Characteristic of cohort studies.

<p>Characteristic of cohort studies.</p

Forest plot of all cohort studies in clinical response.

<p>Pooled estimate of 66.1% (95% CI 43.7%-83.0%).</p

Characteristics of randomized controlled trails.

<p>Characteristics of randomized controlled trails.</p

Forest plot of all cohort studies in clinical remission.

<p>Pooled estimate of 40.5% (95% CI 24.7%-60.4%).</p

Chronic bGH treatment led to insulin resistance.

<p>Mice were treated with bGH at 1 µg/g (controls received saline) daily for 3 weeks. (A) Fasting body weights were measured just before and after the completion of 3-week GH administration. (B) Hepatic Akt activity was examined in mice challenged by insulin 10 minutes prior to sacrifice using Western blotting. (C) Hepatic Akt activity was examined in mice challenged by 10-min saline prior to sacrifice. (D) Liver lysates from mice challenged by 10-min insulin prior to sacrifice were immunoprecipitated with antibody against PTEN, and were blotted with the same antibody. (E) Hepatic PTEN expression was examined in mice challenged by 10-min saline prior to sacrifice. Liver lysates from mice challenged by 10-min insulin (F) or saline (G) prior to sacrifice were immunoprecipitated with antibody against the p85α subunit of PI3K and were blotted with antiserum specific, either for total tyrosine phosphorylation of p85, or for p85 phosphorylated at tyrosine 458 and tyrosine 508. The values in bar graphs were displayed as means ± standard errors.</p

The effect of prolonged GH exposure and PTEN on Akt activity in HepG2 cells.

<p>(A) HepG2 cells were pretreated with GH or 30 min or 4 hours and harvested after insulin stimulation for 10 min. (B) Cells were transfected with wild type PTEN or PTEN mutant C124S, and harvested after insulin stimulation for 10 min. Densitometry absorbance values were averaged after they had been normalized to Akt for equal loading.</p

Knockdown of PTEN gene disrupted chronic GH induced insulin resistance.

<p>Cells were transfected with siRNA targeted for PTEN (A), PTEN mutant C124S (B) or wtPTEN (C), and were stimulated with GH and Insulin as stated in Methods and materials. Densitometry absorbance values were averaged after they had been normalized to Akt for equal loading.</p

The effect of chronic hGH treatment on mice with hypoinsulinemia induced by prolonged fasting.

<p>Mice were treated with daily hGH at 1 µg/g or saline for 3 weeks, and subjected to fasting in the last 3 days. (A) Fasting body weights were measured just before and after the completion of 3-week GH administration. (B) Plasma insulin levels were measured using ELISA Kit. (C) Hepatic Akt activity was examined using Western blotting. (D) Hepatic PTEN expression was examined using Western blotting. (E) Liver lysates were immunoprecipitated with antibody against the p85α subunit of PI3K and were blotted with antiserum specific, either for total tyrosine phosphorylation of p85, or for p85 phosphorylated at tyrosine 458 and tyrosine 508. The values in bar graphs were displayed means ± standard errors.</p

Chronic hGH treatment induced insulin resistance and enhanced the expression of PTEN.

<p>Mice were treated with daily hGH at 1 µg/g (controls received saline) for 3 weeks. (A) Fasting body weights were measured just before and after the completion of 3-week GH administration. (B) Plasma levels of Insulin were measured in mice without pre-sacrifice administration of insulin using ELISA Kit. (C) Hepatic Akt activity was examined in mice challenged by 10-minute insulin prior to sacrifice using Western blotting. (D) Hepatic Akt activity was examined in mice challenged by 10-min saline prior to sacrifice using Western blotting. (E) Hepatic PTEN expression was examined in mice challenged by 10-min insulin prior to sacrifice. (F) Hepatic PTEN expression was examined in mice challenged by 10-min saline prior to sacrifice. Liver lysates from mice challenged by 10-min insulin (G) or saline (H) prior to sacrifice were immunoprecipitated with antibody against the p85α subunit of PI3K and were blotted with antiserum specific, either for total tyrosine phosphorylation of p85, or for p85 phosphorylated at tyrosine 458 and tyrosine 508. The values in bar graphs were displayed as means ± standard errors.</p

Chronic hGH induced insulin resistance without increased PTEN expression in STZ-induced diabetic C57BL/6 mice.

<p>(A) Fasting morning blood glucose of non-STZ and STZ group were measured by OneTouch® UltraVue™ glucometer prior to GH treatment. (B) Fasting body weights were measured before and after the completion of 3-week GH administration. (C) Hepatic Akt activity was examined in mice challenged by 10-minute insulin prior to sacrifice using Western blotting. (D) Hepatic PTEN expression was examined by Western blotting. (E) Liver lysates were immunoprecipitated with antibody against the p85α subunit of PI3K and were blotted with antiserum specific, either for total tyrosine phosphorylation of p85, or for p85 phosphorylated at tyrosine 458 and tyrosine 508. The values in bar graphs were displayed means ± standard errors.</p