scholarly journals Modulation of mitochondrial nitric oxide synthase and energy expenditure in rats during cold acclimation

2003 ◽  
Vol 284 (6) ◽  
pp. H2375-H2383 ◽  
Author(s):  
Jorge Guillermo Peralta ◽  
Paola V. Finocchietto ◽  
Daniela Converso ◽  
Francisco Schöpfer ◽  
Marı́a Cecilia Carreras ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Weight Loss ◽  
Energy Expenditure ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Energy Levels ◽  
Adaptive Responses ◽  
Mitochondrial Nitric Oxide Synthase ◽  
Oxide Synthase

To preserve thermoneutrality, cold exposure is followed by changes in energy expenditure and basal metabolic rate (BMR). Because nitric oxide (NO) modulates mitochondrial O2 uptake and energy levels, we analyzed cold effects (30 days at 4°C) on rat liver and skeletal muscle mitochondrial NO synthases (mtNOS) and their putative impact on BMR. Cold exposure delimited two periods: A ( days 1–10), with high systemic O2 uptake and weight loss, and B ( days 10–30), with lower O2 uptake and fat deposition. mtNOS activity and expression decreased in period A and then increased in period B by 60–100% in liver and skeletal muscle ( P< 0.05). Conversely, mitochondrial O2 uptake remained initially high in the presence of l-arginine and later fell by 30–50% ( P < 0.05). On this basis, the estimated fractional contribution of liver plus muscle to total BMR varied from 40% in period A to 25% in period B. The transitional modulation of mtNOS in rat cold acclimation could participate in adaptive responses that favor calorigenesis or conservative energy-saving mechanisms.

Expression of nitric oxide synthase in skeletal muscle: a novel role for nitric oxide as a modulator of insulin action

Diabetes ◽  
1997 ◽  
Vol 46 (11) ◽  
pp. 1691-1700 ◽  
Author(s):  
S. Kapur ◽  
S. Bedard ◽  
B. Marcotte ◽  
C. H. Cote ◽  
A. Marette
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Nitric Oxide Synthase ◽  
Insulin Action ◽  
Oxide Synthase

Mitochondrial Nitric Oxide Synthase, Oxidative Stress and Apoptosis

Neurosignals ◽  
2001 ◽  
Vol 10 (1-2) ◽  
pp. 57-65 ◽  
Author(s):  
Pedram Ghafourifar ◽  
Urs Bringold ◽  
Sabine D. Klein ◽  
Christoph Richter
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mitochondrial Nitric Oxide Synthase ◽  
Oxide Synthase

scholarly journals Obesity, type 2 diabetes, and impaired insulin-stimulated blood flow: role of skeletal muscle NO synthase and endothelin-1

