Increase In Insulin-like Growth Factor-1 Levels Research Articles

The Role of Physical Activity in the Molecular Impact of Increased Insulin-Like Growth Factor-1 (IGF-1) Levels: A Literature Review

Insulin-like growth factor-1 (IGF-1) is a key mediator of human growth hormone (HGH), which plays an important role in promoting cell growth and differentiation in childhood and continues to exert anabolic effects in adults. IGF-1 is a small peptide that circulates in serum bound to a high affinity binding protein. IGF-1 is part of a vast network of growth factors, receptors, and binding proteins involved in mediating cell proliferation, differentiation, and apoptosis IGF-I-like growth factor has broad anabolic and insulin-sensitising effects, which are generated through endocrine (in circulation) as well as paracrine/autocrine mechanisms. Serum concentrations of IGF-1 steadily increase during childhood and peak at puberty, and continue to decline since then, as does the secretion of human growth hormone. This study aims to determine the role of physical activity in molecular impact on increasing IGF-1 levels. This article is the result of a review of various research references related to the role of physical activity in molecular impact on increasing IGF-1 levels. Physical Activity in Molecular has an impact on increasing IGF-1 levels.

Long-term effect of growth hormone on sleep-disordered breathing in Malaysian children with Prader-Willi syndrome: a retrospective study.

The effect of recombinant human growth hormone (rhGH) on sleep-disordered breathing (SDB) in Malaysian children with Prader-Willi syndrome (PWS) is under-investigated. We determined (1) the short- and long-term effects of rhGH and (2) factors associated with worsening SDB in children with PWS receiving rhGH. This retrospective study included children with PWS (with and without rhGH) who had undergone at least 1 polysomnography. Outcomes measured were the presence of SDB before and after starting rhGH and the progress of SDB with and without rhGH. Serial insulin-like growth factor 1 (IGF-1) measurements were recorded. One-hundred and thirteen polysomnograms were analyzed. The majority (92.3%) of initial polysomnograms showed SDB, with a median (interquartile range) apnea-hypopnea index of 5.0 (2.6, 16.3) events/h. The age for receiving rhGH was a median (IQR) of 1.9 (0.7, 3.4) years. One-third (36.8%) had worsening SDB after initiating rhGH, which was associated with higher IGF-1 levels post-rhGH (P = .007). After a median of 5 years of rhGH, 73.6% maintained or reduced their positive airway pressure settings. Without rhGH, 80% had increased their positive airway pressure settings. Worsening SDB while on rhGH was associated with higher body mass index, lower rhGH dose, higher IGF-1 levels, and non-15q deletion. The majority of Malaysian children with PWS had SDB. At initiation of rhGH, one-third of patients had worsening SDB, associated with increased IGF-1 levels. Stabilization of SDB was more frequently seen in those receiving long-term rhGH. Worsening SDB while on rhGH was associated with a higher body mass index, receiving a lower dose of rhGH, higher IGF-1 levels, and non-15q deletion. Tan YT, Azanan MS, Hng SY, etal. Long-term effect of growth hormone on sleep-disordered breathing in Malaysian children with Prader-Willi syndrome: a retrospective study. J Clin Sleep Med. 2024;20(8):1291-1299.

Association between serum insulin-like growth factor 1 levels and the improvements of cognitive impairments in a subgroup of schizophrenia: Preliminary findings

BackgroundNumerous studies have implicated abnormal insulin-like growth factor 1 (IGF-1) in the pathophysiology of schizophrenia, but findings have been inconsistent. MethodsWe conducted a meta-analysis to compare IGF-1 levels in schizophrenia patients with healthy controls and explored factors contributing to variability between estimates. In an independent sample (58 chronic schizophrenia patients and 30 healthy controls), we investigated differences in IGF-1 levels among schizophrenia subgroups with distinct cognitive profiles, identified using k-means clustering based on five cognitive domains from The Repeatable Battery for the Assessment of Neuropsychological Status. Associations between serum IGF-1 levels and clinical and neurocognitive improvements were also examined. ResultsThe meta-analysis revealed significantly lower serum IGF-1 levels in schizophrenia patients compared to healthy controls, albeit with high heterogeneity. Medication status, BMI, and severity of negative symptoms were identified as potential contributors to this heterogeneity. In our independent study, antipsychotic treatment led to a significant increase in IGF-1 levels, and lower pre-treatment serum IGF-1 levels correlated with greater improvement in cognitive deficits, particularly in a subgroup with more severe cognitive symptoms. ConclusionsOur findings support the “IGF-1 deficiency hypothesis” in the pathogenesis of schizophrenia. Further research is crucial to elucidate the role of IGF-1 in the cognitive impairments associated with schizophrenia.

