Insulin and IGF-I induce pronounced hypertrophy of skeletal myofibers in tissue culture

Vandenburgh, Herman H.; Karlisch, Patricia; Shansky, Janet; Feldstein, Richard

doi:10.1152/ajpcell.1991.260.3.c475

Cited by 180 publications

(101 citation statements)

References 16 publications

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“…The only known factor, added to the medium, which may be involved in the protein turnover rate is the insulin in the culture medium. A high insulin concentration stimulates protein synthesis and inhibits protein degradation in cultures of mammalian, undifferentiated, myotubes (Gulve and Dice, 1989;Vandenburgh et al, 1991;Perrone et al, 1995) and in cultured whole muscle (Ohira et al, 1989). As the concentration of insulin in our culture medium is similar to that showing stimulatory effects on protein synthesis in myotubes, it is possible that for the short fibres the absence of any reduction in the number of sarcomeres in series and tetanic force was due to an insulin effect.…”

Section: Fibre Morphologymentioning

confidence: 69%

Effects of strain on contractile force and number of sarcomeres in series of Xenopus laevis single muscle fibres during long-term culture

Jaspers¹,

Feenstra

Verheyen

et al. 2004

J Muscle Res Cell Motil

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The aim of the present study is to test whether mechanical strain uniquely regulates muscle fibre atrophy/ hypertrophy and adaptation of the number of sarcomeres in series within mature muscle fibres in vitro. Mature single muscle fibres from Xenopus laevis illiofibularis muscle were cultured (4-97 days) while kept at negative strain (20% below passive slack length, 'short fibres') or at positive strain (5% over passive slack length, Ôlong fibresÕ). Before and after culture the number of sarcomeres in series was determined using laser diffraction. During culture, twitch and tetanic force characteristics were measured every day.Survival time of long fibres was substantially less than that of short fibres. Of the long fibres 40% died or became inexcitable within 1 week, whereas this did not occur for short fibres. During culture, twitch and tetanic force of all short fibres increased substantially. Regression analysis showed that the post-culture number of sarcomeres in series was not significantly changed compared to the number before culture. It is concluded that culture at negative strain does not result in atrophy or a reduction of the number of sarcomeres in series, even after 97 days. For the long fibres we did not detect any hypertrophy as tetanic force remained stable or decreased slowly, while twitch force varied. Regression analysis of the change of the number of sarcomeres in series as a function of the culture time showed a positive slope (P ¼ 0.054). Two out of four long fibres that were cultured for at least 2 weeks showed an increase in the number of sarcomeres of 4-5%. Compared with in vivo adaptation to mechanical stimuli this is much less than would be expected. The data suggest that strain may not be the only factor that regulates hypertrophy and the number of sarcomeres in series.

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Section: Fibre Morphologymentioning

confidence: 69%

Effects of strain on contractile force and number of sarcomeres in series of Xenopus laevis single muscle fibres during long-term culture

Jaspers¹,

Feenstra

Verheyen

et al. 2004

J Muscle Res Cell Motil

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“…In particular IGF-1 is a growth stimulating agent for muscle cells in vitro [11,25,28,35] and in vivo [3], although the in vivo role of IGF-1 in stimulating muscle growth in adult animals is less clear and may rely in part on the presence of growth hormone [21]. Recent evidence also suggests that muscle growth in response to stretch is associated with the expression of an alternatively spliced form of IGF-1 [15,39].…”

Section: Discussionmentioning

confidence: 99%

The adaptation of soleus and edl in a rat model of distraction osteogenesis: IGF‐1 and fibrosis

Deyne

Kinsey

Yoshino

et al. 2002

Journal Orthopaedic Research

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The distraction rate of 0.5 mm/day produces good osteogenesis in small rodents; however, the effects of this distraction rate on muscle are not well documented. We evaluated the soleus and the extensor digitorum longus (EDL) after two weeks of lengthening distraction osteogenesis (DO) at 0.5 mm/day in skeletally mature rats. We found a modest but significant local increase of insulin like growth factor-1 (IGF-1) in the EDL, however, muscle growth indicated by developmental forms of myosin heavy chain (MHC) was not detected by mRNA (RT-PCR). To the contrary, the data suggested a decrease in cross-sectional area of the muscle fibers as well as a decrease in mRNA for slow MHC. Immunolabeling of fibronectin in cryosections of the EDL indicated fibrosis of the perimuscular connective tissue while assessment of the passive joint motion did not suggest a lack of excursion on the part of the dorsal flexors. While the literature suggests that IGF-I facilitates muscle growth especially in young animals, excess of IGF-I in muscle from adults may exacerbate DO-induced fibrosis.

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“…Insulin-like growth factor-1 signaling pathways and hypertrophy IGF-1 is a major regulator of skeletal muscle hypertrophic responses [24][25][26][27]. Thus, musclespecific over-expression of IGF-1 has been shown to ameliorate the dystrophic phenotype in the MDX mouse (an animal model for Duchenne muscular dystrophy) [28], and has been shown to accelerate muscle regeneration [29].…”

Section: Heart Failure and Angiotensin IImentioning

confidence: 99%

Angiotensin II as candidate of cardiac cachexia

Delafontaine

Akao

2006

Current Opinion in Clinical Nutrition &Amp; Metabolic Care

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Purpose of review-Congestive heart failure is increasing in prevalence and represents a major public health problem. The syndrome of advanced heart failure often includes muscle wasting, commonly termed cardiac cachexia, which is a predictor of poor outcome. Mechanisms of cardiac cachexia are poorly understood, but there is recent evidence that increased angiotensin II, interacting with the insulin-like growth factor-1 system, plays an important role.Recent findings-In animals, angiotensin II produces weight loss through a pressorindependent mechanism, accompanied by decreased levels of circulating and skeletal muscle insulin-like growth factor-1 and increased mRNA levels of the ubiquitin ligases atrogin-1 and Muscle RING finger-1 in skeletal muscle. Reduced insulin-like growth factor-1 action in muscle leads to increased proteolysis, through the ubiquitin-proteasome pathway, and increased apoptosis. These changes are blocked by muscle-specific expression of insulin-like growth factor-1, likely to be via the Akt/mTOR/p70S6K signaling pathway.Summary-The link between insulin-like growth factor-1, the ubiquitin-proteasome pathway, and angiotensin II effects has widespread clinical implications for the understanding of mechanisms of catabolic conditions. Therapeutic interventions targeting cross-talk mechanisms between angiotensin II and insulin-like growth factor-1 effects could provide new approaches for the treatment of muscle wasting.

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Insulin and IGF-I induce pronounced hypertrophy of skeletal myofibers in tissue culture

Cited by 180 publications

References 16 publications

Effects of strain on contractile force and number of sarcomeres in series of Xenopus laevis single muscle fibres during long-term culture

Effects of strain on contractile force and number of sarcomeres in series of Xenopus laevis single muscle fibres during long-term culture

The adaptation of soleus and edl in a rat model of distraction osteogenesis: IGF‐1 and fibrosis

Angiotensin II as candidate of cardiac cachexia

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