SEARCH · PubMed Health

Results for “Atrophy”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources

PubMed2000

Atrophy of the corpus callosum associated with a decrease in cortical benzodiazepine receptor in large cerebral arterial occlusive diseases.

OBJECTIVES: It remains controversial whether selective neuronal ischaemic change develops in patients with occlusion of the large cerebral arteries. Previous studies have shown atrophy of the corpus callosum with reduced cortical oxygen metabolism in large cerebral arterial occlusive diseases, which might be indirect evidence of loss of the neurons in cortical layer 3. Recent studies of patients with ischaemic cerebrovascular diseases have demonstrated reduced central benzodiazepine receptor (BZR) binding in the normal appearing cortical areas, which might be more direct evidence of changes of the neurons. Although pathophysiology of the decreased BZR is unclear, a decrease in the cortical BZR binding with neuronal loss would cause atrophy of the corpus callosum. The purpose of this study was to determine whether atrophy of the corpus callosum is associated with a decrease in cortical BZR binding in large cerebral arterial occlusive diseases. METHODS: Seven patients with occlusive diseases of the middle cerebral or internal carotid artery and only minor subcortical infarctions were studied. Single photon emission tomographic images of (123)I labelled iomazenil (IMZ) obtained 180 minutes after injection were analysed for BZR binding. The midsagittal corpus callosum area/skull area ratio (on T1 weighted magnetic resonance images) was compared with the cerebral IMZ uptake/cerebellar IMZ uptake ratio. RESULTS: Compared with 23 age and sex matched control subjects, the patients had significantly decreased callosal area/skull area ratio. The degree of corpus callosum atrophy was significantly and strongly (rho=0.99, p<0.02) correlated with that of the decreases in the mean cerebral cortical IMZ uptake ratio. CONCLUSION: Corpus callosum atrophy may occur in association with a decrease in cortical BZR binding in large cerebral arterial occlusive diseases. Corpus callosum atrophy with decreased cortical BZR binding might reflect cortical neuronal damage in large cerebral arterial occlusive diseases.

Aged↗

PubMed2003

The longitudinal relation between brain lesion load and atrophy in multiple sclerosis: a 14 year follow up study.

BACKGROUND: Studies have suggested that T2 lesion activity is prominent in early relapsing-remitting multiple sclerosis, whereas brain atrophy, while seen early, appears more evident in later progressive disease. The temporal relation between these processes remains unclear. OBJECTIVE: To explore the association between changing brain lesion loads and subsequent tissue atrophy in multiple sclerosis. METHODS: 28 subjects with clinically probable or definite multiple sclerosis (mean age 46.0 years; 17 female and 11 male) were followed for 14 years after first onset of symptoms. T2 lesion loads were estimated soon after symptom onset and at around five, 10, and 14 years later. Disease related atrophy was estimated at the 14 year follow up by comparing brain tissue volumes (proportional to total intracranial volumes) determined in the multiple sclerosis group with data from 29 normal control subjects (mean age 36.7 years; 16 female, 13 male) using multiple linear regression analyses to allow for differences in age and sex distributions. RESULTS: Change in lesion load in the first five years was more closely correlated to disease related brain atrophy at 14 years than later changes in lesion load, although the correlation was only moderate (Spearman correlation = -0.528, p = 0.004). CONCLUSIONS: From this, it appears that early rather than later focal lesion accumulation relates to subsequent brain atrophy, but factors unconnected directly with lesion formation probably also play a significant role in determining such atrophy.

Adult↗

PubMed1992

Trace element movement and oxidative stress in skeletal muscle atrophied by immobilization.

The movements of trace elements and the level of oxidative stress in the soleus, a typical slow red muscle which, atrophied by immobilization, were investigated in designated intervals. Male Wistar rats (14 wk old) whose one ankle joints were immobilized in the extended position were killed after 4, 8, and 12 days. Fe, Zn, Mn, and Cu concentrations and the levels of thiobarbituric acid-reactive substance (TBARS) and glutathione were measured. The rate of atrophy increased rapidly until the 8th day and slowly after that. In whole muscle, Fe concentration kept increasing, and Zn and Mn increased temporarily. Their subcellular distributions also changed; especially, the Fe level of the microsomal fraction kept increasing and reached threefold at 12 days. Increased TBARS and glutathione disulfide and decreased total glutathione indicated the increased oxidative stress in atrophy, which might result from an increased Fe level, especially that of the microsomal fraction. Vitamin E injection lessened the rate of atrophy, which showed that oxidative stress accelerated muscle atrophy. This might be mediated by increased intracellular Ca. Also metallothionein was induced in muscle atrophy.