Compensatory Growth Is Accompanied by Changes in Insulin-Like Growth Factor 1 but Not Markers of Cellular Aging in a Long-Lived Seabird.

AbstractDeveloping organisms often plastically modify growth in response to environmental circumstances, which may be adaptive but is expected to entail long-term costs. However, the mechanisms that mediate these growth adjustments and any associated costs are less well understood. In vertebrates, one mechanism that may be important in this context is the highly conserved signaling factor insulin-like growth factor 1 (IGF-1), which is frequently positively related to postnatal growth and negatively related to longevity. To test this idea, we exposed captive Franklin's gulls (Leucophaeus pipixcan) to a physiologically relevant nutritional stressor by restricting food availability during postnatal development and examined the effects on growth, IGF-1, and two potential biomarkers of cellular and organismal aging (oxidative stress and telomeres). During food restriction, experimental chicks gained body mass more slowly and had lower IGF-1 levels than controls. Following food restriction, experimental chicks underwent compensatory growth, which was accompanied by an increase in IGF-1 levels. Interestingly, however, there were no significant effects of the experimental treatment or of variation in IGF-1 levels on oxidative stress or telomeres. These findings suggest that IGF-1 is responsive to changes in resource availability but is not associated with increased markers of cellular aging during development in this relatively long-lived species.

Effect of estradiol and IGF1 on glycogen synthesis in bovine uterine epithelial cells.

Glucose is an important nutrient for the endometrium and embryo during pregnancy. This study shows that estradiol (E2)/IGF1 signaling stimulates glycogen synthesis in the uterine epithelium of cows, which could provide glucose when needed. Glycogen storage in the uterine epithelium peaks near estrus and is a potential source of glucose for the endometrium and embryos. However, the hormonal regulation of glycogen synthesis in the uterine epithelium is poorly understood. Our objective was to evaluate the effect of E2 and insulin-like growth factor 1 (IGF1) on glycogenesis in immortalized bovine uterine epithelial (BUTE) cells. Treatment of BUTE cells with E2 (0.1-10 nM) did not increase glycogen levels. However, treatment of BUTE cells with IGF1 (50 or 100 ng/mL) resulted in a >2-fold increase in glycogen. To determine if the uterine stroma produced IGF1 in response to E2, bovine uterine fibroblasts were treated with E2, which increased IGF1 levels. Immunohistochemistry showed higher levels of IGF1 in the stroma on day 1 than on day 11, which coincides with higher glycogen levels in the uterine epithelium. Western blots revealed that IGF1 treatment increased the levels of phospho-AKT, phospho-GSKβ, hexokinase 1, and glycogen synthase in BUTE cells. Metabolomic (GC-MS) analysis showed that IGF1 increased 3-phosphoglycerate and lactate, potentially indicative of increased flux through glycolysis. We also found higher levels of N-acetyl-glucosamine and protein glycosylation after IGF1 treatment, indicating increased hexosamine biosynthetic pathway activity. In conclusion, IGF1 is produced by uterine fibroblasts due to E2, and IGF1 increases glucose metabolism and glycogenesis in uterine epithelial cells. Glycogen stored in the uterine epithelium due to E2/IGF1 signaling at estrus could provide glucose to the endometrium or be secreted into the uterine lumen as a component of histotroph.

Trends in insulin-like growth factor-1 levels after bariatric surgery: a systematic review and meta-analysis.

