For the present, to determine growth hormone(GH) deficiency in patients with short stature, many provocative tests using various pharmacological agents such as glucagon, insulin, clonidine, arginine, growth hormone releasing factor, etc. should be done. These are not only complicated but are also misleading in some patients. In search of a simple and accurate method of detecting GH deficiency that may replace the more complicated provocative tests, we measured basal plasma insulin-like growth factor-I (IGF-I) to see the correlation with the peak GH values in the GH stimulation test. But, in each group of patients with different types of short stature, IGF-I values were poorly correlated. In addition, IGF-I values of the patients with short stature compared to the age- and sex-matched normal ranges showed a significant overlap, and the difference between the proportion of patients with subnormal values in GH deficient patients and non-GH deficient patients was not prominent. Nevertheless, in response to human growth hormone (hGH) administration, both the yearly growth rate and IGF-I levels increased conspicuously. Therefore, even though it may not be feasible to use IGF-I as a single diagnostic measure of patients with short stature, the change in IGF-I values in the follow up of hGH therapy may well represent the response to hGH.
Adolescent ; *Body Height ; Child ; Child, Preschool ; Female ; Growth Disorders/*blood/diagnosis ; Growth Hormone/blood/*deficiency ; Human ; Insulin-Like Growth Factor I/*analysis/metabolism ; Male ; Somatomedins/*analysis

For the present, to determine growth hormone(GH) deficiency in patients with short stature, many provocative tests using various pharmacological agents such as glucagon, insulin, clonidine, arginine, growth hormone releasing factor, etc. should be done. These are not only complicated but are also misleading in some patients. In search of a simple and accurate method of detecting GH deficiency that may replace the more complicated provocative tests, we measured basal plasma insulin-like growth factor-I (IGF-I) to see the correlation with the peak GH values in the GH stimulation test. But, in each group of patients with different types of short stature, IGF-I values were poorly correlated. In addition, IGF-I values of the patients with short stature compared to the age- and sex-matched normal ranges showed a significant overlap, and the difference between the proportion of patients with subnormal values in GH deficient patients and non-GH deficient patients was not prominent. Nevertheless, in response to human growth hormone (hGH) administration, both the yearly growth rate and IGF-I levels increased conspicuously. Therefore, even though it may not be feasible to use IGF-I as a single diagnostic measure of patients with short stature, the change in IGF-I values in the follow up of hGH therapy may well represent the response to hGH.
Adolescent ; *Body Height ; Child ; Child, Preschool ; Female ; Growth Disorders/*blood/diagnosis ; Growth Hormone/blood/*deficiency ; Human ; Insulin-Like Growth Factor I/*analysis/metabolism ; Male ; Somatomedins/*analysis

Obesity worldwide is constantly increasing. Obesity acts as an independent significant risk factor for malignant tumors of various organs including colorectal cancer. Visceral adipose tissue is physiologically more important than subcutaneous adipose tissue. The relative risk of colorectal cancer of obese patients is about 1.5 times higher than the normal-weight individuals, and obesity is also associated with premalignant colorectal adenoma. The colorectal cancer incidence of obese patients has gender-specific and site-specific characteristics that it is higher in men than women and in the colon than rectum. Obesity acts as a risk factor of colorectal carcinogenesis by several mechanisms. Isulin, insulin-like growth factor, leptin, adiponectin, microbiome, and cytokines of chronic inflammation etc. have been understood as its potential mechanisms. In addition, obesity in patients with colorectal cancer negatively affects the disease progression and response of chemotherapy. Although the evidence is not clear yet, there are some reports that weight loss as well as life-modification such as dietary change and physical activity can reduce the risk of colorectal cancer. It is very important knowledge in the point that obesity is a potentially modifiable risk factor that can alter the incidence and outcome of the colorectal cancer.
Adipokines/metabolism/physiology ; Body Mass Index ; Colorectal Neoplasms/*etiology/prevention & control ; Energy Intake ; Exercise ; Humans ; Insulin Resistance ; Meta-Analysis as Topic ; Obesity/*complications ; Somatomedins/metabolism/physiology ; Weight Loss

Insulin-like growth factor (IGF)/IGF binding protein (IGFBP) abnormalities may be important in the pathogenesis of growth failure in chronic renal failure (CRF). We induced experimental CRF by 5/6 nephrectomy in Sprague Dawley rats (100 g) and observed for 2 weeks comparing with sham-operated pair-fed control rats (Sham- C). CRF rats gained 30% less height than Sham- C rats (P<0.01). Serum IGFBP profiles by Western ligand blot revealed that IGFBP4 was elevated two fold in CRF rats (P<0.01 vs. Sham-C). However, IGFBP4 mRNA levels in liver or skeletal muscle were not different in two groups. To determine if the increase of serum IGFBP4 in CRF retarded the growth of cartilage, epiphyseal chondrocytes were isolated from CRF or control rats and cultured in the presence of control or CRF rat sera. Incubation with 10% CRF serum reduced proliferations of normal chondrocytes and L6 rat skeletal muscle cells. In contrast, 10% CRF serum did not inhibit the growth of CRF chondrocytes. Rat sera from two groups were separated into two different fractions, high (>10 kDa, containing IGFBPs) and low (<10 kDa, containing free IGF) molecular weight fractions using a gel filtration column. Both fractions obtained from CRF sera decreased the growth of control chondrocytes up to 40% compared with those from control sera. We suggest that the pathogenesis of growth failure in CRF may be involved in the increase of circulating IGFBP4 as well as the unidentified small molecular weight uremic serum factors which block the growth of chondrocytes in growth plate.
Animals ; Cell Proliferation ; Cells, Cultured ; Chondrocytes/*cytology/metabolism ; Insulin-Like Growth Factor Binding Protein 4/analysis/*blood/genetics ; Kidney Failure, Chronic/*blood/metabolism/physiopathology ; Liver/chemistry ; Male ; Muscle, Skeletal/chemistry ; RNA, Messenger/analysis/metabolism ; Rats ; Rats, Sprague-Dawley ; Somatomedins/analysis/metabolism