Animals↗

PubMed1990

Glucocorticoid-induced muscle atrophy prevention by exercise in fast-twitch fibers.

Exercise has been shown to be effective in preventing glucocorticoid-induced atrophy in muscles containing high proportions of type II or fast-twitch fibers. This investigation was undertaken to further evaluate this response in type IIa and IIb fibers, determined by histochemical staining for myofibrillar adenosinetriphosphatase with alkaline and acid preincubation. Steroid [cortisol acetate (CA), 100 mg/kg body wt] and exercise (running 90 min/day, 29 m/min) treatments were initiated simultaneously for 11 consecutive days in female rats. Fiber distribution and area measurements were performed in a deep and superficial region of plantaris muscle. The exercise regimen spared approximately 40% of the CA-induced plantaris muscle atrophy. In the deep region, the fiber population, which contained approximately 13% type I (slow-twitch), 24% type IIa, and 63% IIb fibers, was not affected by either treatment. In the superficial section, which consisted solely of type II fibers, the proportion of type IIa fibers was higher (27 vs. 9%, P less than 0.01) in the steroid- than in the vehicle-treated groups. Within each region, type IIa fibers were less susceptible to atrophy than type IIb fibers, and within each fiber type, the deep region had less atrophy than the superficial region. Type I fibers were unchanged by steroid treatment. For type IIa fibers, exercise prevented 100% of the atrophy in the deep region and 50% in the superficial region. For type IIb fibers, the activity spared 67 and 40% of the atrophy in these same regions, respectively. These results show that glucocorticoids are capable of changing the myosin phenotype.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Centrifugal intensity and duration as countermeasures to soleus muscle atrophy.

Mechanical acceleration is a countermeasure that may be employed to prevent atrophy of slow-twitch muscle during non-weight bearing. In the present study, daily centrifugation of rats for different durations (1 or 2 h) and at different gravitational intensities (1.5 or 2.6 G) was used to test whether mechanical acceleration could ameliorate the atrophy of the soleus muscle induced by non-weight bearing (tail-traction model). The soleus muscle atrophied 32% during 7 days of non-weight bearing without countermeasures. Centrifugation treatment did not completely prevent atrophy relative to precontrol wet weight of the soleus muscle. Non-weight-bearing groups receiving 2-h daily treatments of 1, 1.5, or 2.6 G had 48, 56, and 65%, respectively, of the atrophy observed in the non-weight-bearing-only group compared with the precontrol group. No evidence was obtained that centrifugation at 2.6 G was more effective than exposure to 1 or 1.5 G as a countermeasure to non-weight-bearing-induced atrophy of the soleus muscle.

Animals↗

PubMed2004

Dialysis-related hypotension as a cause of progressive frontal lobe atrophy in chronic hemodialysis patients: a 3-year prospective study.

BACKGROUND/AIM: Brain atrophy is known to develop more rapidly in hemodialysis (HD) patients than other individuals. The present study was designed to examine the role of HD-related hypotension in brain atrophy in patients on chronic HD. METHODS: By using magnetic resonance imaging, whole brain atrophy was assessed by the ventricular-brain ratio (VBR; ventricular area/whole brain area). Frontal brain atrophy was assessed by the frontal atrophy index (FAI; frontal brain area/intracranial frontal space). The number of lacunae was also counted. We studied 32 HD patients without symptomatic neurological abnormalities or diabetes mellitus: male/female ratio 19/13; mean age +/- SD 53 +/- 10 (range 28-77) years; mean HD duration +/- SD 11 +/- 6 (range 1-22) years. Magnetic resonance imagings were taken in 1995 and 1998. All dialysis-related hypotension episodes during the same period were identified from the medical records and counted. RESULTS: The VBR ranged from 8.8 to 18.7% in 1995 (12.8 +/- 2.2%) and was not different in 1998 (13.1 +/- 2.7%). However, the VBR increased by more than 5% in 14 patients, and their HD duration of 13 +/- 6 years was significantly longer than that of 18 patients with stable VBR (p < 0.05). The FAI in 1995 was 62.2 +/- 4.2% (range 55.8-71.3%) and decreased significantly to 59.7 +/- 4.7% (range 50.2-70.9%) in 1998 (p < 0.05). The change in FAI correlated significantly with both the total number of dialysis-related hypotension episodes (r = 0.45, p < 0.05) and the increase in number of lacunae (r = 0.42, p < 0.05). CONCLUSION: Our results suggest that dialysis-related hypotension plays a role in progressive frontal lobe atrophy in HD patients.