According to studies, there are many inconsistencies in how IGF-1 levels change after bariatric surgery compared to before surgery, as well as its effects. These discrepancies can be attributed to various factors such as age, body mass index (BMI), and duration of intervention. Therefore, the aim of this study was to evaluate the level of insulin-like growth factor-1 (IGF-1) after bariatric surgery. A systematic review and meta-analysis based on the PRISMA guidelines was conducted from inception until 2021. From 1871 articles initially selected, 24 studies with 28 treatment arms met the eligible criteria and were included. Pooled findings from the random-effects model indicated that IGF-1 levels increased significantly [weighted mean difference (WMD) = 8.84 ng/ml; 95% confidence interval (CI) 0.30-17.39; p = 0.043] after bariatric surgery compared to before surgery. No significant heterogeneity was noted among the studies (Cochran Q test, p = 0.90, I2 = 0.0%). In subgroup analysis, bariatric surgery significantly increased IGF-1 levels at age <40 years but not at age ≤40 years. Bariatric surgery is capable of increasing the IGF-1 levels compared to the period prior to surgery but with a modest clinical magnitude.

Evaluation of Changes in Serum Insulin like Growth Factor-1 Levels with Growth Modulation via Twin Block TherapyA Prospective Clinical Study

Introduction: Serum insulin like growth factor is a pertinent growth regulator in bone and cartilage, therefore assessment of changes in serum Insulin like Growth Factor (IGF) levels in patients undergoing functional appliance therapy can act as valuable tool to understand the mode of action of functional appliances. Aim: To evaluate the changes in serum Insulin like Growth Factor-1 (IGF-1) levels in the patients undergoing twin block therapy and to establish IGF-1 as a biochemical marker produced in response to mechanical disturbance in the condylar region by twin block appliance. Materials and Methods: This prospective clinical trial was conducted in the Department of Orthodontics and Dentofacial Orthopedics, Postgraduate Institute of Dental Sciences, Rohtak, Haryana, India from May 2014 to November 2015. Total 27 patients included in study, divided into two groups, the test group which comprised of 15 patients treated with standard twin block appliance therapy and the control group which comprised of 12 patients not treated with the same. Serum samples were collected from test group and control group patients at four time intervals (pretreatment (T0), 1 month (T1), 3 months (T3) and 6 months (T6)) and subjected to EnzymeLinked Immunosorbent Assay (ELISA) to measure IGF-1 levels. The data thus obtained was subjected to statistical analysis using Statistical Package for the Social Sciences (SPSS) for windows 20.0. Intragroup differences were evaluated using paired t-test, while intergroup differences were evaluated using independent sample t-test. The p-value&lt;0.05 was considered as statistically significant. Results: The data was obtained from 11 patients (6 males and 5 females) in the test group and 10 patients (6 males and 4 females) in the control group after elimination of dropouts. Mean age of the test group subjects was 12.8±0.9 years and that of control group subjects was 13.1±0.9 years. The mean IGF-1 levels in the test group were 124.5 ng/mL (T0), 126.27 ng/mL (T1), 130.90 ng/mL (T3) and 135.54 ng/mL (T6). In the control group, 151.5 ng/mL (T0), 140.8 ng/mL (T1), 157.8 ng/mL (T3) and 120.2 ng/ mL (T6). In the test group, mean levels of serum IGF-1 did not change significantly when baseline levels were compared with the serum IGF-1 levels at T1 (0.467), T3 (0.729) and T6 (0.62) of functional appliance therapy, although an increase in IGF-1 levels was noted at each interval. Comparison of serum IGF-1 levels of test and control group showed no statistically significant difference between the groups at T0, T1, T3 and T6. Conclusion: Functional appliance therapy was not found to be associated with concomitant increase in serum IGF-1 levels.

Effects of experimental increase in insulin-like growth factor 1 on feather growth rate, moult intensity and feather quality in a passerine bird.

