Regulation of glucose and fatty acid metabolism in skeletal muscle during contraction

The glucose-fatty acid cycle explains the preference for fatty acid during moderate and long duration physical exercise. In contrast, there is a high glucose availability and oxidation rate in response to intense physical exercise. The reactive oxygen species (ROS) production during physical exercise suggests that the redox balance is important to regulate of lipids/carbohydrate metabolism. ROS reduces the activity of the Krebs cycle, and increases the activity of mitochondrial uncoupling proteins. The opposite effects happen during moderate physical activity. Thus, some issues is highlighted in the present review: Why does skeletal muscle prefer lipids in the basal and during moderate physical activity? Why does glucose-fatty acid fail to carry out their effects during intense physical exercise? How skeletal muscles regulate the lipids and carbohydrate metabolism during the contraction-relaxation cycle?     

Effect of short-term creatine supplementation on markers of skeletal muscle damage after strenuous contractile activity

The protective effect of short-term creatine supplementation (CrS) upon markers of strenuous contractile activity-induced damage in human and rat skeletal muscles was investigated. Eight Ironman triathletes were randomized into the placebo (Pl; n = 4) and creatine-supplemented (CrS; n = 4) groups. Five days prior to the Ironman competition, the CrS group received creatine monohydrate (20 g day⁻¹) plus maltodextrin (50 g) divided in two equal doses. The Pl group received maltodextrin (50 g day⁻¹) only. The effect of CrS (5 g day⁻¹/kg body weight for 5 days) was also evaluated in a protocol of strenuous contractile activity induced by electrical stimulation in rats. Blood samples were collected before and 36 and 60 h after the competition and were used to determine plasma activities of creatine kinase (CK), lactate dehydrogenase (LDH), aldolase (ALD), glutamic oxaloacetic acid transaminase (GOT), glutamic pyruvic acid transaminase (GPT), and C-reactive protein (CRP) level. In rats, plasma activities of CK and LDH, muscle vascular permeability (MVP) using Evans blue dye, muscle force and fatigue were evaluated. Activities of CK, ALD, LDH, GOT, GTP, and levels of CRP were increased in the Pl group after the competition as compared to basal values. CrS decreased plasma activities of CK, LDH, and ALD, and prevented the rise of GOT and GPT plasma activities. In rats, CrS delayed the fatigue, preserved the force, and prevented the rise of LDH and CK plasma activities and MVP in the gastrocnemius muscle. CrS presented a protective effect on muscle injury induced by strenuous contractile activities.     

Viruses exploit the function of epidermal growth factor receptor

Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase that regulates cellular homeostatic processes. Following ligand binding, EGFR activates different downstream signalling cascades that promote cell survival, proliferation, motility, and angiogenesis and induces F‐actin‐dependent EGFR endocytosis, which relocalises the activated receptors for degradation or recycling. The responses that are induced by ligand binding to EGFR, including cell signalling activation, protein kinase phosphorylation and cytoskeletal network rearrangement, resemble those induced by virus infection. Increasing evidence demonstrates that many viruses usurp EGFR endocytosis or EGFR‐mediated signalling for entry, replication, inflammation, and viral antagonism to the host antiviral system. In addition, viruses have acquired sophisticated mechanisms to regulate EGFR functions by interrupting the EGFR‐recycling process and modulating EGFR expression. In this review, we provide an overview of the mechanisms by which viruses alter EGFR signalling in favour of their continued survival. Copyright © 2014 John Wiley & Sons, Ltd.     

Analysis of Helicobacter pylori binding site on HEp-2 cells and three cell lines from human gastric carcinoma

Helicobacter pylori (H. pylori) is a pathogen responsible for chronic gastritis and peptic ulcer diseases. It colonises the gastric mucus layer and adheres to the gastric epithelial cell surface. As this adherence is the first step of infection, it is important to study the adherence mechanism. The aim of this study was to analyse the specific binding assay of H. pylori to HEp-2 cells and three gastric phenotype cell lines, AGS, MKN-45 and AZ-521. H. pylori NCTC 11637 grown on agar plates was harvested and used in experiments. H. pylori was inoculated to pre-cultured cell monolayers. Adhered bacteria were labelled with an anti-H. pylori antibody and an FITC-conjugated secondary antibody and quantified by using a fluorescent plate reader. Microbial adherence to HEp-2 cells increased with incubation time and incubated concentration of H. pylori. No further increase was obtained with four or more hours of incubation or with a concentration of 4 x 10(7) bacteria/well or more. Scatchard analysis revealed a linear plot and the Bmax value was 88.3. Similar adherence patterns were obtained when AGS, AZ-521 and MKN-45 cells were used for adherence assays, but they had a lower binding affinity than HEp-2 cells and AZ-521. MKN-45 cells had less receptors than HEp-2 and AGS cells. In conclusion, H. pylori adhered to the cell surface could be quantified by this assay method. H. pylori adhesion to cell surfaces has a single population of binding site and one type of binding site on HEp-2, AGS, AZ-521 and MKN-45 cells.     

Mode of inhibitory action of propiverine hydrochloride on the micturition movements of the bladder in dogs

Propiverine hydrochloride (P-4) is a new derivative of benzilic acid. The effect of P-4 on the vesico-detrusor reflex (corresponding to the first reflex of Barrington) in anesthetized or decerebrated dogs was studied to elucidate the mode of action of the drug. When bladder contraction was induced by electrical stimulation of the distal ending of the pelvic nerve under the bilateral pelvic nerve and hypogastric nerve transection, P-4 (2, 5 and 10 mg/kg, i.v.) significantly inhibited the contraction. A similar effect was also observed following intravenous administration of flavoxate (10 and 20 mg/kg), verapamil (1 mg/kg) or propantheline (2 mg/kg), while thiopental (4 mg/kg, i.v.) had no significant effect. When the bladder was filled under the bilateral pelvic nerve and hypogastric nerve transection, an increase of afferent impulses from the distal ending of a pelvic vesical branch was observed. P-4 (10 mg/kg, i.v.) had no effect on the afferent impulses. When the central endings of the pelvic vesical branches were electrically stimulated, reflex discharges were noted from a pelvic vesical branch on the contralateral side. Thiopental (2 and 4 mg/kg, i.v.) markedly decreased the reflex discharge, whereas P-4 (10 mg/kg, i.v.) caused no such inhibition. These findings suggest that the inhibition of the vesico-detrusor reflex by P-4 may result from its inhibitory action on the efferent terminal of the pelvic nerve.