 μg/ml) inhibited the enzyme 20–30% both in the absence and presence of Ca2+/calmodulin, whereas PE, PC and PA did not affect the enzyme activity. ATP (1 mm) did not affect the particulate or supernatant fraction phosphodiesterase either in the absence or presence of Ca2+/calmodulin or Ca2+/phospholipid. It is concluded that, contrary to islet adenylate cyclase, islet cyclic AMP phosphodiesterase may be regulated by Ca2+/calmodulin.


Author(s):  
William J. Marshall

Summary The properties of the hepatic microsomal, drug detoxicating, enzyme system are reviewed with particular reference to its inducibility. Induction is modified by various factors of which the diet is particularly important. A theoretical model system for induction has been proposed and this is discussed. There are a number of methods for assessing microsomal enzyme induction in man, none of which is ideal. Nevertheless, induction is a well recognised phenomenon in man and has a bearing on the metabolism of a number of endogenous substances. The effect of induction on steroid metabolism and the relationship between inducers, vitamin D, and metabolic bone disease is discussed. Bilirubin metabolism is affected by changes in microsomal enzyme activity and inducers have been used therapeutically in some cases of hyperbilirubinaemia. The relationship between drugs and the hepatic porphyrias is reviewed. The hepatic microsomal enzyme system is but one of many inducible enzymes and the role of induction in general in metabolic regulation is emphasised.


2020 ◽  
Author(s):  
Chuan Yu ◽  
Fuyu Du ◽  
Chunjie Zhang ◽  
Yinju Li ◽  
Chengshui Liao ◽  
...  

Abstract Background: Salmonella enterica serovar Typhimurium (S. Typhimurium) is an important infectious disease pathogen that can survive and replicate in macrophages. Glycolysis is essential for immune responses against S. Typhimurium infection in macrophages, and is also associated with apoptosis. S. Typhimurium secreted effector K3 (SseK3) was recently identified as a novel translated and secreted protein. However, there is no study about the role of sseK3 in the relationship between apoptosis and glycolysis in cells infected with S. Typhimurium. It is unclear whether this protein exerts a significant role in the progress of apoptosis and glycolysis in S. Typhimurium-infected macrophages.Results: Macrophages were infected with S. Typhimurium SL1344 wild-type (WT), ΔsseK3 mutant or sseK3-complemented strain, and the effects of sseK3 on apoptosis and glycolysis were determined. The adherence and invasion in the ΔsseK3 mutant group were similar to that in the WT and sseK3-complemented groups, indicating that SseK3 was not essential for the adherence and invasion of S. Typhimurium in macrophages. However, the percentage of apoptosis in the ΔsseK3 mutant group was much lower than that in the WT and sseK3-complemented groups. Caspase-3, caspase-8, and caspase-9 enzyme activity in the ΔsseK3 mutant group were significantly lower than in the WT group and sseK3-complemented groups, indicating that sseK3 could improve the caspase-3, caspase-8, and caspase-9 enzyme activity. We also found that there were no significant differences in pyruvic acid levels between the three groups, but the lactic acid level in the ΔsseK3 mutant group was much lower than that in the WT and sseK3-complemented groups. The ATP levels in the ΔsseK3 mutant group were remarkably higher than those in the WT and sseK3-complemented groups. These indicated that the sseK3 enhanced the level of glycolysis in macrophages infected by S. Typhimurium.Conclusions: S. Typhimurium sseK3 is likely involved in promoting macrophage apoptosis and modulating glycolysis in macrophages. Our results could improve our understanding of the relationship between apoptosis and glycolysis in macrophages induced by S. Typhimurium sseK3.


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