hypoglycemia/phosphatase

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Estrogen regulates energy metabolic pathway and upstream adenosine 5'-monophosphate-activated protein kinase and phosphatase enzyme expression in dorsal vagal complex metabolosensory neurons during glucostasis and hypoglycemia.

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The ability of estrogen to shield the brain from the bioenergetic insult hypoglycemia is unclear. Estradiol (E) prevents hypoglycemic activation of the energy deficit sensor adenosine 5'-monophosphate-activated protein kinase (AMPK) in hindbrain metabolosensory A2 noradrenergic neurons. This study

Liver Glucokinase(A456V) Induces Potent Hypoglycemia without Dyslipidemia through a Paradoxical Induction of the Catalytic Subunit of Glucose-6-Phosphatase.

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Recent reports point out the importance of the complex GK-GKRP in controlling glucose and lipid homeostasis. Several GK mutations affect GKRP binding, resulting in permanent activation of the enzyme. We hypothesize that hepatic overexpression of a mutated form of GK, GK(A456V), described in a

Reactive hypoglycaemia in association with disordered islet function and abnormal hepatic glucose-6-phosphatase activity: response to diazoxide.

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Severe reactive hypoglycaemia was confirmed in a non-diabetic male patient by a counter-regulatory hormone (GH, cortisol and catecholamine) response to profound hypoglycaemia induced by an intravenous glucose load. There was also evidence of disordered pancreatic islet cell paracrine regulation with

A hypothesis linking hypoglycemia, hyperuricemia, lactic acidemia, and reduced gluconeogenesis in alcoholics to inactivation of glucose-6-phosphatase activity by acetaldehyde.

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Preliminary data have been obtained indicating that glucose-6-phosphatase is inactivated upon preincubation with 447 and 224 mM acetaldehyde for 30 min at room temperature, resulting in a loss of 67% and 33% of the original activity, respectively. The reaction with acetaldehyde is rapid because 44%

Elevated aminotransferases and alkaline phosphatases in unstable diabetes mellitus without ketoacidosis or hypoglycemia.

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Four patients with unstable diabetes mellitus and pronounced elevations of serum aminotransferases and alkaline phosphatases are reported. Thorough investigations revealed no cause for the abnormalities. The enzyme elevations were associated with hepatomegaly, and in some instances, abdominal pain

Effect of anabolic steroid, methylandrostenediol, on the intravenous insulin hypoglycemia and on liver glucose-6-phosphatase activity in male rats.

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Liver glucose-6-phosphatase activity and blood fatty acid level in rats with insulin-induced hypoglycemia.

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[STUDIES ON NEONATAL HYPOGLYCEMIA. 1. ACTIVITY OF GLUCOSE-6-P PHOSPHATASE IN LIVER OF THE NEWBORN].

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[Effects of butter yellow on 6-phosphorylglucose phosphatase activity. Choice of the reference basis and interpretation of hypoglycemia].

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[Study of the metabolism of carbon hydrates in dermatology I. Behavior of blood inorganic phosphorus and of alkaline and acid phosphatases after sugar load and in induced hypoglycemia in psoriasis and other skin diseases].

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[Serum acid and alkaline phosphatase in insulin hypoglycemia].

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Reactive oxygen species-mediated pancreatic beta-cell death is regulated by interactions between stress-activated protein kinases, p38 and c-Jun N-terminal kinase, and mitogen-activated protein kinase phosphatases.

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Pancreatic beta-cells are susceptible to reactive oxygen species (ROS), which are known to be generated by high or low glucose (LG), hypoxic, or cytokine-producing conditions. When we cultured mouse beta-cell-derived MIN6 cells in a LG condition, we detected a significant generation of ROS,

Nutrient limitations alter cell division control and chromosome segregation through growth-related kinases and phosphatases.

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In dividing fission yeast Schizosaccharomyces pombe cells, the balance between Wee1 kinase and Cdc25 phosphatase which control the cyclin-dependent kinase (CDK) at the G2-M transition determines the rod-shaped cell length. Under nitrogen source starvation or glucose limitation, however, cell size

Deletion of the gene encoding the ubiquitously expressed glucose-6-phosphatase catalytic subunit-related protein (UGRP)/glucose-6-phosphatase catalytic subunit-beta results in lowered plasma cholesterol and elevated glucagon.

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In liver, glucose-6-phosphatase catalyzes the hydrolysis of glucose-6-phosphate (G6P) to glucose and inorganic phosphate, the final step in the gluconeogenic and glycogenolytic pathways. Mutations in the glucose-6-phosphatase catalytic subunit (G6Pase) give rise to glycogen storage disease (GSD)

Insulin resistance and the transcription of the glucose-6-phosphatase gene in newborn dogs.

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In the present report changes in the mRNA level of glucose-6-phosphatase (G6Pase; EC 3.1.39) in newborn and adult dogs in vivo were studied to further test the hypotheses that neonatal hyperglycemia may be due to unsuppressed gluconeogenesis by insulin and that the antidiabetic role of insulin-like

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