2017 ◽  
Vol 122 (1) ◽  
pp. 38-47 ◽  
Author(s):  
Leryn J. Reynolds ◽  
Daniel P. Credeur ◽  
Camila Manrique ◽  
Jaume Padilla ◽  
Paul J. Fadel ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Vastus Lateralis ◽  
Glucose Disposal ◽  
Endothelin 1 ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Increased endothelin-1 (ET-1) and reduced endothelial nitric oxide phosphorylation (peNOS) are hypothesized to reduce insulin-stimulated blood flow in type 2 diabetes (T2D), but studies examining these links in humans are limited. We sought to assess basal and insulin-stimulated endothelial signaling proteins (ET-1 and peNOS) in skeletal muscle from T2D patients. Ten obese T2D [glucose disposal rate (GDR): 6.6 ± 1.6 mg·kg lean body mass (LBM)−1·min−1] and 11 lean insulin-sensitive subjects (Lean GDR: 12.9 ± 1.2 mg·kg LBM−1·min−1) underwent a hyperinsulinemic-euglycemic clamp with vastus lateralis biopsies taken before and 60 min into the clamp. Basal biopsies were also taken in 11 medication-naïve, obese, non-T2D subjects. ET-1, peNOS (Ser1177), and eNOS protein and mRNA were measured from skeletal muscle samples containing native microvessels. Femoral artery blood flow was assessed by duplex Doppler ultrasound. Insulin-stimulated blood flow was reduced in obese T2D (Lean: +50.7 ± 6.5% baseline, T2D: +20.8 ± 5.2% baseline, P < 0.05). peNOS/eNOS content was higher in Lean under basal conditions and, although not increased by insulin, remained higher in Lean during the insulin clamp than in obese T2D ( P < 0.05). ET-1 mRNA and peptide were 2.25 ± 0.50- and 1.52 ± 0.11-fold higher in obese T2D compared with Lean at baseline, and ET-1 peptide remained 2.02 ± 1.9-fold elevated in obese T2D after insulin infusion ( P < 0.05) but did not increase with insulin in either group ( P > 0.05). Obese non-T2D subjects tended to also display elevated basal ET-1 ( P = 0.06). In summary, higher basal skeletal muscle expression of ET-1 and reduced peNOS/eNOS may contribute to a reduced insulin-stimulated leg blood flow response in obese T2D patients. NEW & NOTEWORTHY Although impairments in endothelial signaling are hypothesized to reduce insulin-stimulated blood flow in type 2 diabetes (T2D), human studies examining these links are limited. We provide the first measures of nitric oxide synthase and endothelin-1 expression from skeletal muscle tissue containing native microvessels in individuals with and without T2D before and during insulin stimulation. Higher basal skeletal muscle expression of endothelin-1 and reduced endothelial nitric oxide phosphorylation (peNOS)/eNOS may contribute to reduced insulin-stimulated blood flow in obese T2D patients.

Glucose uptake during contraction in isolated skeletal muscles from neuronal nitric oxide synthase μ knockout mice

2015 ◽  
Vol 118 (9) ◽  
pp. 1113-1121 ◽  
Author(s):  
Yet Hoi Hong ◽  
Tony Frugier ◽  
Xinmei Zhang ◽  
Robyn M. Murphy ◽  
Gordon S. Lynch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Nitric Oxide Synthase ◽  
Glucose Uptake ◽  
Ex Vivo ◽  
Organ Bath ◽  
Skeletal Muscle Glucose Uptake ◽  
Nos Inhibitor ◽  
Amp Activated Protein Kinase ◽  
Oxide Synthase

Inhibition of nitric oxide synthase (NOS) significantly attenuates the increase in skeletal muscle glucose uptake during contraction/exercise, and a greater attenuation is observed in individuals with Type 2 diabetes compared with healthy individuals. Therefore, NO appears to play an important role in mediating muscle glucose uptake during contraction. In this study, we investigated the involvement of neuronal NOSμ (nNOSμ), the main NOS isoform activated during contraction, on skeletal muscle glucose uptake during ex vivo contraction. Extensor digitorum longus muscles were isolated from nNOSμ−/−and nNOSμ+/+mice. Muscles were contracted ex vivo in a temperature-controlled (30°C) organ bath with or without the presence of the NOS inhibitor NG-monomethyl-l-arginine (L-NMMA) and the NOS substrate L-arginine. Glucose uptake was determined by radioactive tracers. Skeletal muscle glucose uptake increased approximately fourfold during contraction in muscles from both nNOSμ−/−and nNOSμ+/+mice. L-NMMA significantly attenuated the increase in muscle glucose uptake during contraction in both genotypes. This attenuation was reversed by L-arginine, suggesting that L-NMMA attenuated the increase in muscle glucose uptake during contraction by inhibiting NOS and not via a nonspecific effect of the inhibitor. Low levels of NOS activity (∼4%) were detected in muscles from nNOSμ−/−mice, and there was no evidence of compensation from other NOS isoform or AMP-activated protein kinase which is also involved in mediating muscle glucose uptake during contraction. These results indicate that NO regulates skeletal muscle glucose uptake during ex vivo contraction independently of nNOSμ.

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