Effect of Age on the Oxygen Consumption and Glucose Uptake by the Elastic Cartilage of Rat

Gerontology ◽  
1967 ◽  
Vol 13 (3) ◽  
pp. 173-176 ◽  
Author(s):  
B.K. Patnaik
Keyword(s):  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Elastic Cartilage ◽  
Effect Of Age

Influence of endogenous norepinephrine on cerebral blood flow and metabolism

1976 ◽  
Vol 231 (2) ◽  
pp. 489-494 ◽  
Author(s):  
ET MacKenzie ◽  
J McCulloch ◽  
AM Harper
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Cerebral Circulation ◽  
Brain Metabolism ◽  
Cerebral Metabolism ◽  
Cerebral Oxygen ◽  
Brain Norepinephrine ◽  
Cerebral Oxygen Consumption

The influence of brain norepinephrine on cerebral metabolism and blood flow was examined because exogenous norepinephrine, administered in a way that the blood-brain barrier is bypassed, has been shown to effect pronounced changes in the cerebral circulation. Reserpine (40 mug/kg, by intracarotid infusion) was administered in order to release brain norepinephrine in five anesthetized baboons. Reserpine significantly increased cerebral oxygen consumption (23%) and cerebral blood flow (50%). This response lasted for approximately 60 min. In a further five animals, effects of central beta-adrenoreceptor blockade were studied. Pro pranolol (12 mug/kg-min) produced an immediate, significant reduction in both cerebral oxygen consumption (40%) and cerebral glucose uptake (39%). Cerebral blood flow was reduced minimally. However, the responsiveness of the cerebral circulation to induced hypercapnia was severely attenuated from a gradient of 3.22 before, to 1,11 after, administration. These experiments suggest that central norepinephrine can influence the cerebral circulation primarily through noradrenergic effects on brain metabolism.

scholarly journals Role of TRIB3 in regulation of insulin sensitivity and nutrient metabolism during short-term fasting and nutrient excess

2012 ◽  
Vol 303 (7) ◽  
pp. E908-E916 ◽  
Author(s):  
Jiarong Liu ◽  
Wei Zhang ◽  
Gin C. Chuang ◽  
Helliner S. Hill ◽  
Ling Tian ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Oxygen Consumption Rate ◽  
Glucose Oxidation ◽  
Consumption Rate ◽  
Negative Regulator ◽  
Short Term

We have suggested previously that Tribbles homolog 3 (TRIB3), a negative regulator of Akt activity in insulin-sensitive tissues, could mediate glucose-induced insulin resistance in muscle under conditions of chronic hyperglycemia (Liu J, Wu X, Franklin JL, Messina JL, Hill HS, Moellering DR, Walton RG, Martin M, Garvey WT. Am J Physiol Endocrinol Metab 298: E565–E576, 2010). In the current study, we have assessed short-term physiological regulation of TRIB3 in skeletal muscle and adipose tissues by nutrient excess and fasting as well as TRIB3's ability to modulate glucose transport and mitochondrial oxidation. In Sprague-Dawley rats, we found that short-term fasting enhanced insulin sensitivity concomitantly with decrements in TRIB3 mRNA (66%, P < 0.05) and protein (81%, P < 0.05) in muscle and increments in TRIB3 mRNA (96%, P < 0.05) and protein (∼10-fold, P < 0.05) in adipose tissue compared with nonfasted controls. On the other hand, rats fed a Western diet for 7 days became insulin resistant concomitantly with increments in TRIB3 mRNA (155%, P < 0.05) and protein (69%, P = 0.0567) in muscle and a decrease in the mRNA (76%, P < 0.05) and protein (70%, P < 0.05) in adipose. In glucose transport and mitochondria oxidation studies using skeletal muscle cells, we found that stable TRIB3 overexpression impaired insulin-stimulated glucose uptake without affecting basal glucose transport and increased both basal glucose oxidation and the maximal uncoupled oxygen consumption rate. With stable knockdown of TRIB3, basal and insulin-stimulated glucose transport rates were increased, whereas basal glucose oxidation and the maximal uncoupled oxygen consumption rate were decreased. In conclusion, TRIB3 impacts glucose uptake and oxidation oppositely in muscle and fat according to levels of nutrient availability. The above data for the first time implicate TRIB3 as a potent physiological regulator of insulin sensitivity and mitochondrial glucose oxidation under conditions of nutrient deprivation and excess.

