Disease relevance of Lipg

• Ischemia and denervation of EDL muscle of adult rat induce a large central zone of degeneration surrounded by a thin zone of peripheral surviving muscle fibers [1].
• The aim of this study was to determine whether exogenous glucose metabolism influences the pH in superfused EDL muscle from growing rats fed or starved for 48 h (body weight 55 and 45 g, respectively) [2].
• RESULTS: At day 27 the electrophoretic analysis of myosin heavy chains (MHCs) demonstrated in the CHF rats the occurrence of a myopathy, with disappearance of slow MHC1 in the Tibialis Anterior (TA), and a significant shift from the slow to the fast isoforms in the soleus and EDL [3].
• TA muscle ablation caused hypertrophy of EDL muscle, characterized by a significant increase in muscle mass and the size of type IIx and type IIb fibers, and a proportional increase in the number of myonuclei [4].
• Both 5-fluoro-uracil and vincristine prevent the development of denervation hypersensitivity both in soleus and EDL muscles [5].

Psychiatry related information on Lipg

• We conclude that glucose was routed mainly toward both oxidative phosphorylation and glycogen synthesis in EDL muscles after food deprivation of rats [2].

High impact information on Lipg

• Western blot analysis showed the presence of two immunopositive bands with apparent molecular masses of 30 and 32 kD specifically present in membrane fraction of a fast-twitch rat skeletal muscle (extensor digitorum longus, EDL) and not revealed in a slow-twitch muscle (soleus) [6].
• There is a progressive refinement of enzyme levels in the soleus into a more uniform fiber population, while the fibers in the EDL progressively diverge into 2 distinct phenotypes [7].
• The effect of exogenous hydrogen peroxide (H(2)O(2)) on excitation-contraction (E-C) coupling and sarcoplasmic reticulum (SR) function was compared in mechanically skinned slow twitch fibres (prepared from the soleus muscles) and fast twitch fibres (prepared from the extensor digitorum longus; EDL muscles) of adult rats [8].
• Incubation of isolated rat soleus and EDL muscles in the presence of 10 mM leucine resulted in a decreased proteolytic rate as measured by the release of tyrosine into the incubation medium [9].
• Increases in resting force were first detectable at about 0.5 mmol l-1 caffeine for soleus muscles and 5.0 mmol l-1 caffeine for EDL muscles and occurred in the range 0.2-0.4 mumol l-1 [Ca2+]i for soleus and 0.7-0.9 mumol l-1 for EDL [10].

Chemical compound and disease context of Lipg

• The effect of ischemia on ATP levels in the SOL was similar to ATP levels in the EDL, 1 h of ischemia also resulted in a large decrement in PCr, from 50.1 +/- 2.9 to 11.7 +/- 2.4 mmol/kg dry weight, and a large increase in lactate, from 25.0 +/- 3.0 to 114 +/- 10 mmol/kg dry weight [11].
• Chronic administration of an anabolic hormone, nandrolone phenylpropionate, in sedentary female rats for 6 weeks gave a 20% increase in body weight and the same proportional increase in all muscles sampled (heart, diaphragm, soleus, TA, EHP and EDL), such that the muscle/body weight ratio was unchanged [12].
• 3. In order to identify the cellular mechanisms of skeletal muscle atrophy during fasting and diabetes mellitus, we have studied protein turnover in soleus and EDL muscles from control and fasted (for 24 h) or diabetic rats (1, 3, 5 and 10 days after streptozotocin injection) [13].
• The twitch, tetanus, and double pulse responses with a number of interval times have been investigated for a fast (EDL) and a slow (soleus) muscle of the rat at three muscle lengths (in vivo, at 37 degrees C, pentobarbital sodium anesthesia) [14].

Biological context of Lipg

• Part of the nucleotide sequence of the Lipg gene in the rat was established using primers based on the mRNA sequence described in the mouse [15].
• The Lipg gene was found to be located on rat chromosome 18 in the vicinity of the marker D18Mit11; a region reported to be homologous with both human and mouse chromosome 18 [15].
• However, oxygen consumption rate assessed in situ in saponin skinned fibers (12.5 +/- 0.8 in C and 15.1 +/- 0.9 micromol O2/min/g dw in HS soleus compared to 7.3 +/- 1.3 micromol O2/min/g dw in control EDL), as well as mitochondrial CK (mi-CK) and citrate synthase activities, were preserved in HS soleus [16].
• We used an array of specific antibodies to identify adult and developmental MHC isoforms within EDL and soleus muscle fibers, and show a marked multiple expression of MHCs with a general shift towards slower and more energy efficient MHC profiles after 2 weeks of denervation or TTX nerve conduction block [17].
• We find that the mature pattern of differences in release arise through co-ordinated increases in presynaptically dependent release properties (quantal content, spontaneous release frequency and evoked potential amplitude), beginning at three weeks, which are particularly substantial in EDL [18].

Anatomical context of Lipg

• Functional experiments carried out on isolated skeletal muscle bundle fibers demonstrated that the osmotic response is faster in EDL than in soleus fibers isolated from the same rat [6].
• Ca2+ release and uptake by the sarcoplasmic reticulum has also been investigated directly on skinned EDL fibres at 1 mmol/l BDM at 23 degrees C. 2 [19].
• Four days after sciatic nerve section, taurine concentration in the EDL but not in the SL was increased by 2.5-fold [20].
• Provided that the major part of muscle NADH is located in the mitochondria it can be calculated that the mitochondrial NADH content in skeletal muscle at rest is about 36 (soleus) and 60% (EDL) of the anoxic value, respectively [21].
• To gain further insight into metabolic and mechanical properties of deconditioned slow-twitch (soleus) or fast-twitch (EDL) skeletal muscles, we induced experimental muscle deconditioning by hindlimb suspension (HS) in rats for 3 weeks [16].

Associations of Lipg with chemical compounds

• The soleus was more sensitive in this respect, with 50% potentiation occurring at 1 mmol l-1 caffeine compared with 3.5 mmol l-1 for the EDL [10].
• Tenotomy did not increase the total taurine content of the EDL [20].
• The increase in taurine concentration of the denervated EDL was prevented by simultaneous ingestion of guanidinoethane sulfonate, a competitive inhibitor of taurine transport [20].
• In EDL muscles from starved rats superfused with glucose for 4 h, intracellular pH was elevated (7-7.3), lactate concentration low, glycogen repletion very intense and citrate synthase activity high [2].
• The purpose of the present study was to compare dexamethasone-induced glycogen increases in normal EDL and SOL muscles with that in free muscle grafts [22].

Analytical, diagnostic and therapeutic context of Lipg

• A rat-hamster radiation hybrid (RH) panel was used for chromosomal assignment of the rat Lipg gene [15].
• LPL mRNA levels were quantitated by both Northern blotting and reverse transcriptase-polymerase chain reaction (RT-PCR), and were approximately equal in heart and soleus, and 5-fold lower in EDL [23].
• In contrast, the electrical stimulation of sciatic nerve accelerated the uptake of taurine by EDL and SL of the control but not of the curare-treated rats [20].
• We studied the ionic and water content and the resting membrane potential of rat extensor digitorum longus EDL muscles at different times after unilateral nerve crush [24].
• The transcript levels of the myogenic regulatory factors (myoD, myf5, myogenin and MRF4) were measured by RT PCR in rat soleus (slow) and EDL (fast) muscles which were regenerating from notexin-induced necrosis [25].

References