Moulting is a crucial, yet often overlooked life-history stage in many animals, when they renew their integumental structures. This life-history stage is an energetically demanding somatic growth event that has particular importance in birds because feathers play a crucial role in flight, insulation and communication. Somatic growth processes are regulated by the evolutionarily conserved peptide hormone insulin-like growth factor 1 (IGF-1). However, the role of IGF-1 in feather growth remains unknown. In this study, we captured 41 juvenile free-living bearded reedlings (Panurus biarmicus) that had started their first complete moult and brought them into captivity. Then, we manipulated their circulating IGF-1 levels using poly-(lactic-co-glycolid acid) microparticles (microspheres) that provide a sustained release of IGF-1. The treatment increased IGF-1 levels but did not affect the feather growth rate. However, 2weeks after the treatment, birds in the increased IGF-1 group were moulting more feathers simultaneously than the controls and were at a more advanced stage of moult. Birds with experimentally increased IGF-1 levels had better quality feathers (measured by a lower number of fault bars) than the controls. These results suggest that an increase in IGF-1 does not speed up feather growth, but may alter moult intensity by initiating the renewal of several feathers simultaneously. This may shorten the overall moulting time but may imply costs in terms of IGF-1-induced oxidative stress.

Variants of FOXO3 and RPA3 genes affecting IGF-1 levels alter the risk of development of primary osteoarthritis.

Pathologically high growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels in patients with acromegaly are associated with arthropathy. Several studies highlight the potential role of the GH/IGF-1 axis in primary osteoarthritis (OA). We aimed to disentangle the role of IGF-1 levels in primary OA pathogenesis. Patients from the Genetics osteoARthritis and Progression (GARP) Study with familial, generalized, symptomatic OA (n = 337, mean age: 59.8 ± 7.4 years, 82% female) were compared to Leiden Longevity Study (LLS) controls (n = 456, mean age: 59.8 ± 6.8 years, 51% female). Subjects were clinically and radiographically assessed, serum IGF-1 levels were measured, and 10 quantitative trait loci (QTL) in the FOXO3, IGFBP3/TNS3, RPA3, SPOCK2 genes, previously related to serum IGF-1 levels, were genotyped. Linear or binary logistic generalized estimating equation models were performed. Serum IGF-1 levels were increased in OA patients, with male patients exhibiting the strongest effect (males OR = 1.10 (1.04-1.17), P=0.002 vs females OR = 1.04 (1.01-1.07), P = 0.02). Independent of the increased IGF-1 levels, male carriers of the minor allele of FOXO3 QTL rs4946936 had a lower risk to develop hip OA (OR = 0.41 (0.18-0.90), P = 0.026). Additionally, independent of IGF-1 levels, female carriers of the minor alleles of RPA3 QTL rs11769597 had a higher risk to develop knee OA (OR = 1.90 (1.20-2.99), P = 0.006). Patients with primary OA had significantly higher IGF-1 levels compared to controls. Moreover, SNPs in the FOXO3 and RPA3 genes were associated with an altered risk of OA. Therefore, altered IGF-1 levels affect the development of OA, and are potentially the result of the pathophysiological OA process.

Peripheral Circulation and Astrocytes Contribute to the MSC-Mediated Increase in IGF-1 Levels in the Infarct Cortex in a dMCAO Rat Model.

Materials and Methods Ischemic brain injury was induced by dMCAO in Sprague-Dawley rats. The transplantation group received MSC infusion 1 h after dMCAO. Expression of IGF-1 in GFAP+ astrocytes, Iba-1+ microglia/macrophages, CD3+ lymphocytes, Ly6C+ monocytes/macrophages, and neutrophil elastase (NE)+ neutrophils was examined to determine the contribution of these cells to the increase of IGF-1. ELISA was performed to examine IGF-1 levels in blood plasma at days 2, 4, and 7 after ischemia onset. Results In total, only 5-6% of Iba-1+ microglia were colabeled with IGF-1 in the infarct cortex, corpus callosum, and striatum at day 2 post-dMCAO. MSC transplantation did not lead to a higher proportion of Iba-1+ cells that coexpressed IGF-1. In the infarct cortex, all Iba-1+/IGF-1+ double-positive cells were also positive for CD68. In the infarct, corpus callosum, and striatum, the majority (50-80%) of GFAP+ cells were colabeled with ramified IGF-1 signals. The number of GFAP+/IGF-1+ cells was further increased following MSC treatment. In the infarct cortex, approximately 15% of IGF-1+ cells were double-positive for CD3. MSC treatment reduced the number of infiltrated CD3+/IGF-1+ cells by 70%. In the infarct, few Ly6C+ monocytes/macrophages or NE+ neutrophils expressed IGF-1, and MSC treatment did not induce a higher percentage of these cells that coexpressed IGF-1. The IGF-1 level in peripheral blood plasma was significantly higher in the MSC group than in the ischemia control group. Conclusion The MSC-mediated increase in IGF-1 levels in the infarct cortex mainly derives from two sources, astrocytes in brain and blood plasma in periphery. Manipulating the IGF-1 level in the peripheral circulation may lead to a higher level of IGF-1 in brain, which could be conducive to recovery at the early stage of dMCAO.

