ABSTRACT
The mammalian kidney contributes significantly to glucose homeostasis through gluconeogenesis. Considering that stanniocalcin 1 (STC1) regulates ATP production, is synthesized and acts in different cell types of the nephron, the present study hypothesized that STC1 may be implicated in the regulation of gluconeogenesis in the vertebrate kidney. Human STC1 strongly reduced gluconeogenesis from (14)C-glutamine in rat renal medulla (MD) slices but not in renal cortex (CX), nor from (14)C-lactic acid. Total PEPCK activity was markedly reduced by hSTC1 in MD but not in CX. Pck2 (mitochondrial PEPCK isoform) was down-regulated by hSTC1 in MD but not in CX. In fish (Dicentrarchus labrax) kidney slices, both STC1-A and -B isoforms decreased gluconeogenesis from (14)C-acid lactic, while STC1-A increased gluconeogenesis from (14)C-glutamine. Overall, our results demonstrate a role for STC1 in the control of glucose synthesis via renal gluconeogenesis in mammals and suggest that it may have a similar role in teleost fishes.
Subject(s)
Bass/metabolism , Fish Proteins/metabolism , Gluconeogenesis , Glycoproteins/metabolism , Kidney Medulla/metabolism , Animals , Bass/genetics , Gene Expression Regulation , Glutamine/metabolism , Humans , Intracellular Signaling Peptides and Proteins/genetics , Intracellular Signaling Peptides and Proteins/metabolism , Kidney Cortex/metabolism , Lactic Acid/metabolism , Male , Mammals/metabolism , Mitochondria/enzymology , Phosphoenolpyruvate Carboxykinase (GTP)/genetics , Phosphoenolpyruvate Carboxykinase (GTP)/metabolism , Rats , Rats, WistarABSTRACT
The present study assesses the effects of starvation and refeeding on 1-[(14)C]-methyl aminoisobutyric acid ((14)C-MeAIB) uptake, (14)C-total lipids, (14)CO(2) production from (14)C-glycine, (14)C-protein synthesis from (14)C-leucine and Na(+)-K(+)-ATPase activity in jaw muscle of Neohelice granulata previously maintained on a carbohydrate-rich (HC) or high-protein (HP) diet. In N. granulata the metabolic adjustments during starvation and refeeding use different pathways according to the composition of the diet previously offered to the crabs. During starvation, (14)CO(2) production from (14)C-glycine, and (14)C-protein synthesis from (14)C-leucine were reduced in HC-fed crabs. In crabs maintained on the HP or HC diet, (14)C-total lipid synthesis increased after 15 days of starvation. In crabs fed HP diet, (14)C-MeAIB uptake and Na(+)-K(+)-ATPase activity decreased in refeeding state. In crabs refeeding HC diet, (14)C-MeAIB uptake and (14)CO(2) production decreased during the refeeding. In contrast, the (14)C-protein synthesis increased after 120h of refeeding. In both dietary groups, (14)C-total lipid synthesis increased during refeeding. Changes in the carbon amino acid flux between different metabolic pathways in muscle are among the strategies used by this crab to face starvation and refeeding. Protein or carbohydrate levels in the diet administered to this crab modulate the carbon flux between the different metabolic pathways.
Subject(s)
Brachyura/metabolism , Dietary Carbohydrates/metabolism , Dietary Proteins/metabolism , Food Deprivation , Glycine/metabolism , Muscles/metabolism , Aminoisobutyric Acids/metabolism , Animals , Biological Transport , Brachyura/physiology , Carbon/metabolism , Carbon Dioxide/metabolism , Carbon Radioisotopes/metabolism , Enzyme Activation , Leucine/metabolism , Lipid Metabolism , Male , Muscles/physiology , Protein Biosynthesis , Sodium-Potassium-Exchanging ATPase/metabolism , Time FactorsABSTRACT
We reported previously that intrauterine asphyxia acutely affects the rat hippocampus. For this reason, the early effects of this injury were studied in the cerebral cortex, immediately after hysterectomy (acute condition) or following a recovery period at normoxia (recovery condition). Lactacidemia and glycemia were determined, as well as glycogen levels in the muscle, liver and cortex. Cortical tissue was also used to assay the ATP levels and glutamate uptake. Asphyxiated pups exhibited bluish coloring, loss of movement, sporadic gasping and hypertonia. However, the appearance of the controls and asphyxiated pups was similar at the end of the recovery period. Lactacidemia and glycemia were significantly increased by asphyxia in both the acute and recovery conditions. Concerning muscle and hepatic glycogen, the control group showed significantly higher levels than the asphyxic group in the acute condition and when compared with groups of the recovery period. In the recovery condition, the control and asphyxic groups showed similar glycogen levels. However, in the cortex, the control groups showed significantly higher glycogen levels than the asphyxic group, in both the acute and recovery conditions. In the cortical tissue, asphyxia reduced ATP levels by 70 % in the acute condition, but these levels increased significantly in asphyxic pups after the recovery period. Asphyxia did not affect glutamate transport in the cortex of both groups. Our results suggest that the cortex uses different energy resources to restore ATP after an asphyxia episode followed by a reperfusion period. This strategy could sustain the activity of essential energy-dependent mechanisms.
