Background. Insulin-like growth factor 1 (IGF-1) is known as somatomedin C. This polypeptide hormone is functionally and structurally similar to insulin. IGF-1 effects on tissue by the IGF-1R and the insulin-like growth factor-binding protein also known as IGFBP. Abnormal IGF-1 and IGFBP signaling are positively correlated with a high risk of selected civilization diseases development. Physical inactivity is a one of the main causes of majority of chronic diseases and it is associated with eg. IGF-1 and IGFBPs level. Objective. The aim of the study was to explanation the effect of physical activity on IGF-1 and its binding protein – IGFBPs concentration in the context of selected civilization diseases prevention. The review of clinical trial. Material and Methods. The review of articles had published in databases: MEDLINE, EMBASE, Scopus and Web of Science until December 2015. The selected prospective studies about the effect of exercise on IGF-1 level and its binding protein IGFBP in the context of selected civilization diseases prevention were collected. Results. The majority of the included studies indicate that mechanical loading is a key mechanism linking IGF-1/IGFBPs concentration and selected chronic diseases development. The duration and intensity of physical activity have a significant impact on IGF-1 and IGFBP serum. The highest concentration of IGF-1 in serum was after eccentric training. “Overtraining” increases unfavorable and unbound IGF-1 levels and contributes to the increased incidence of hormone-cancer and osteoarthritis. Conclusions. Irregularity of the GH/IGF-1 axis may affect on the development of rheumatic diseases, cardiovascular diseases (regulate cardiac growth and metabolism) and metabolic syndrome.
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Insulin-like growth factor-1 (IGF-1) and other growth factors overexpression was reported in acute pancreatitis. Previous studies have shown the protective effect of epidermal growth factor (EGF), Hepatocyte Growth Factor (HGF) and Fibroblast Growth Factor (FGF) in the course of experimental acute pancreatitis. The aim of our studies was to determine the effect of IGF-1 administration on the development of caerulein-induced pancreatitis. Methods: Acute pancreatitis was induced by infusion of caerulein (10 µg/kg/h) for 5 h. IGF-1 was administrated twice at the doses: 2, 10, 50, or 100 µg/kg s.c. Results: Administration of IGF-1 without induction of pancreatitis increased plasma interleukin-10 (IL-10). Infusion of caerulein led to development of acute edematous pancreatitis. Histological examination showed pancreatic edema, leukocyte infiltration and vacuolization of acinar cells. Also, acute pancreatitis led to an increase in plasma lipase and interleukin 1ß (IL-1ß) level, whereas pancreatic DNA synthesis and pancreatic blood flow were decreased. Treatment with IGF-1, during induction of pancreatitis, increased plasma IL-10 and attenuated the pancreatic damage, what was manifested by histological improvement of pancreatic integrity, the partial reversion of the drop in pancreatic DNA synthesis and pancreatic blood flow, and the reduction in pancreatitis-evoked increase in plasma amylase, lipase and IL-1ß level. Protective effect of IGF-1 administration was dose-dependent. Similar strong protective effect was observed after IGF-1 at the dose 2 x 50 and 2 x 100 µg/kg. Conclusions: (1) Administration of IGF-1 attenuates pancreatic damage in caerulein-induced pancreatitis; (2) This effect is related, at least in part, to the increase in IL-10 production, the reduction in liberation of IL-1ß and the improvement of pancreatic blood flow.
The type 1 insulin-like growth factor receptor (IGF-1R), which is over-expressed or activated in many human cancers, including lung cancer, mediates cancer cell proliferation and metastasis. Several studies indicate that blocking IGF-1R expression can inhibit tumor cell proliferation and metastasis. In this study, inhibition of the endogenous IGF-1R by recombinant adenoviruses encoding short hairpin RNAs against IGF-1R was found to significantly suppress IGF-1R expression, arrest the cell cycle, enhance the apoptotic response, and inhibit proliferation, adhesion, invasion and migration in A549 cells. Moreover, silencing IGF-1R decreases the expression of invasive-related genes including matrix metalloproteinase-2 (MMP-2), MMP-9, and urokinase-plasminogen activator (u-PA), and the phosphorylation of Akt and ERK1/2. These results suggest that the silencing of IGF-1R has the potential to be an effective cancer gene therapy strategy for human lung cancer.
Polymorphism of insulin like growth factor IGF-1gene in selected Polish sheep breeds. Research was carried out in 2009-2013 on 1751 sheep bred in Poland (1366 ♀; 385♂) - 4 meat-wool breeds: Polish Merino, Old type Polish Merino, Corriedale and Żelaźnieńska sheep and 3 meat breeds (Berrichone du cher, Suffolk, Charolaise) from 34 flocks selected randomly across the country. All animals were subjected to identification factor insulin-IGF-1 gene, in the assessment of C and T alleles. Summing up, it should be noted that in 4 meat-wool breeds and 2 meat breeds (Berrichone du cher , Suffolk) there were no polymorphism of alleles and genotypes of insulin-like growth factor (IGF-1) gene, limiting its scope to determine C allele and CC genotype. Only one Charolaise ewe (breed imported from France) had T allele and C:T genotype. That result indicates the need for further research about sheep imported and adapted in Polish production conditions and assess the adaptation process.