Insulin-like growth factor-1 and site-specific cancers: A Mendelian randomization study.

Insulin‐like growth factor‐1 (IGF‐1) is involved in several processes relevant to carcinogenesis. We used 416 single‐nucleotide polymorphisms robustly associated with serum IGF‐1 levels to assess the potential causal associations between this hormone and site‐specific cancers through Mendelian randomization. Summary‐level genetic association estimates for prostate, breast, ovarian, and lung cancer were obtained from large‐scale consortia including individuals of European‐descent. Furthermore, we estimated genetic associations with 14 site‐specific cancers in European‐descent individuals in UK Biobank. Supplementary analyses were conducted for six site‐specific cancers using summary‐level data from the BioBank Japan Project. Genetically predicted serum IGF‐1 levels were associated with colorectal cancer. The odds ratio (OR) per standard deviation increase of IGF‐1 levels was 1.11 (95% confidence interval [CI] 1.01‐1.22; P = .03) in UK Biobank and 1.22 (95% CI 1.09‐1.36; P = 3.9 × 10−4) in the BioBank Japan Project. For prostate cancer, the corresponding OR was 1.10 (95% CI 1.01‐1.21; P = .04) in UK Biobank, 1.03 (95% CI 0.97‐1.09; P = .41) in the prostate cancer consortium, and 1.08 (95% CI 0.95‐1.22; P = .24) in the BioBank Japan Project. For breast cancer, the corresponding OR was 0.99 (95% CI 0.92‐1.07; P = .85) in UK Biobank and 1.08 (95% CI 1.02‐1.13; P = 4.4 × 10−3) in the Breast Cancer Association Consortium. There was no statistically significant association between genetically predicted IGF‐1 levels and 14 other cancers. This study found some support for a causal association between elevated serum IGF‐1 levels and increased risk of colorectal cancer. There was inconclusive or no evidence of a causal association of IGF‐1 levels with prostate, breast, and other cancers.

Вплив ожиріння, гіперінсулінемії IGF-1 та гіперглікемії у розвитку колоректального раку у хворих на цукровий діабет 2-го типу

The latest studies prove an increased risk of colorectal cancer in patients with type 2 diabetes mellitus. The pathogenetic factors of type 2 diabetes have been recognized as mechanisms of association between these diseases. The objective: to investigate the effects of obesity, hyperinsulinemia, IGF-1 and hyperglycemia on the development of colorectal cancer in patients with type 2 diabetes. Materials and methods. 36 patients were divided into groups: I – healthy (control group), II – patients with type 2 diabetes mellitus, III – patients with colorectal cancer without diabetes, IV – patients with a combination of two diseases. Using the method of enzyme-linked immunosorbent assay were determined levels of insulin and insulin-like growth factor-1 (IGF-1). DM compensation was assessed by the level of glycosylated hemoglobin (HbA1c) that was determined by immuno-exchange chromatography. The data obtained were analyzed using Statistica 12.0 (StatSoft Inc.,USA). Differences between the values in the control and experimental groups were determined by the Student’s t-test. The differences were considered significant at р&lt;0.05. Results. According to the data obtained, colorectal cancer was diagnosed in patients with the age of over 60 years old with obesity. The body mass index (BMI) in patients of all study groups was higher than 30 kg/m2. Patients of group IV with a combination of type 2 diabetes and a circle of rectal cancer had significantly higher BMI compared to the control group (р&lt;0.05). Significant hyperinsulinemia and increased IGF-1 levels were detected in patients in all study groups (р&lt;0.05). Most patients with diabetes in both groups had HbA1c levels higher than 7.5%. Conclusions. Obesity, hyperinsulinemia, increased bioavailability of IGF-1, and hyperglycemia are pathogenetic factors in the risk of colorectal cancer in patients with type 2 diabetes. Patients over the age of 55 with diabetes, obesity, and hyperinsulinemia are advised to be screened for colorectal cancer.

