Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.1.1 (hexokinase)
 5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an attempt to evaluate early signs of placental insufficiency, the functional state of placental and chorionic mitochondria was studied in 62 pregnant women. The group included 18 women who decided to terminate pregnancy at 8-10 weeks of gestation, 13 women with normal delivery at term, 16 women who had miscarriages at 10-12 weeks of gestation, and 15 women who had miscarriages at 18-26 weeks of gestation. Functional state of mitochondria was estimated by oxygen consumption in the absence and presence of the acceptor system (hexokinase-glucose-adenosine diphosphate). Succinic and alpha-ketoglutaric acids were used as oxidation substrates. During normal pregnancy the rate of succinic acid oxidation in the absence of acceptor system (free respiration) was 12.1 and 11.8 microA 02/mg at 8-10 weeks and at term, respectively; the rate of oxygen consumption during oxidation of alpha-ketoglutarate was 7.6 and 6.2 microA 02/mg, respectively. The rate of oxygen consumption in the presence of acceptor system (coupled respiration) was 18.1 and 16.5 microA 02/mg for succinic acid and 14.4 and 11.2 microA 02/mg for alpha-ketoglutaric acid, respectively. Spontaneous miscarriage was characterized by significant decrease in the rate of oxygen consumption. Free respiration at 8-10 and 18-26 weeks was 8.6 and 63 microA 02/mg, respectively, for succinic acid and 6.8 and 5.9 microA 02/mg for alpha-ketoglutaric acid, respectively. Coupled respiration at 8-10 and 18-26 weeks was 11.2 and 5.7 for succinic acid and 9.5 and 6.5 microA 02/mg for alpha-ketoglutaric acid, respectively. These findings indicated that spontaneous miscarriage was preceded by inhibition of oxidative phosphorylation. It was suggested that functional impairment of placenta can be corrected by administration of preparations containing thiol group (cysteine).
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PMID:[Characteristics of the functional state of the placental mitochondria in interrupted pregnancy]. 337 22

The monomethyl ester of succinic acid (SME) was recently found to protect pancreatic islet B-cells against the impairment of glucose-stimulated insulin release caused by either glucopenia or starvation. The possible metabolic determinants of such a protective action are now scrutinized. After 180 min preincubation at 2.8 mM D-glucose in the presence of SME (10 mM), the oxidation of D-[U-14C]glucose, relative to either the utilization of D-[5-3H]glucose or the generation of 14C-labeled acidic metabolites, was higher than that after preincubation in the absence of SME and became close to that otherwise found after preincubation at 16.7 mM D-glucose. Likewise, after 3 days of culture at a low concentration of D-glucose (2.8 mM), the presence of SME in the culture medium tended to increase the subsequent oxidation of D-[6-14C]glucose and utilization of D-[5-3H]glucose. These two variables increased as a function of the concentration of D-glucose in the culture medium, this coinciding with a modest increase in hexokinase activity and a more pronounced increase in glucokinase activity. The presence of SME in the culture medium failed, however, to exert any obvious effect upon the respiration of the islets, suggesting that the protective action of the ester against glucopenia may also involve variables distinct from the metabolism of either endogenous or exogenous nutrients. Likewise, the fact that SME infusion to starved rats prevents the impairment of glucose-induced insulin release otherwise attributable to starvation may involve enzymatic determinants, such as a less severe decrease in glucokinase activity, metabolic variables, such as a greater relative increase in D-[U-14C]glucose oxidation relative to D-[5-3H]glucose utilization in response to a rise in extracellular D-glucose concentration, and other factors yet to be identified that participate in the secretory sequence at a site distal to those metabolic events triggered by D-glucose in the islet cells.
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PMID:Protective action of succinic acid monomethyl ester against the impairment of glucose-stimulated insulin release caused by glucopenia or starvation: metabolic determinants. 785 80

Utilization of the tricarboxylic acid (TCA) cycle intermediates, L-malic acid and succinic acid, by the yeast Pachysolen tannophilus is repressed in the presence of glucose. Strains of P. tannophilus containing mutations in two hexokinases and a glucokinase were characterized for growth on glucose plus L-malic acid or succinic acid. Increased specific utilization rates of malic acid and succinic acid in the presence of glucose were observed in mutants containing a lesion in hexokinase A, an enzyme associated with catabolite repression. Such derepressed mutants may have application in winemaking in which utilization of a major grape acid, L-malic acid, is often desirable for acidity reduction.
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PMID:Derepressed utilization of L-malic acid and succinic acid by mutants of Pachysolen tannophilus. 924 68

Rats were fasted for 48 h, but infused with either NaCl or the sodium salt of monoethyl succinic acid (EMS), both delivered at a rate of 80 mumol/g body weight per day. The infusion of EMS, as compared to NaCl, failed to affect paraovarian adipose tissue or liver weight, liver or muscle glycogen, and insulinemia. It accentuated the starvation-induced fall in body weight, and decreased both liver and muscle protein content. Nevertheless, the succinate ester increased plasma D-glucose concentration, delayed the rise in ketonemia, maintained a higher glucokinase/hexokinase activity ratio in liver and pancreatic islets, and allowed for a more efficient stimulation of insulin release by D-glucose or 2-ketoisocaproate in isolated pancreatic islets. These findings indicate that monoethyl succinate displays a significant nutritional value when infused in starved rats.
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PMID:Nutritional value of succinic acid monoethyl ester in starvation. 926 86