Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.9 (glucose-6-phosphatase)
 3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intestinal hexose absorption and gluconeogenesis have been studied in relation to refeeding after two different fasting phases: a long period of protein sparing during which energy expenditure is derived from lipid oxidation (phase II), and a later phase characterized by a rise in plasma corticosterone triggering protein catabolism (phase III). Such a switch in body fuel uses, leading to changes in body reserves and gluconeogenic precursors, could modulate intestinal gluconeogenesis and glucose transport. The gene and protein levels, and the cellular localization of the sodium-glucose cotransporter SGLT1, and of GLUT5 and GLUT2, as well as that of the key gluconeogenic enzymes phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (Glc6Pase) were measured. PEPCK and Glc6Pase activities were also determined. In phase III fasted rats, SGLT1 was up-regulated and intestinal glucose uptake rates were higher than in phase II fasted and fed rats. PEPCK and Glc6Pase mRNA, protein levels and activities also increased in phase III. GLUT5 and GLUT2 were down-regulated throughout the fast, but increased after refeeding, with GLUT2 recruited to the apical membrane. The increase in SGLT1 expression during phase III may allow glucose absorption at low concentrations as soon as food is available. Furthermore, an increased epithelial permeability due to fasting may induce a paracellular movement of glucose. In the absence of intestinal GLUT2 during fasting, Glc6Pase could be involved in glucose release to the bloodstream via membrane trafficking. Finally, refeeding triggered GLUT2 and GLUT5 synthesis and apical recruitment of GLUT2, to absorb larger amounts of hexoses.
 ...
PMID:Intestinal gluconeogenesis and glucose transport according to body fuel availability in rats. 1587 50

Dairy goats are often fed a high-concentrate (HC) diet to meet their lactation demands; however, long-term concentrate feeding is unhealthy and leads to milk yield and lactose content decreases. Therefore, we tested whether a buffering agent is able to increase the output of glucose in the liver and influence lactose synthesis. Eight lactating goats were randomly assigned to two groups: one group received a HC diet (Concentrate : Forage = 6:4, HG) and the other group received the same diet with a buffering agent added (0.2 % NaHCO(3), 0.1 % MgO, BG) over a 19-week experimental period. The total volatile fatty acids and lipopolysaccharide (LPS) declined in the rumen, which led the rumen pH to become stabile in the BG goats. The milk yield and lactose content increased. The alanine aminotransferase, aspartate transaminase, alkaline phosphatase, pro-inflammatory cytokines, LPS and lactate contents in the plasma significantly decreased, whereas the prolactin and growth hormone levels increased. The hepatic vein glucose content increased. In addition, pyruvate carboxylase (PC), phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6PC) expression in the liver was significantly up-regulated. In the mammary glands, the levels of glucose transporter type 1, 8, 12 as well as of sodium-glucose cotransporter 1 increased. Cumulative buffering agent treatment increased the blood concentrations of glucose via gluconeogenesis and promoted its synthesis in the liver. This treatment may contribute to the increase of the milk yield and lactose synthesis of lactating goats.
 ...
PMID:Buffering agent-induced lactose content increases via growth hormone-mediated activation of gluconeogenesis in lactating goats. 2930 9