Role of the Sympathoadrenal System in the Regulation of Glycogen Metabolism in Resting and Exercising Skeletal Muscles

1992 ◽  
Vol 24 (06) ◽  
pp. 266-271 ◽  
Author(s):  
Carole Lavoie ◽  
F. Péronnet ◽  
J.-L. Chiasson
Keyword(s):  
Skeletal Muscles ◽  
Glycogen Metabolism ◽  
Sympathoadrenal System

Role of the sympathoadrenal system in exercise-induced inhibition of insulin secretion. Effects of islet transplantation

Diabetes ◽  
1995 ◽  
Vol 44 (5) ◽  
pp. 565-571 ◽  
Author(s):  
H. Houwing ◽  
K. M. Frankel ◽  
J. H. Strubbe ◽  
P. T. van Suylichem ◽  
A. B. Steffens
Keyword(s):  
Insulin Secretion ◽  
Islet Transplantation ◽  
Sympathoadrenal System ◽  
Exercise Induced

Role of insulin and IGF-I in activation of muscle protein synthesis after oral feeding

1996 ◽  
Vol 270 (4) ◽  
pp. E614-E620 ◽  
Author(s):  
E. Svanberg ◽  
H. Zachrisson ◽  
C. Ohlsson ◽  
B. M. Iresjo ◽  
K. G. Lundholm
Keyword(s):  
Protein Synthesis ◽  
Skeletal Muscles ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Oral Feeding ◽  
Myofibrillar Proteins ◽  
Diabetic Mice ◽  
Igf I ◽  
Stimulation Of

The aim was to evaluate the role of insulin and insulin-like growth factor I (IGF-I) in activation of muscle protein synthesis after oral feeding. Synthesis rate of globular and myofibrillar proteins in muscle tissue was quantified by a flooding dose of radioactive phenylalanine. Muscle tissue expression of IGF-I mRNA was measured. Normal (C57 Bl) and diabetic mice (type I and type II) were subjected to an overnight fast (18 h) with subsequent refeeding procedures for 3 h with either oral chow intake or provision of insulin, IGF-I, glucose, and amino acids. Anti-insulin and anti-IGF-I were provided intraperitoneally before oral refeeding in some experiments. An overnight fast reduced synthesis of both globular (38 +/- 3%) and myofibrillar proteins (54 +/- 3%) in skeletal muscles, which was reversed by oral refeeding. Muscle protein synthesis, after starvation/ refeeding, was proportional and similar to changes in skeletal muscle IGF-I mRNA expression. Diabetic mice responded quantitatively similarly to starvation/refeeding in muscle protein synthesis compared with normal mice (C57 Bl). Both anti-insulin and anti-IGF-I attenuated significantly the stimulation of muscle protein synthesis in response to oral feeding, whereas exogenous provision of either insulin or IGF-I to overnight-starved and freely fed mice did not clearly stimulate protein synthesis in skeletal muscles. Our results support the suggestion that insulin and IGF-I either induce or facilitate the protein synthesis machinery in skeletal muscles rather than exerting a true stimulation of the biosynthetic process during feeding.

scholarly journals The microRNA, miR-133b, functions to slow Duchenne muscular dystrophy pathogenesis

2020 ◽  
Author(s):  
Thomas Taetzsch ◽  
Dillon Shapiro ◽  
Randa Eldosougi ◽  
Tracey Myers ◽  
Robert Settlage ◽  
...  
Keyword(s):  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Skeletal Muscles ◽  
Tibialis Anterior Muscle ◽  
Muscle Fibers ◽  
Progressive Degeneration ◽  
Protein Encoding ◽  
Small Muscle ◽  
Encoding Genes

AbstractDuchenne muscular dystrophy (DMD) is characterized by progressive degeneration of skeletal muscles. To date, there are no treatments available to slow or prevent the disease. Hence, it remains essential to identify molecular factors that promote muscle biogenesis since they could serve as therapeutic targets for treating DMD. While the muscle enriched microRNA, miR-133b, has been implicated in the biogenesis of muscle fibers, its role in DMD remains unknown. To assess the role of miR-133b in DMD-affected skeletal muscles, we genetically ablated miR-133b in the mdx mouse model of DMD. In the absence of miR-133b, the tibialis anterior muscle of juvenile and adult mdx mice is populated by small muscle fibers with centralized nuclei, exhibits increased fibrosis, and thickened interstitial space. Additional analysis revealed that loss of miR-133b exacerbates DMD-pathogenesis partly by altering the number of satellite cells and levels of protein-encoding genes, including previously identified miR-133b targets as well as genes involved in cell proliferation and fibrosis. Altogether, our data demonstrate that skeletal muscles utilize miR-133b to mitigate the deleterious effects of DMD.

Role of conjugation and red blood cells for inactivation of circulating normetanephrine

1984 ◽  
Vol 247 (1) ◽  
pp. R208-R211
Author(s):  
S. Yoneda ◽  
N. Alexander ◽  
N. D. Vlachakis ◽  
R. F. Maronde
Keyword(s):  
Immobilization Stress ◽  
Glucuronic Acid ◽  
Simultaneous Increase ◽  
Sympathoadrenal System ◽  
Methyltransferase Activity ◽  
Substrate Saturation ◽  
The Mean ◽  
Catechol Methyltransferase ◽  
Mean Concentration

