scholarly journals Effects of glimepiride on growth, glucose metabolism and expression of p38MAPK, JNK in skeletal muscles of GIFT tilapia

2021 ◽  
Vol 21 ◽  
pp. 100873
Author(s):  
Huiwen Sun ◽  
Dongyan Guan ◽  
Jiting Wang ◽  
Zhen Wang ◽  
Yang Li ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Skeletal Muscles ◽  
Gift Tilapia

Prolonged suppression of glucose metabolism causes insulin resistance in rat skeletal muscle

1997 ◽  
Vol 272 (2) ◽  
pp. E288-E296 ◽  
Author(s):  
J. K. Kim ◽  
J. H. Youn
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Skeletal Muscles ◽  
Glycogen Synthesis ◽  
Whole Body ◽  
Metabolic Fluxes ◽  
Phosphate Inhibition ◽  
Intracellular Glucose

To determine whether an impairment of intracellular glucose metabolism causes insulin resistance, we examined the effects of suppression of glycolysis or glycogen synthesis on whole body and skeletal muscle insulin-stimulated glucose uptake during 450-min hyperinsulinemic euglycemic clamps in conscious rats. After the initial 150 min to attain steady-state insulin action, animals received an additional infusion of saline, Intralipid and heparin (to suppress glycolysis), or amylin (to suppress glycogen synthesis) for up to 300 min. Insulin-stimulated whole body glucose fluxes were constant with saline infusion (n = 7). In contrast, Intralipid infusion (n = 7) suppressed glycolysis by approximately 32%, and amylin infusion (n = 7) suppressed glycogen synthesis by approximately 45% within 30 min after the start of the infusions (P < 0.05). The suppression of metabolic fluxes increased muscle glucose 6-phosphate levels (P < 0.05), but this did not immediately affect insulin-stimulated glucose uptake due to compensatory increases in other metabolic fluxes. Insulin-stimulated whole body glucose uptake started to decrease at approximately 60 min and was significantly decreased by approximately 30% at the end of clamps (P < 0.05). Similar patterns of changes in insulin-stimulated glucose fluxes were observed in individual skeletal muscles. Thus the suppression of intracellular glucose metabolism caused decreases in insulin-stimulated glucose uptake through a cellular adaptive mechanism in response to a prolonged elevation of glucose 6-phosphate rather than the classic mechanism involving glucose 6-phosphate inhibition of hexokinase.

scholarly journals Rosiglitazone promotes glucose metabolism of GIFT tilapia based on the PI3K/Akt signaling pathway

2021 ◽  
Vol 9 (5) ◽  
Author(s):  
Dong‐Yan Guan ◽  
Hui‐Wen Sun ◽  
Ji‐Ting Wang ◽  
Zhen Wang ◽  
Yang Li ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Gift Tilapia

scholarly journals p38 MAPK in Glucose Metabolism of Skeletal Muscle: Beneficial or Harmful?

2020 ◽  
Vol 21 (18) ◽  
pp. 6480 ◽  
Author(s):  
Eyal Bengal ◽  
Sharon Aviram ◽  
Tony Hayek
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Syndrome ◽  
Glucose Metabolism ◽  
P38 Mapk ◽  
Glucose Intolerance ◽  
Skeletal Muscles ◽  
Fiber Type ◽  
Caloric Intake ◽  
Mitogen Activated Protein Kinase ◽  
Metabolic Adaptation

Skeletal muscles respond to environmental and physiological changes by varying their size, fiber type, and metabolic properties. P38 mitogen-activated protein kinase (MAPK) is one of several signaling pathways that drive the metabolic adaptation of skeletal muscle to exercise. p38 MAPK also participates in the development of pathological traits resulting from excessive caloric intake and obesity that cause metabolic syndrome and type 2 diabetes (T2D). Whereas p38 MAPK increases insulin-independent glucose uptake and oxidative metabolism in muscles during exercise, it contrastingly mediates insulin resistance and glucose intolerance during metabolic syndrome development. This article provides an overview of the apparent contradicting roles of p38 MAPK in the adaptation of skeletal muscles to exercise and to pathological conditions leading to glucose intolerance and T2D. Here, we focus on the involvement of p38 MAPK in glucose metabolism of skeletal muscle, and discuss the possibility of targeting this pathway to prevent the development of T2D.

