• Title/Summary/Keyword: IGF-I lipid metabolism

Search Result 5, Processing Time 0.016 seconds

Insulin-like Growth Factor-I Induces FATP1 Expression in C2C12 Myotubes (C2C12 myotube에서 Insulin-like growth factor-I 이 FATP1 발현에 미치는 영향)

  • Kim, Hye Jin;Lee, Won Jun
    • Journal of Life Science
    • /
    • v.24 no.12
    • /
    • pp.1284-1290
    • /
    • 2014
  • Fatty acid transporter protein 1 (FATP1) is highly expressed in skeletal muscle and modulates fatty acid uptake and metabolism. However, the influence of insulin-like growth factor-I (IGF-I), a master regulator of skeletal muscle cells, on FATP1 in skeletal muscle cells has not been demonstrated. To investigate the effect of IGF-I on FATP1 and the expression of the IGFBP5 protein, differentiated C2C12 murine skeletal muscle cells were treated with 20 ng/ml of IGF-I at different time points. The results showed that IGF-I increased FATP1 and IGFBP5 protein expression in a time-dependent manner. To determine whether this induction of FATP1 by the IGF-I treatment was regulated pretranslationally, the mRNA level of FATP1 was measured by real-time quantitative PCR. The IGF-I treatment resulted in very rapid induction of the FATP1 mRNA transcript in C2C12 myotubes. FATP1 mRNA increased 169% and 132% after 24 and 48 h of the IGF-I treatment, respectively, and it returned to control levels after 72 h of the treatment, suggesting that the FATP1 gene is regulated pretranslationally by IGF-I in skeletal muscle cells. This is the first evidence that IGF-I can regulate the expression of FATP1. In conclusion, IGF-I induced rapid transcriptional modification of the FATP1 gene in C2C12 skeletal muscle cells and had modulating effects on fatty acid uptake proteins and oxidative proteins.

Insulin-like Growth Factor-I Induces FABPpm Expression in C2C12 Myotubes (C2C12 myotube에서 insulin-like growth factor-I 이 FABPpm과 FAT/CD36 발현에 미치는 영향)

  • Kim, Hye Jin;Yoon, Hae Min;Lee, Won Jun
    • Journal of Life Science
    • /
    • v.25 no.10
    • /
    • pp.1098-1102
    • /
    • 2015
  • FABPpm (plasma membrane-bound fatty acid binding protein ) is highly expressed in skeletal muscle. The principal role of this protein is modulating fatty acid uptake and metabolism. The influence of insulin-like growth factor-I (IGF-I), which is a major regulator of skeletal muscle cells, on FABPpm in skeletal muscle cells has not been investigated. To determine the effect of IGF-I on the expression of FABPpm, differentiated C2C12 murine skeletal muscle cells were treated with 20 ng/ml of IGF-I for different times. IGF-I increased the expression of FABPpm in a time-dependent manner. The mRNA level of FABPpm was measured by real-time quantitative PCR to determine whether the IGF-1-induced induction of FABPpm was regulated pretranslationally. The IGF-I treatment resulted in very rapid induction of the FABPpm mRNA transcript in the C2C12 myotubes. After 24 and 48 hr of the IGF-I treatment, FABPpm mRNA increased 130 and 179%, respectively. The increase in the protein expression returned to control levels after 72 hr of the IGF-I treatment, suggesting that IGF-1 regulated the FABPpm gene pretranslationally in skeletal muscle cells. This is the first evidence that IGF-I has a modulatory effect on the expression of FABPpm. In conclusion, IGF-I induced rapid transcriptional modification of the FABPpm gene in C2C12 skeletal muscle cells and exerted modulatory effects on FABPpm.

Growth Hormone Signaling in the Regulation of Acid Labile Subunit

  • Kim, Jin Wook;Boisclair, Yves R.
    • Asian-Australasian Journal of Animal Sciences
    • /
    • v.21 no.5
    • /
    • pp.754-768
    • /
    • 2008
  • The past decades have seen enormous advances in our understanding of how GH acts. GH is a pituitary-derived polypeptide hormone that has diverse physiological effects including the regulation of bone growth, carbohydrate and lipid metabolism. The effects of GH are mediated directly and indirectly through IGF-I. In addition, GH stimulates the hepatic production of ALS. In postnatal life, IGF-I and -II circulate as 150 kDa ternary complexes consisting of one molecule each of IGFBP-3 or IGFBP-5, IGF-I or IGF-II and ALS. It is now known that ALS increases significantly the half-lives of the IGFs, IGFBP-3 and -5, and therefore is responsible for maintaining a circulating reservoir for each of these proteins.