Adult↗

PubMed2005

Genomic susceptibility loci for brain atrophy in hypertensive sibships from the GENOA study.

We measured 366 microsatellite markers genome-wide to search for loci contributing to subcortical white matter ischemic damage (leukoariosis) and brain atrophy in 488 non-Hispanic white subjects (193 men, 295 women; mean age+/-SD=64.1+/-7.7 years; 79% hypertensive) from 223 sibships recruited through > or =2 members with essential hypertension diagnosed before age 60. Leukoariosis was quantitated by magnetic resonance imaging (MRI), brain atrophy by the difference between intracranial and brain volumes, and calculated mean arterial pressure and pulse pressure provided measures of steady-state level and pulsatile components of blood pressure. After adjustment for sex and age, variance components models estimated significant heritability of leukoariosis (0.72), brain atrophy (0.52), mean arterial pressure (0.084), and pulse pressure (0.294) (P<0.0001 for each trait). Univariate maximum logarithm of odds scores (MLS) were observed for leukoariosis on chromosome 5 (MLS=1.91; P=0.00150); for brain atrophy on 1q and 17p (MLS=2.76, P=0.00018); for mean arterial pressure on 11p (MLS=1.57; P=0.00354); and for pulse pressure on 11p (MLS=3.02; P=0.00070). Bivariate linkage analyses provided evidence of loci with pleiotropic effects on brain atrophy and pulse pressure on chromosomes 11p (MLS = 5.07 at 16 cM; P=0.00001) and 16q (MLS of 4.56 at 124 cM; P=0.00003). These results demonstrate usefulness of multivariate linkage analyses to detect loci with pleiotropic effects on genetically correlated traits and suggest overlap between the genes influencing blood pressure and those contributing to brain atrophy.

Aged↗

PubMed2003

Influence of cilioretinal arteries on neuroretinal rim and parapapillary atrophy in glaucoma.

PURPOSE: The pattern of neuroretinal rim loss and increase in the area of parapapillary atrophy in glaucoma depend on the localization of the central retinal vessel trunk in the lamina cribrosa. The purpose of the present study was to determine whether, in a similar way, the pattern of rim loss and progression of parapapillary atrophy are influenced by the presence and position of cilioretinal arteries. METHODS: Color stereo optic disc photographs (15 degrees) for morphometric evaluation of the optic nerve head were used to compare the appearance of the optic disc in 41 patients exhibiting unilateral or bilateral cilioretinal arteries in the temporal horizontal disc region with the optic disc morphology of 127 patients without cilioretinal arteries. The areas of the neuroretinal rim and alpha and beta zones of parapapillary atrophy were measured in the total disc and in four disc sectors. RESULTS: Eyes with and eyes without cilioretinal arteries did not differ significantly in the areas of neuroretinal rim and alpha and beta zones of parapapillary atrophy, when measured in the whole optic disc and in the four disc sectors separately; in ratios of the temporal horizontal area to total area of rim and parapapillary atrophy; and in the ratio of temporal horizontal rim area-to-nasal rim area, neither in an interindividual comparison nor in an intraindividual intereye comparison. CONCLUSIONS: In contrast to the position of the central retinal vessel trunk, presence and position of cilioretinal arteries do not markedly influence the pattern of neuroretinal rim loss and progression of parapapillary atrophy in glaucoma.

Chronic Disease↗

PubMed2004

Disruption of either the Nfkb1 or the Bcl3 gene inhibits skeletal muscle atrophy.

