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Different effects of IGF-I on insulin-stimulated glucose uptake in adipose tissue and skeletal muscle.

Artikel i vetenskaplig tidskrift
Författare Fredrik Frick
Jan Oscarsson
K Vikman-Adolfsson
Malin Ottosson
N Yoshida
Staffan Edén
Publicerad i American journal of physiology. Endocrinology and metabolism
Volym 278
Nummer/häfte 4
Sidor E729-37
ISSN 0193-1849
Publiceringsår 2000
Publicerad vid Institutionen för fysiologi och farmakologi
Institutionen för invärtesmedicin
Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Sidor E729-37
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adipocytes, drug effects, metabolism, Adipose Tissue, drug effects, metabolism, Animals, Blood Glucose, metabolism, C-Peptide, blood, Female, Glucose, metabolism, Glycogen, metabolism, Hypoglycemic Agents, pharmacology, Hypophysectomy, Insulin, blood, pharmacology, Insulin-Like Growth Factor I, metabolism, pharmacology, Lipid Metabolism, Lipolysis, drug effects, Muscle, Skeletal, drug effects, metabolism, Organ Size, drug effects, Rats, Rats, Sprague-Dawley, Spleen, drug effects, growth & development, Weight Gain, drug effects
Ämneskategorier Fysiologi

Sammanfattning

The effect of insulin-like growth factor I (IGF-I) on insulin-stimulated glucose uptake was studied in adipose and muscle tissues of hypophysectomized female rats. IGF-I was given as a subcutaneous infusion via osmotic minipumps for 6 or 20 days. All hypophysectomized rats received L-thyroxine and cortisol replacement therapy. IGF-I treatment increased body weight gain but had no effect on serum glucose or free fatty acid levels. Serum insulin and C-peptide concentrations decreased. Basal and insulin-stimulated glucose incorporation into lipids was reduced in adipose tissue segments and isolated adipocytes from the IGF-I-treated rats. In contrast, insulin treatment of hypophysectomized rats for 7 days increased basal and insulin-stimulated glucose incorporation into lipids in isolated adipocytes. Pretreatment of isolated adipocytes in vitro with IGF-I increased basal and insulin-stimulated glucose incorporation into lipids. These results indicate that the effect of IGF-I on lipogenesis in adipose tissue is not direct but via decreased serum insulin levels, which reduce the capacity of adipocytes to metabolize glucose. Isoproterenol-stimulated lipolysis, but not basal lipolysis, was enhanced in adipocytes from IGF-I-treated animals. In the soleus muscle, the glycogen content and insulin-stimulated glucose incorporation into glycogen were increased in IGF-I-treated rats. In summary, IGF-I has opposite effects on glucose uptake in adipose tissue and skeletal muscle, findings which at least partly explain previous reports of reduced body fat mass, increased body cell mass, and increased insulin responsiveness after IGF-I treatment.

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