Preventive effects of insulinlike growth factor‐I on steroid‐induced muscle atrophy

Kanda, Fumio; Takatani, Keiko; Okuda, Shiho; Matsushita, Tatsuo; Chihara, Kazuo

doi:10.1002/(sici)1097-4598(199902)22:2<213::aid-mus9>3.3.co;2-d

Cited by 18 publications

(25 citation statements)

References 31 publications

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“…In the present study, glucocorticoid treatment caused a 31% decrease in mean muscle fiber CSA of TA muscle compared to controls. These findings are similar to previous animal studies, which have shown a 26% decrease in extensor digitorum longus and soleus muscles in rats (22) and a 26% decrease in diaphragm muscle in hamsters (18) after glucocorticoid administration.…”

Section: Discussionmentioning

confidence: 86%

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Effects of a vitamin D analog, alfacalcidol, on bone and skeletal muscle in glucocorticoid-treated rats

et al. 2010

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Glucocorticoids cause secondary osteoporosis and myopathy. The efficacy of vitamin D on osteoporotic fractures is thought to be through direct effects on bone and indirect effects on muscles that help to prevent falls. However, effects of vitamin D on muscles under glucocorticoid treatment remain unclear. Six-month-old female Wistar rats were randomized to four groups: vehicletreated controls; a prednisolone (PSL)-administered group (PSL group); an alfacalcidol-administered group (D group); and a group administered both PSL and alfacalcidol (PSL+D group). After a 4-week treatment period, maximum contractile strength and strength decrement index (SDI), an indicator of muscle fatigue, were measured in the calf muscle by electrical stimulation of the sciatic nerve. Cross-sectional area (CSA) of muscle fibers in the tibialis anterior muscle and bone mineral density (BMD) of the femur were evaluated. The PSL group showed significantly lower muscle strength, BMD and CSA of muscle fibers, and significantly higher SDI compared to the other three groups (P < 0.05). No significant differences were observed in any of these parameters among control, D, and PSL+D groups. These results suggest that in glucocorticoid-treated rats, alfacalcidol preserved not only BMD, but also muscle strength and muscle volume, and prevented muscle fatigue.

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Section: Discussionmentioning

confidence: 86%

“…Glucocorticoids stimulate muscle proteolysis (10,22) and inhibit protein synthesis (10, 41), resulting in muscle atrophy and muscle dysfunction. Glucocorticoid-induced myopathy is characterized by a decrease in the size of muscle fibers (13).…”

Section: Discussionmentioning

confidence: 99%

Effects of a vitamin D analog, alfacalcidol, on bone and skeletal muscle in glucocorticoid-treated rats

et al. 2010

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“…Thus IGF-I is a dominant signal over glucocorticoids in determination of muscle protein balance in vitro, as has been suggested for insulin in vivo (17). Simultaneous administration of IGF-I with glucocorticoids to rats significantly attenuates the glucocorticoid-induced muscle atrophy and myofibrillar protein breakdown as measured by 3-MH excretion (21). Accordingly, only when insulin is low (such as during fasting) are the catabolic effects of glucocorticoids on muscle evident (54).…”

Section: Discussionmentioning

confidence: 99%

IGF-I stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin ligases, atrogin-1 and MuRF1

Sacheck¹,

Ohtsuka²,

McLary³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

542

455

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“…Acute treatment with high-dose glucorticosteroids decreases IGF-1 and IGF-2 expression in the rat diaphragm and gastrocnemius [14]. In vitro and experimental studies have shown that IGF treatment can reverse detrimental effects of corticosteroid-induced muscle wasting [15,16].…”

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confidence: 99%

Hypoxia, nitrogen balance and body weight

Schols¹,

Westerterp²

2002

Eur Respir J

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Recent clinical studies have shown that acute exacerbations of chronic obstructive pulmonary disease (COPD) are characterised by disturbances in the balance between dietary intake and energy expenditure [1,2] as well as by a negative nitrogen balance [3]. Since weight loss prior to and during hospitalisation for an acute exacerbation has been related to poor outcome in terms of mortality and readmission rate [4,5], it is important to prevent or treat this complication. It is yet unclear to what extent factors contributing to weight loss, during acute disease exacerbations, are similar to stable disease. Elevated energy requirement of physical activity has been implicated during stable disease [6] but is unlikely to be an important factor during acute disease, when the activity level is probably very low. Hypoxia is otherwise implicated as a potential trigger of reduced dietary intake and metabolic alterations during acute exacerbations, while in stable disease, there is no strong relationship between resting arterial oxygen tension and nutritional status.Hypobaric hypoxia, as applied in high-altitude studies, clearly induces weight loss and is an interesting human model to investigate the influence of acute hypoxia. There is evidence that the altitude limit for the maintenance of body weight in humans isy5,000 m [7]. Acute transfer from sea level to altitude usually results in weight loss, but the rate of weight loss diminishes when the food supply is adequate. Reduced dietary intake is initially the result of a reduced meal size because of a rapid increase in satiety during the meal [8]. Part of the effect of reduced meal size on daily dietary intake can be compensated for by an increase in meal frequency. At altitudes of o7,000 m, acute mountain symptoms result in suppression of hunger and the desire to eat [8], possibly related to a reduction in appetite through leptin, a key mediator in the neuroendocrine regulation of food intake [9]. The effect of hypobaric hypoxia on resting metabolic rate is unclear. High-altitude studies are limited by the fact that subjects are often highly trained and have a physical activity related energy expenditure that is comparable to that of endurance athletes. A more specific study on nitrogen balance during a prolonged stay at 5,000 m showed no impairment of protein digestibility [10]. However, glycine metabolism, as measured with glycine ( 15 N), changed as a function of altitude exposure. Urinary excretion of 15 N from intravenous glycine administration, as a fraction of urinary nitrogen, increased from 20.6% after 4 days to 38.0% after 13 days at altitude (pv0.05). It was hypothesised that the increased 15 N excretion was due to increased oxidation of glycine as a function of altitude exposure. Others have also observed an altitude-induced increase in capillary leakage resulting in a renal loss of amino acids [11].Experimental models subjecting animals to a hypoxic environment, i.e. that of IIOKA et al. [12] in the current issue of this journal, are comparable to an altit...

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Preventive effects of insulinlike growth factor‐I on steroid‐induced muscle atrophy

Cited by 18 publications

References 31 publications

Effects of a vitamin D analog, alfacalcidol, on bone and skeletal muscle in glucocorticoid-treated rats

Effects of a vitamin D analog, alfacalcidol, on bone and skeletal muscle in glucocorticoid-treated rats

IGF-I stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin ligases, atrogin-1 and MuRF1

Hypoxia, nitrogen balance and body weight

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