The intracellular signals that mediate skeletal muscle protein loss and functional deficits due to muscular disuse are just beginning to be elucidated. Previously we showed that the activity of an NF-kappaB-dependent reporter gene was markedly increased in unloaded muscles, and p50 and Bcl-3 proteins were implicated in this induction. In the present study, mice with a knockout of the p105/p50 (Nfkb1) gene are shown to be resistant to the decrease in soleus fiber cross-sectional area that results from 10 days of hindlimb unloading. Furthermore, the marked unloading-induced activation of the NF-kappaB reporter gene in soleus muscles from WT mice was completely abolished in soleus muscles from Nfkb1 knockout mice. Knockout of the B cell lymphoma 3 (Bcl3) gene also showed an inhibition of fiber atrophy and an abolition of NF-kappaB reporter activity. With unloading, fast fibers from WT mice atrophied to a greater extent than slow fibers. Resistance to atrophy in both strains of knockout mice was demonstrated clearly in fast fibers, while slow fibers from only the Bcl3(-/-) mice showed atrophy inhibition. The slow-to-fast shift in myosin isoform expression due to unloading was also abolished in both Nfkb1 and Bcl3 knockout mice. Like the soleus muscles, plantaris muscles from Nfkb1(-/-) and Bcl3(-/-) mice also showed inhibition of atrophy with unloading. Thus both the Nfkb1 and the Bcl3 genes are necessary for unloading-induced atrophy and the associated phenotype transition.

Animals↗

PubMed1999

Morphological and functional characteristics of acinar atrophy and recovery in the duct-ligated parotid gland of the rat.

Although acinar atrophy occurs frequently in salivary diseases, the relationship between structural changes and functional decrements is not well-established, and the potential for recovery of histological and functional integrity has not been wholly quantified. We aimed, therefore, to develop further our understanding of pathological acinar atrophy. Stensen's duct was ligated for periods up to six weeks and, in separate experiments, was de-ligated after two weeks and allowed to recover for up to two weeks. Qualitative and quantitative histological analyses were carried out. Additionally, the ability of enzymatically dispersed cells from ligated and de-ligated glands to respond to neurohormonal stimuli was also measured. The results confirmed that totally obstructed glands undergo a rapid, progressive severe atrophy amounting to absolute losses of over 85% of acinar tissue by two weeks. Acinar shrinkage and cell losses through apoptosis accounted for the glandular atrophy. Remaining intralobular epithelia consisted of extremely atrophic acini and numerous duct-like structures with intermediate forms. Dispersed cells from atrophic glands exhibited agonist-induced release of chloride similar to normal. Together, these structural-functional results confirm the persistent viability of acinar-like cells in the obstructed gland and suggest that the duct-like structures are derived from surviving atrophic acini. De-ligated glands exhibited a near-normal recovery of structure by two weeks. Their enzymatically dispersed cells responded normally to agonist stimulation. The results support the view that pathological atrophy is largely similar to physiological atrophy, providing a mechanism for acinar cell survival under adverse conditions, with the possibility of eventual recovery.

Animals↗

PubMed2002

Severe spinal muscular atrophy variant associated with congenital bone fractures.

Infantile autosomal recessive spinal muscular atrophy (type I) represents a lethal disorder leading to progressive symmetric muscular atrophy of limb and trunk muscles. Ninety-six percent cases of spinal muscular atrophy type I are caused by deletions or mutations in the survival motoneuron gene (SMNI) on chromosome 5q11.2-13.3. However, a number of chromosome 5q-negative patients with additional clinical features (respiratory distress, cerebellar hypoplasia) have been designated in the literature as infantile spinal muscular atrophy plus forms. In addition, the combination of severe spinal muscular atrophy and neurogenic arthrogryposis has been described. We present clinical, molecular, and autopsy findings of a newborn boy presenting with generalized muscular atrophy in combination with congenital bone fractures and extremely thin ribs but without contractures.

Bone and Bones↗

PubMed2003

Evoked potentials in spinal muscular atrophy.

Visual evoked potentials, brainstem evoked responses, and somatosensory evoked potentials were evaluated in 22 children with spinal muscular atrophy, types I and II. Eleven of the children had the severe form of spinal muscular atrophy (type I) and 11 children had the intermediate form (type II). The results of visual evoked potentials, brainstem evoked responses, and somatosensory evoked potentials were compared with those obtained in a control group. Statistical analysis showed abnormalities in the different sensory modalities. A significant increase in the visual evoked potential latencies was observed and was found more often in patients with spinal muscular atrophy type I. Alterations of the somatosensory thalamocortical responses were also observed, as well as a delay in the central conduction time. Although spinal muscular atrophy is usually considered to be a purely motor disorder involving neurons of the spinal anterior horn and nuclei of the lower cranial nerves, lesions of the posterior roots, spinal ganglia, ascending tracts, lateral geniculated corpus, and thalamus have been reported. Our results suggest that sensory neuron degeneration occurs more commonly in spinal muscular atrophy than previously thought and that this process probably develops more slowly than motoneuron degeneration. Such degeneration may be associated with brain atrophy.

