Integration of carbohydrate and lipid metabolism in skeletal muscle during postnatal development

Challiss, R. A. John; Ferré, Pilar

doi:10.1051/rnd:19880515

Cited by 8 publications

(3 citation statements)

References 65 publications

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“…Furthermore, with higher frequency electrical stimulation we found increased abundance of long-chain acylcarnitines, which increase with exercise intensity in humans [105]. The changes in acylcarnitine species profile are indicative of increased fatty acid oxidation and increased longer chain fatty acid metabolism which occurs with developmental maturation and limited glucose availability [102,106,107].…”

Section: Discussionmentioning

confidence: 74%

Electrical stimulation increases hypertrophy and metabolic flux in tissue-engineered human skeletal muscle

et al. 2019

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In vitro models of contractile human skeletal muscle hold promise for use in disease modeling and drug development, but exhibit immature properties compared to native adult muscle. To address this limitation, 3D tissue-engineered human muscles (myobundles) were electrically stimulated using intermittent stimulation regimes at 1 Hz and 10 Hz. Dystrophin in myotubes exhibited mature membrane localization suggesting a relatively advanced starting developmental maturation. One-week stimulation significantly increased myobundle size, sarcomeric protein abundance, calcium transient amplitude (∼2-fold), and tetanic force (∼3-fold) resulting in the highest specific force generation (19.3mN/mm) reported for engineered human muscles to date. Compared to 1 Hz electrical stimulation, the 10 Hz stimulation protocol resulted in greater myotube hypertrophy and upregulated mTORC1 and ERK1/2 activity. Electrically stimulated myobundles also showed a decrease in fatigue resistance compared to control myobundles without changes in glycolytic or mitochondrial protein levels. Greater glucose consumption and decreased abundance of acetylcarnitine in stimulated myobundles indicated increased glycolytic and fatty acid metabolic flux. Moreover, electrical stimulation of myobundles resulted in a metabolic shift towards longer-chain fatty acid oxidation as evident from increased abundances of medium- and long-chain acylcarnitines. Taken together, our study provides an advanced in vitro model of human skeletal muscle with improved structure, function, maturation, and metabolic flux.

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Section: Discussionmentioning

confidence: 74%

Electrical stimulation increases hypertrophy and metabolic flux in tissue-engineered human skeletal muscle

et al. 2019

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“…The suckling-weaning nutritional and developmental transition is characterized by important nutritional (36), hormonal (7), and metabolic changes affecting both carbohydrate (8,9,37) and lipid metabolism (8,9,38). This nutritional breakpoint seems to play a key role in the evolution of alanine transport into the parenchymal liver cell, because the apparent KM for this uptake is sharply increased immediately after weaning.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, typical gluconeogenic amino acids such as alanine play only a minor part as substrates for glucose production along the whole suckling period (1,6). This lack of information is particularly noticeable regarding the sucklingweaning developmental transition, a period of trascendental metabolic changes in which carbohydrate and lipid metabolism are very well studied (7)(8)(9). Furthermore, most of the studies on amino acid transport during development have been performed on cultured hepatocytes from protease-treated livers (10-12), with some controverted results.…”

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confidence: 99%

Ontogeny of L-Alanine Uptake in Plasma Membrane Vesicles from Rat Liver

et al. 1995

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Alanine uptake into liver plasma membrane vesicles was studied at different stages of postnatal rat development. Before weaning, alanine hepatic uptake showed lower values for the global K, than after weaning (0.34,0.77, 1.45, and 1.61 mM for I-, 1 5 , and 28-d-old and adult rats, respectively). Alanine uptake capacity increased progressively until reaching maximum values in the adult state (values for V,,,: 0.078,0.199,0.317, and 0.613 nmol alaninelmg protein13 s for I-, 1 5 , and 28-d-old and adult rats, respectively). These results seem to point to a prevalence of a high affinity, low capacity alanine transport component (traditionally assumed to be attributable to system A) in newborn and suckling rats, in agreement with our previous results on isolated hepatocytes (Martinez-Mas JV, Casado J, Felipe A, Marin JJG, Pastor-Anglada M: Biochem J 293: 819-824, 1993). The suckling-weaning developmental transition seems to play a role in establishing the pattern of adult hepatic alanine transport characterized by a higher capacity but a lower affinity (because most alanine is taken up by system ASC) inasmuch as K, values show a 100% increase after weaning, although V, , , values continue to increase steadily until the adult age. Amino acid transport and utilization during postnatal development have not been extensively studied in spite of their role in sustaining growth. Amino acids are mainly used for anabolic purposes, such as protein accretion (1) with rates even higher than in the adult (2-4) or purine and pyrimidine biosynthesis (5). Moreover, typical gluconeogenic amino acids such as alanine play only a minor part as substrates for glucose production along the whole suckling period (1, 6). This lack of information is particularly noticeable regarding the sucklingweaning developmental transition, a period of trascendental metabolic changes in which carbohydrate and lipid metabolism are very well studied (7-9). Furthermore, most of the studies on amino acid transport during development have been performed on cultured hepatocytes from protease-treated livers (10-12), with some controverted results. Different approaches applied to amino acid transport during development are quite scarce (13). Recently, we have reported the kinetic study of alanine transport in freshly isolated hepatocytes from rat fetuses and neonates by a less injurious methodology (14). In that report, it was shown that, in fetal and neonatal hepatocytes,

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