Differential effects of EGF on repair of cellular functions after dichlorovinyl-l-cysteine-induced injury

1999 ◽  
Vol 276 (2) ◽  
pp. F228-F236 ◽  
Author(s):  
Graz˙yna Nowak ◽  
Kenneth B. Keasler ◽  
Douglas E. McKeller ◽  
Rick G. Schnellmann
Keyword(s):  
Cell Death ◽  
Oxygen Consumption ◽  
Atpase Activity ◽  
Glucose Uptake ◽  
Mitochondrial Function ◽  
Cellular Functions ◽  
Sublethal Injury ◽  
Epidermal Growth ◽  
Death And Loss ◽  
Over Time

This study examined the repair of renal proximal tubule cellular (RPTC) functions following sublethal injury induced by the nephrotoxicant S-(1,2-dichlorovinyl)-l-cysteine (DCVC). DCVC exposure resulted in 31% cell death and loss 24 h following the treatment. Monolayer confluence recovered through migration/spreading but not proliferation after 6 days. Basal, uncoupled, and ouabain-sensitive oxygen consumption (Qo 2) decreased 47, 76, and 62%, respectively, 24 h after DCVC exposure. Na+-K+-ATPase activity and Na+-dependent glucose uptake were inhibited 80 and 68%, respectively, 24 h after DCVC exposure. None of these functions recovered over time. Addition of epidermal growth factor (EGF) following DCVC exposure did not prevent decreases in basal, uncoupled, and ouabain-sensitive Qo 2 values and Na+-K+-ATPase activity but promoted their recovery over 4–6 days. In contrast, no recovery of Na+-dependent glucose uptake occurred in the presence of EGF. These data show that: 1) DCVC exposure decreases mitochondrial function, Na+-K+-ATPase activity, active Na+ transport, and Na+-dependent glucose uptake in sublethally injured RPTC; 2) DCVC-treated RPTC do not proliferate nor regain their physiological functions in this model; and 3) EGF promotes recovery of mitochondrial function and active Na+ transport but not Na+-dependent glucose uptake. These results suggest that cysteine conjugates may cause renal dysfunction, in part, by decreasing RPTC functions and inhibiting their repair.

The Effect of Age on the Oxygen Consumption of Normal and Transplanted Ear Skin in Mice

Gerontology ◽  
1965 ◽  
Vol 11 (1-2) ◽  
pp. 45-56 ◽  
Author(s):  
Jennifer Mundy ◽  
P.L. Krohn
Keyword(s):  
Oxygen Consumption ◽  
Effect Of Age

The effect of age on glucose uptake and GLUT1 and GLUT4 expression in rat skeletal muscle

2011 ◽  
Vol 30 (3) ◽  
pp. 191-197 ◽  
Author(s):  
J. M. Santos ◽  
S. A. Benite-Ribeiro ◽  
G. Queiroz ◽  
J. A. Duarte
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Rat Skeletal Muscle ◽  
Glut4 Expression ◽  
Effect Of Age

scholarly journals SGLT2 Inhibition Does Not Affect Myocardial Fatty Acid Oxidation or Uptake, But Reduces Myocardial Glucose Uptake and Blood Flow in Individuals With Type 2 Diabetes– a Randomized Double-Blind, Placebo-Controlled Crossover Trial

2020 ◽  
Author(s):  
Katrine M. Lauritsen ◽  
Bent R.R. Nielsen ◽  
Lars P. Tolbod ◽  
Mogens Johannsen ◽  
Jakob Hansen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Acid Oxidation ◽  
Double Blind ◽  
Double Blind Placebo ◽  
Myocardial Glucose Uptake ◽  
Pet Ct ◽  
Sglt2 Inhibition