Adolescent↗

PubMed2005

Type I spinal muscular atrophy can mimic sensory-motor axonal neuropathy.

Spinal muscular atrophy is a group of allelic autosomal recessive disorders characterized by progressive motoneuron loss, symmetric weakness, and skeletal muscle atrophy. It is traditionally considered a pure lower motoneuron disorder, for which a current definitive diagnosis is now possible by molecular genetic testing. We report two newborns with a clinical phenotype consistent with that of spinal muscular atrophy type I and nerve conduction studies and electromyography suggesting more extensive sensory involvement than classically described with spinal muscular atrophy. Molecular testing confirmed spinal muscular atrophy in patient 1 but not in patient 2. Thus, in the setting of a suspected congenital axonal neuropathy, molecular testing might be necessary to distinguish spinal muscular atrophy type I from infantile polyneuropathy.

Diagnosis, Differential↗

PubMed1997

Gene deletions in Arab patients with spinal muscular atrophy.

Spinal muscular atrophy is an autosomal recessive disorder characterized by degeneration of lower motor neurons. We have investigated the presence of survival motor neuron gene and neuronal apoptosis inhibitory protein gene deletions in 17 Arab and 1 Indian families with spinal muscular atrophy (15 type I and 3 type II). Homologous deletions were detected in exons 7 and 8 of the survival motor neuron gene and exon 5 of the neuronal apoptosis inhibitory protein gene in all patients with type I spinal muscular atrophy. Exon 13 of the neuronal apoptosis inhibitory protein gene was deleted in only one patient with type I spinal muscular atrophy. In two patients with type II spinal muscular atrophy, only exons 7 and 8 of the survival motor neuron gene were deleted whereas exons 5 and 13 of the neuronal apoptosis inhibitory protein gene were present. In another patient with spinal muscular atrophy type II, exons 7 and 8 of the survival motor neuron gene and exon 5 of the neuronal apoptosis inhibitory protein gene were deleted. This latter patient also had the Pierre Robin syndrome. No deletion was detected in healthy siblings or the parents. The deletions found in our patients are similar to those reported in other population groups.

Apoptosis↗

PubMed2004

Pathogenesis of brain and spinal cord atrophy in multiple sclerosis.

For more than a century, multiple sclerosis was viewed as a disease process characterized by oligodendrocyte and myelin loss, and research into the pathogenesis of multiple sclerosis was mainly focused on the mechanisms of inflammation. However, with development of more sophisticated neuroimaging and molecular biology techniques, attention has shifted to new aspects of pathogenesis of multiple sclerosis: axonal loss and neurodegeneration. Evidence is increasing that tissue destruction, primarily axonal loss and neurodegeneration, is a key element in the pathogenesis of multiple sclerosis. In addition, it is now known that brain and spinal cord atrophy begins early in the disease process of multiple sclerosis and advances relentlessly throughout the course of the disease. Cumulative data suggest that axonal loss is the major determinant of progressive neurologic disability in patients with multiple sclerosis. Magnetic resonance imaging and magnetic resonance spectroscopy in patients with multiple sclerosis for < 5 years indicate brain atrophy and loss of axonal integrity. Neurodegeneration and axonal loss in patients with multiple sclerosis are initially accompanied by a local response from oligodendrocyte progenitor cells and some remyelination. However, these repair mechanisms eventually fail, and patients typically develop generalized brain atrophy, cognitive decline, and permanent disability. Although the exact mechanisms underlying central nervous system atrophy in patients with multiple sclerosis are largely unknown, evidence exists that atrophy may represent an epiphenomenon related to the effects of dynamic inflammation within the central nervous system, including demyelination, axonal injury, neuronal loss, Wallerian degeneration, and possibly iron deposition. This article summarizes the potential mechanisms involved in central nervous system atrophy in patients with multiple sclerosis.

Apoptosis↗

PubMed2000

Brain atrophy in relapsing multiple sclerosis: relationship to relapses, EDSS, and treatment with interferon beta-1a.