Plasma and red blood cell (RBC) concentrations of normetanephrine (NMN), in both free and glucuronide-conjugated forms, were measured before, during, and after forced immobilization, an intense stressor of the sympathoadrenal system of rats. In this study NMN glucuronide was deconjugated by enzymatic hydrolysis; free and total NMN were assayed by radioenzymatic, thin-layer chromatographic procedures. In plasma, free NMN and NMN glucuronide are 777 +/- 99 and 792 +/- 74 pg/ml, respectively, when rats are at rest. Both free NMN and NMN glucuronide increased about 200% after 15 min of stress; in absolute amounts, increases were equivalent to that of the simultaneous increase in norepinephrine (NE). At 2 h of stress, NMN glucuronide, but not free NMN, increased further and significantly. The mean concentration of RBC-free NMN is about 50 times higher than that of plasma-free NMN, and it did not change significantly during stress; RBCs do not contain conjugated NMN. RBC NMN levels showed a strong correlation with RBC catechol methyltransferase activity. The latter seems to operate under conditions of substrate saturation; an acute release of NE leads to temporary storage of NE in RBCs but not conversion to NMN. The results indicate that conjugation of NMN with glucuronic acid is an important route for inactivation of plasma NMN formed during forced immobilization stress, whereas free NMN does not accumulate in RBCs during stress.

Time course of changes in lipoprotein lipase activity in rat skeletal muscles during denervation-reinnervation

2002 ◽  
Vol 92 (2) ◽  
pp. 535-540 ◽  
Author(s):  
E. Z˙ernicka ◽  
E. Smol ◽  
J. Langfort ◽  
M. Górecka
Keyword(s):  
Lipoprotein Lipase ◽  
Skeletal Muscles ◽  
Time Course ◽  
Sciatic Nerve Crush ◽  
Lipoprotein Lipase Activity ◽  
Predominant Role ◽  
Nerve Crush ◽  
Gastrocnemius Muscles ◽  
Muscle Potential

The effects of denervation-reinnervation after sciatic nerve crush on the activity of extracellular and intracellular lipoprotein lipase (LPL) were examined in the soleus and red portion of gastrocnemius muscles. The activity of both LPL fractions was decreased in the two muscles within 24 h after the nerve crush and remained reduced for up to 2 wk. During the reinnervation period, LPL activity was still reduced in the soleus and started to increase only on the 40th day. In the red gastrocnemius, LPL activity increased progressively with reinnervation, exceeding control values on the 30th day postcrush. The LPL activity in the soleus from the contralateral to denervated hindlimb was also affected, being increased on the postoperation day and then gradually decreased during the following days. In conclusion, the time course of changes in muscle LPL activity after nerve crush confirmed the predominant role of nerve conduction in controlling muscle potential to take up free fatty acids derived from the plasma triacylglycerols. However, other factors, such as muscle fiber composition and the fiber transformation, should also be considered in this aspect of the denervation-reinnervation process. Moreover, it was found that denervation of muscles from one hindlimb may influence LPL activity in muscles from the contralateral leg.

Sa1952 Unraveling the Mechanisms Involved in Exercise Prevention of Colorectal Cancer: The Role of Skeletal Muscles

2015 ◽  
Vol 148 (4) ◽  
pp. S-365
Author(s):  
Mart DeLaCruz ◽  
Anuj Chhaparia ◽  
Navneet Momi ◽  
Ramesh K. Wali ◽  
Hemant K. Roy
Keyword(s):  
Colorectal Cancer ◽  
Skeletal Muscles

Coronary nitric oxide production controls cardiac substrate metabolism during pregnancy in the dog

2008 ◽  
Vol 294 (6) ◽  
pp. H2516-H2523 ◽  
Author(s):  
Jeffrey G. Williams ◽  
Caroline Ojaimi ◽  
Khaled Qanud ◽  
Suhua Zhang ◽  
Xiaobin Xu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glucose Oxidation ◽  
Atp Synthesis ◽  
Glycogen Metabolism ◽  
Cardiac Metabolism ◽  
Atp Production ◽  
Oxidative Pathway ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

The aim of this study was to examine the role of nitric oxide (NO) in the control of cardiac metabolism at 60 days of pregnancy (P60) in the dog. There was a basal increase in diastolic coronary blood flow during pregnancy and a statistically significant increase in cardiac output (55 ± 4%) and in cardiac NOx production (44 ± 4 to 59 ± 3 nmol/min, P < 0.05). Immunohistochemistry of the left ventricle showed an increase in endothelial nitric oxide synthase staining in the endothelial cells at P60. NO-dependent coronary vasodilation (Bezold-Jarisch reflex) was increased by 20% and blocked by NG-nitro-l-arginine methyl ester (l-NAME). Isotopically labeled substrates were infused to measure oleate, glucose uptake, and oxidation. Glucose oxidation was not significantly different in P60 hearts (5.4 ± 0.5 vs. 6.2 ± 0.4 μmol/min) but greatly increased in response to l-NAME injection (to 19.9 ± 0.9 μmol/min, P < 0.05). Free fatty acid (FFA) oxidation was increased in P60 (from 5.3 ± 0.6 to 10.4 ± 0.5 μmol/min, P < 0.05) and decreased in response to l-NAME (to 4.5 ± 0.5 μmol/min, P < 0.05). There was an increased oxidation of FFA for ATP production but no change in the respiratory quotient during pregnancy. Genes associated with glucose and glycogen metabolism were downregulated, whereas genes involved in FFA oxidation were elevated. The acute inhibition of NO shifts the heart away from FFA and toward glucose metabolism despite the downregulation of the carbohydrate oxidative pathway. The increase in endothelium-derived NO during pregnancy results in a tonic inhibition of glucose oxidation and reliance on FFA uptake and oxidation to support ATP synthesis in conjunction with upregulation of FFA metabolic enzymes.

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