Insulin-like Growth Factor-I Regulates the FAT/CD36 Expression in C2C12 Skeletal Muscle Cells (C2C12 골격근 세포에서 FAT/CD36 발현 조절에 있어 Insulin-like growth factor-I이 미치는 영향)

  • Kim, Hye Jin;Yoon, Hae Min;Kim, Tae Young;Lee, Won Jun
    • Journal of Life Science
    • /
    • v.26 no.7
    • /
    • pp.758-763
    • /
    • 2016
  • Fatty acid transporters are key mediators of skeletal muscle lipid metabolism. Several protein groups have been implicated in cellular long-chain fatty acid uptake or oxidation, including fatty acid transporter proteins (FATPs), the plasma membrane fatty acid-binding protein (FABPpm), and the fatty acid translocase (FAT/CD36). FAT/CD36 is highly expressed in skeletal muscle and known to be regulated by various factors such as exercise and hormones. Insulin-like growth factor-I (IGF-I) is a well-known regulator of skeletal muscle cells. However, it has not been studied whether there is any interaction between IGF-I and FAT/CD36 in skeletal muscle cells. In this study, the effects of IGF-I treatment on FAT/CD36 induction were examined. Differentiated C2C12 cells were treated with 20 ng/ml of IGF-I at different time points. Treatment of C2C12 cells with IGF-I resulted in increased FAT/CD36 mRNA and protein expression. After 24 and 48 hr of IGF-I treatment, FAT/CD36 mRNA increased 89% and 24% respectively. The increase of both proteins returned to the control level after 72 hr of IGF-I treatment, suggesting that the FAT/CD36 gene is regulated pretranslationally by IGF-I in skeletal muscle cells. These results suggest that IGF-I can regulate the expression of FAT/CD36 in skeletal muscle cells. In conclusion, IGF-I induces a rapid transcriptional modification of the FAT/CD36 gene in C2C12 skeletal muscle cells and has modulating effects on fatty acid uptake proteins as well as oxidative proteins.

Effect of Chromium Picolinate on Growth Performance, Carcass Characteristics, Serum Metabolites and Metabolism of Lipid in Pigs

  • Xi, Gang;Xu, Zirong;Wu, Si-hung;Chen, Shijiang
    • Asian-Australasian Journal of Animal Sciences
    • /
    • v.14 no.2
    • /
    • pp.258-262
    • /
    • 2001
  • The study was conducted to evaluate the effects of chromium picolinate (CrP) on growth, carcass characteristics and serum metabolites in growing-finishing pigs. A total of 96 Landrace$\times$Yorkshire$\times$Duroc hybrid pigs, initial live weight about $38.12{\pm}00kg$, were randomly assigned to 2 groups (16 pigs per pen, 3 pens per group), each group had 48 pigs with an equal number of barrows and gilts. The pigs were fed the diet with or without $200{\mu}g/kg$ Cr from CrP. The results indicated that the addition of $200{\mu}g/kg$ CrP increased ADG by 3.58% and decreased feed conversion rate (FCR) by 3.00% compared to the control group. Pigs fed CrP had 7.58% (p<0.05) higher carcass lean percentage, 15.55% (p<0.05) larger longissimus muscle area (LMA) and 10.90% (p<0.05) lower back fat thickness, 15.17% (p<0.05) lower carcass fat percentage. In addition, the IGF-I level in serum was elevated by 79.20% (p<0.05), the Insulin and cortisol level decreased by 27.35% (p<0.05) and 34.58% (p<0.05) respectively with supplementation of CrP. Analysis of subcutaneous fat (10th rib) showed that the activity of hormone sensitive lipase (HSL) increased by 79.58% (p<0.05) and the activities of isocitrate dehydrogenase (ISD) and malate dehydrogenase (MDH) decreased significantly by 15.06% (p<0.05) and 54.53% (p<0.05) respectively in the $200{\mu}g/kg$ CrP group. The concentration of RNA, RNA/DNA in LMA increased by 31.89% (p<0.05) and 5.41% (p<0.05) respectively with the addition of CrP. These results suggest that CrP reduced fat deposits by decreasing lipogenic enzyme activities and increasing HSL activity and may have promoted muscle anabolic metabolism through elevated IGF-I levels.