Brain atrophy is a relevant surrogate marker of the disease process in multiple sclerosis (MS) because it represents the net effect of various pathological processes leading to brain tissue loss. There are various approaches to quantifying central nervous system atrophy in MS. We have focused on a normalized measure of whole brain atrophy, the brain parenchymal fraction (BPF). BPF is defined as the brain parenchymal volume, divided by the volume within the surface of the brain. We applied this method to an MRI data set generated during a phase III clinical trial of interferon beta-1a (AVONEX). The purpose of the current study is to further explore clinical and MRI correlates of the BPF, particularly as they relate to relapse rate and Kurtzke's Expanded Disability Status Score (EDSS); and to further explore the therapeutic effects observed in interferon beta-1a recipients. Of all demographic and disease measures in the clinical trial data base, T2 lesion volume most closely correlated with BPF in cross sectional studies, and was the baseline factor most closely correlated with progressive brain atrophy in the subsequent 2 years. We also observed that change in T2 lesion volume was the disease measure most closely correlated with change in BPF during 2 years of observation. Of interest, relapse number and EDSS change during 2 years were only weakly correlated with BPF change during the same period. Disability progression, defined as sustained worsening of at least 1.0 EDSS points from baseline, persisting at least 6 months, was associated with significantly greater brain atrophy progression. We observed a therapeutic effect of interferon beta-1a in the second year of the clinical trial, and this beneficial effect was not accounted for by change in gadolinium enhanced lesion volume, or by corticosteroid medication within 40 days of the final MRI scan. The BPF is an informative surrogate marker for destructive pathological processes in relaping MS patients, and is useful in demonstrating treatment effects in controlled clinical trials. The significance of progressive brain atrophy during relapsing MS will be assessed by measuring clinical and MRI changes in prospective follow up studies.

Adjuvants, Immunologic↗

PubMed1999

Frontal lobe atrophy and central motor conduction time in chronic alcoholics.

The central motor conduction time (CMCT) was investigated in 12 cases of chronic alcoholism with frontal lobe atrophy, 12 cases of chronic alcoholism without frontal lobe atrophy, and 12 age-matched healthy controls. The CMCT was significantly prolonged in the chronic alcoholics with frontal lobe atrophy as compared to the chronic alcoholics without frontal lobe atrophy and the healthy controls. A significant positive correlation was noted between the CMCT and the degree of frontal lobe atrophy. The CMCT may be prolonged in chronic alcoholics with frontal lobe atrophy.

Alcoholism↗

PubMed2005

Insulin-like growth factor-I gene transfer by electroporation prevents skeletal muscle atrophy in glucocorticoid-treated rats.

Catabolic states caused by injury are characterized by a loss of skeletal muscle. The anabolic action of IGF-I on muscle and the reduction of its muscle content in response to injury suggest that restoration of muscle IGF-I content might prevent skeletal muscle loss caused by injury. We investigated whether local overexpression of IGF-I protein by gene transfer could prevent skeletal muscle atrophy induced by glucocorticoids, a crucial mediator of muscle atrophy in catabolic states. Localized overexpression of IGF-I in tibialis anterior (TA) muscle was performed by injection of IGF-I cDNA followed by electroporation 3 d before starting dexamethasone injections (0.1 mg/kg.d sc). A control plasmid was electroporated in the contralateral TA muscle. Dexamethasone induced atrophy of the TA muscle as illustrated by reduction in muscle mass (403 +/- 11 vs. 461 +/- 19 mg, P < 0.05) and fiber cross-sectional area (1759 +/- 131 vs. 2517 +/- 93 mum(2), P < 0.05). This muscle atrophy was paralleled by a decrease in the IGF-I muscle content (7.2 +/- 0.9 vs. 15.7 +/- 1.4 ng/g of muscle, P < 0.001). As the result of IGF-I gene transfer, the IGF-I muscle content increased 2-fold (15.8 +/- 1.2 vs. 7.2 +/- 0.9 ng/g of muscle, P < 0.001). In addition, the muscle mass (437 +/- 8 vs. 403 +/- 11 mg, P < 0.01) and the fiber cross-sectional area (2269 +/- 129 vs. 1759 +/- 131 mum(2), P < 0.05) were increased in the TA muscle electroporated with IGF-I DNA, compared with the contralateral muscle electroporated with a control plasmid. Our results show therefore that IGF-I gene transfer by electroporation prevents muscle atrophy in glucocorticoid-treated rats. Our observation supports the important role of decreased muscle IGF-I in the muscle atrophy caused by glucocorticoids.

Animals↗