Effect of acute hyperglycemia on glucose metabolism in skeletal muscles in IDDM patients

Diabetes ◽  
1992 ◽  
Vol 41 (2) ◽  
pp. 174-182 ◽  
Author(s):  
A. Vaag ◽  
O. Hother-Nielsen ◽  
P. Skott ◽  
P. Andersen ◽  
E. A. Richter ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Skeletal Muscles ◽  
Acute Hyperglycemia

Alcohol and glucose metabolism in skeletal muscles in the rat

1996 ◽  
Vol 1 (1) ◽  
pp. 71-83 ◽  
Author(s):  
DAN XU ◽  
AMARDEEP DHILLON ◽  
CHRISTOPHER DAVEY ◽  
PAUL FOURNIER ◽  
T. NORMAN PALMER
Keyword(s):  
Glucose Metabolism ◽  
Skeletal Muscles

scholarly journals Glucose Metabolic Changes in the Brain and Muscles of Patients with Nonspecific Neck Pain Treated by Spinal Manipulation Therapy: A [18F]FDG PET Study

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Akie Inami ◽  
Takeshi Ogura ◽  
Shoichi Watanuki ◽  
Md. Mehedi Masud ◽  
Katsuhiko Shibuya ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Fdg Pet ◽  
Skeletal Muscles ◽  
Spinal Manipulation ◽  
Sympathetic Nerve Activity ◽  
Muscle Tension ◽  
Amylase Level ◽  
Salivary Amylase ◽  
Nerve Activity ◽  
The Brain

Objective. The aim of this study was to investigate changes in brain and muscle glucose metabolism that are not yet known, using positron emission tomography with [18F]fluorodeoxyglucose ([18F]FDG PET).Methods. Twenty-one male volunteers were recruited for the present study. [18F]FDG PET scanning was performed twice on each subject: once after the spinal manipulation therapy (SMT) intervention (treatment condition) and once after resting (control condition). We performed the SMT intervention using an adjustment device. Glucose metabolism of the brain and skeletal muscles was measured and compared between the two conditions. In addition, we measured salivary amylase level as an index of autonomic nervous system (ANS) activity, as well as muscle tension and subjective pain intensity in each subject.Results. Changes in brain activity after SMT included activation of the dorsal anterior cingulate cortex, cerebellar vermis, and somatosensory association cortex and deactivation of the prefrontal cortex and temporal sites. Glucose uptake in skeletal muscles showed a trend toward decreased metabolism after SMT, although the difference was not significant. Other measurements indicated relaxation of cervical muscle tension, decrease in salivary amylase level (suppression of sympathetic nerve activity), and pain relief after SMT.Conclusion. Brain processing after SMT may lead to physiological relaxation via a decrease in sympathetic nerve activity.

scholarly journals Effects of epinephrine on glucose metabolism in contracting rat skeletal muscles

1998 ◽  
Vol 275 (3) ◽  
pp. E448-E456 ◽  
Author(s):  
Rune Aslesen ◽  
Jørgen Jensen
Keyword(s):  
Glucose Metabolism ◽  
Glucose Transport ◽  
Skeletal Muscles ◽  
Contractile Activity ◽  
Phosphate Concentration ◽  
Insulin Stimulation ◽  
Glucose Phosphorylation ◽  
Slow Twitch ◽  
Fast Twitch

The effects of epinephrine on glucose metabolism during contractile activity and insulin stimulation were investigated in fast-twitch (epitrochlearis) and slow-twitch (soleus) muscles from Wistar rats. All muscles were mounted on contraction apparatuses, and some muscles were stimulated electrically for 30 min in vitro. Glucose uptake and glucose phosphorylation were measured with 2-[1,2-3H(N)]deoxy-d-glucose and glucose transport with 3- O-[ methyl-3H]methyl-d-glucose.d-[1-14C]mannitol was used to correct for extracellular space. In epitrochlearis, both contraction and insulin increased glucose transport by threefold, and combined they showed an additive effect. Epinephrine (10−6 M) did not influence glucose transport across the membrane during contractile activity or insulin stimulation. In the absence of epinephrine, similar glucose phosphorylation was obtained during contraction and during insulin stimulation in epitrochlearis (∼12 mmol ⋅ kg dry wt−1 ⋅ 30 min−1). In the presence of epinephrine, 9.5 ± 0.6 mmol ⋅ kg dry wt−1 ⋅ 30 min−1 glucose was phosphorylated during contraction, whereas only 2.0 ± 0.3 mmol ⋅ kg dry wt−1 ⋅ 30 min−1 was phosphorylated during insulin stimulation ( P < 0.01), despite a similar glucose 6-phosphate concentration. Comparable results were obtained in soleus. In conclusion, our data suggest that epinephrine inhibits glucose phosphorylation much less during contraction than during insulin stimulation.

scholarly journals WWOX somatic ablation in skeletal muscles alters glucose metabolism

2019 ◽  
Vol 22 ◽  
pp. 132-140 ◽  
Author(s):  
Muhannad Abu-Remaileh ◽  
Monther Abu-Remaileh ◽  
Rania Akkawi ◽  
Ibrahim Knani ◽  
Shiran Udi ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Skeletal Muscles
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