The objective of the study was to evaluate the effect of energy contents in a dry period diets in “7+1” feeding strategy of dry cow including 7 weeks of the dry period (far-off) and 1 week of a close-up period, on colostrum quality and the immune status of calves. Forty Holstein multiparous cows were dried at 56d before the expected date of calving and were assigned to the higher energy diet group (HE; 0.69 UFL/kg DM, NDF 52% DM), or the lower energy diet group (LE; 0.61 UFL/1kg DM, NDF 56% DM). From -7d to the expected calving date up to 21 d of lactation, all cows were fed the same fresh, lactation diet. Samples of colostrum were collected within 2h after parturition and its density, dry matter content and concentrations of immunoglobulins, fat, protein, lactose, urea and somatic cell counts were measured. Calves were weighed 2 h after calving and on the 21d of life. On 3d and 21d of calves’ life blood samples were collected and the concentration of IgG, IgA, IgM, insulin-like growth factor 1 (IGF-1) as well as total protein and albumin concentrations were determined. Treatments had no significant effect on composition of colostrum and serum immunoglobulins and IGF-1 concentration. In both groups the weight of calves at birth was similar, still daily body weight gain during 21 day of rearing period in HE group was higher than in the LE group (P=0.05).
Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, has been primarily isolated from the human and rat stomach. Ghrelin has been shown to stimulate appetite and fat deposition in adult rats and humans. The aim of this study was to investigate the effect of ghrelin administration on pancreatic growth in suckling, weaned and peripubertal seven week old rats. Rats were treated with saline or ghrelin (4, 8 or 16 nmol/kg/dose) intraperitoneally twice a day: suckling rats were treated for 7 or 14 days starting from the first postnatal day, three week old weaned rats and seven weeks old rats were treated for 5 days. Treatment with ghrelin did not affect animal weight in suckling or weaned rats, whereas in young seven week old rats, ghrelin caused a significant increase in body weight. Ghrelin decreased food intake in weaned rats; whereas in seven week old rats, food intake was enhanced. In suckling rats, ghrelin decreased the pancreatic weight, pancreatic amylase content, DNA synthesis and DNA content. In contrast, ghrelin increased pancreatic weight, DNA synthesis, DNA content and amylase content in weaned or young seven week old rats. Pancreatic blood flow was not affected by ghrelin in any group of rats tested. Ghrelin increased serum level of growth hormone in all rats. This effect was weak in suckling rats, higher in weaned and the highest in seven week old animals. Ghrelin did not affect serum level of insulin-like growth factor-1 (IGF-1) in suckling rats. In weaned and in seven week old rats, treatment with ghrelin caused increase in serum level of IGF-1. We conclude that ghrelin reduces pancreatic growth in suckling rats; whereas in weaned and young seven week old animals, treatment with ghrelin increases pancreatic growth. This biphasic effect of ghrelin in young animals on pancreatic growth seems to be related to age-dependent changes of the release of anabolic IGF-1.
The search for genes with that positively affect physical fitness is a difficult process. Physical fitness is determined by numerous genes, and its genetic determinants are modified by environmental factors. The map of candidate genes that can potentially affect physical fitness becomes larger every year, and currently it contains more than 200 genes associated with such aspects as respiratory and cardiovascular stability; body build and composition – especially muscle mass and strength; carbohydrate and lipid metabolism; response to training; and exercise intolerance. The inclusion of the genetic component in physiological and biochemical studies would permit drawing a representation of predispositions for each athlete interested in practicing high performance sports and would be a valuable coaching aid in the process of training individualization.
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Recent studies have shown that ghrelin exhibits gastroprotective effects. The aim of present study was to examine the influence of ghrelin administration on the healing of chronic gastric and duodenal ulcers and to evaluate the role of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) in this process. In pituitary-intact or hypophysectomized rats, chronic gastric and duodenal ulcers were induced by acetic acid. After induction of ulcers, rats were treated intraperitoneally twice a day with saline, ghrelin (4, 8 or 16 nmol/kg/dose) or IGF-1 (20 nmol/kg/dose) for six or ten days. In animals with intact pituitary, treatment with ghrelin increased serum level of GH and IGF-1. These effects were accompanied by the increase in mucosal cell proliferation, mucosal blood flow and healing rate of gastric and duodenal ulcers. After hypophysectomy, the significant increase in serum level of endogenous ghrelin was observed, but the healing of gastric and duodenal ulcers was delayed. This effect was accompanied by a significant decrease in serum concentration of endogenous GH and IGF-1, and reduction in mucosal blood flow and DNA synthesis. In hypophysectomized rats, administration of exogenous ghrelin was without any effect on serum level of GH and IGF-1, healing rate of gastroduodenal ulcers or mucosal cell proliferation. In contrast to this effect, administration of IGF-1 increased mucosal cell proliferation, healing rate of gastroduodenal ulcers and mucosal blood flow in hypophysectomized rats. Conclusion: Treatment with ghrelin accelerates healing of chronic gastroduodenal ulcers and this effect is mediated by the release of endogenous GH and IGF-1.