Sodium-glucose cotransporter 2 (SGLT2) inhibition reduces cardiovascular morbidity and mortality in individuals with type 2 diabetes. Beneficial effects have been attributed to increased ketogenesis, reduced cardiac fatty acid oxidation and diminished cardiac oxygen consumption. We therefore studied whether SGLT2 inhibition altered cardiac oxidative substrate consumption, efficiency, and perfusion. <p>13 individuals with type 2 diabetes were studied after four weeks treatment with empagliflozin and placebo in a randomized, double-blind, placebo-controlled crossover study. Myocardial palmitate and glucose uptake were measured with <sup>11</sup>C-palmitate and <sup>18</sup>F-FDG PET/CT. Oxygen consumption and myocardial external efficiency (MEE) were measured with <sup>11</sup>C-acetate PET/CT. Resting and adenosine stress myocardial blood flow (MBF) and myocardial flow reserve (MFR) were measured using <sup>15</sup>O-H<sub>2</sub>O PET/CT. </p> <p>Empagliflozin did not affect myocardial FFA uptake but reduced myocardial glucose uptake by 57% (p<0.001). Empagliflozin did not change myocardial oxygen consumption or MEE. Empagliflozin reduced resting MBF by 13% (p<0.01), but did not significantly affect stress MBF or MFR.</p> <p>In conclusion, SGLT2 inhibition did not affect myocardial FFA uptake, but channeled myocardial substrate utilization from glucose towards other sources and reduced resting MBF. However, the observed metabolic and hemodynamic changes were modest and most likely contribute only partially to the cardioprotective effect of SGLT2 inhibition. </p>

Unraveling the metabolome in prostate tumorigenesis: Effects by an oncogenic isopeptidase

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e16148-e16148
Author(s):  
C. Priolo ◽  
M. Loda
Keyword(s):  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Fdg Pet ◽  
Metabolic Profiling ◽  
De Novo ◽  
Imaging Techniques ◽  
Genetic Alterations ◽  
Cancer Diagnostics ◽  
Normal Prostate ◽  
Prostate Tumorigenesis

e16148 Background: Cancer cells undergo fundamental changes in their metabolism, including a higher rate of glycolysis and an increase in de novo fatty acid synthesis. The high incorporation of glucose into tumor cells has already been exploited in cancer diagnostics with the generation of the FDG-PET scan technology. However, some tumors including those arising in the prostate are less prone to FDG-PET imaging and could benefit from other imaging techniques based on alternative metabolic features. We asked whether prostate epithelial cell transformation driven by specific oncogenes results in a typical metabolic profiling, whose characterization may be useful to improve diagnostics and to address new therapeutics. Methods: Normal prostate epithelial cells (RWPE-1 and PrEC) were transformed by overexpressing known oncogenes, such as the protein kinase AKT1 and the de-ubiquitinating enzyme (isopeptidase) USP2a. These cells were then subjected to mass spectrometry-based metabolomics, gene expression analysis, oxygen consumption and glucose uptake assays. Multiple bioinformatic tools were utilized for data mining and pathway visualization. Results: We integrated data from different high-throughput technologies to map metabolic changes induced during prostate tumorigenesis by genes that are often altered in prostate cancer. A different metabolic profiling was found in association to each specific oncogene. In fact, extremely significant alterations were found in the glycolytic pathways in the case of AKT-driven transformation, whereas changes in the lipid metabolism and in some aminoacids were prevalent in USP2a-overexpressing cells. Complementary assays including oxygen consumption and glucose uptake measurement confirmed the global metabolic analysis. Conclusions: These results suggest that tumors showing different genetic alterations may be characterized by a different metabolic profiling, whose assessment can potentially improve diagnostics and individualized treatment. Metabolic profiling analysis of human prostate tumors is currently ongoing. No significant financial relationships to disclose.

scholarly journals The fuel of the spleen. Studies using a new method for perfusing the rat spleen with whole blood

1989 ◽  
Vol 263 (2) ◽  
pp. 325-332 ◽  
Author(s):  
M A Mindham ◽  
P A Mayes
Keyword(s):  
Oxygen Consumption ◽  
Fatty Acid ◽  
Glucose Uptake ◽  
Whole Blood ◽  
Glucose Oxidation ◽  
The Other ◽  
Cell Populations ◽  
Total Oxygen ◽  
Total Glucose ◽  
Oxidation Of Glucose

1. An improved rat spleen perfusion is described incorporating a method of defibrination which avoids the use of heparin and enables the spleen to be perfused with rat blood for several hours at a haematocrit of 40% and for 12 h or more at a haematocrit of 20%. 2. Glucose oxidation accounted for 11.6% of the total oxygen consumption but this represented only 8% of total glucose uptake, which was largely converted to lactate and released into the perfusate. However, significant amounts of lactate were oxidized. These results can be explained by the presence of at least two cell populations, one emphasizing the anaerobic oxidation of glucose and the other aerobic metabolism, particularly of lactate. 3. Non-esterified fatty acid and 3-hydroxybutyrate, when available at physiological concentrations, were shown to be major oxidative fuels of the spleen. 4. Chylomicron triacylglycerol was hydrolysed readily and taken up, but not oxidized extensively.

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