Obesity, Hyperinsulinemia, IGF-1, and Hyperglycemia as Risk Factors for Colorectal Cancer in Patients with Type 2 Diabetes mellitus

The latest studies prove an increased risk of colorectal cancer in patients with type 2 diabetes mellitus. The pathogenetic factors of type 2 diabetes have been recognized as mechanisms of association between these diseases.The objective: to investigate the effects of obesity, hyperinsulinemia, IGF-1 and hyperglycemia on the development of colorectal cancer in patients with type 2 diabetes.Materials and methods. 36 patients were divided into groups: I – healthy (control group), II – patients with type 2 diabetes mellitus, III – patients with colorectal cancer without diabetes, IV – patients with a combination of two diseases. Using the method of enzyme-linked immunosorbent assay were determined levels of insulin and insulin-like growth factor-1 (IGF-1). DM compensation was assessed by the level of glycosylated hemoglobin (HbA1c) that was determined by immuno-exchange chromatography. The data obtained were analyzed using Statistica 12.0 (StatSoft Inc.,USA). Differences between the values in the control and experimental groups were determined by the Student’s t-test. The differences were considered significant at р&lt;0.05.Results. According to the data obtained, colorectal cancer was diagnosed in patients with the age of over 60 years old with obesity. The body mass index (BMI) in patients of all study groups was higher than 30 kg/m2. Patients of group IV with a combination of type 2 diabetes and a circle of rectal cancer had significantly higher BMI compared to the control group (р&lt;0.05). Significant hyperinsulinemia and increased IGF-1 levels were detected in patients in all study groups (р&lt;0.05). Most patients with diabetes in both groups had HbA1c levels higher than 7.5%.Conclusions. Obesity, hyperinsulinemia, increased bioavailability of IGF-1, and hyperglycemia are pathogenetic factors in the risk of colorectal cancer in patients with type 2 diabetes. Patients over the age of 55 with diabetes, obesity, and hyperinsulinemia are advised to be screened for colorectal cancer.

Oral delivery of novel human IGF-1 bioencapsulated in lettuce cells promotes musculoskeletal cell proliferation, differentiation and diabetic fracture healing

Human insulin-like growth factor-1 (IGF-1) plays important roles in development and regeneration of skeletal muscles and bones but requires daily injections or surgical implantation. Current clinical IGF-1 lacks e-peptide and is glycosylated, reducing functional efficacy. In this study, codon-optimized Pro-IGF-1 with e-peptide (fused to GM1 receptor binding protein CTB or cell penetrating peptide PTD) was expressed in lettuce chloroplasts to facilitate oral delivery. Pro-IGF-1 was expressed at high levels in the absence of the antibiotic resistance gene in lettuce chloroplasts and was maintained in subsequent generations. In lyophilized plant cells, Pro-IGF-1 maintained folding, assembly, stability and functionality up to 31 months, when stored at ambient temperature. CTB-Pro-IGF-1 stimulated proliferation of human oral keratinocytes, gingiva-derived mesenchymal stromal cells and mouse osteoblasts in a dose-dependent manner and promoted osteoblast differentiation through upregulation of ALP, OSX and RUNX2 genes. Mice orally gavaged with the lyophilized plant cells significantly increased IGF-1 levels in sera, skeletal muscles and was stable for several hours. When bioencapsulated CTB-Pro-IGF-1 was gavaged to femoral fractured diabetic mice, bone regeneration was significantly promoted with increase in bone volume, density and area. This novel delivery system should increase affordability and patient compliance, especially for treatment of musculoskeletal diseases.

Hormone replacement therapy in children with growth hormone deficiency: impact on immune profile

Growth hormone (GH) may influence the immune system. The aim of this study was to assess the immune profile after treatment with GH in pre-pubertal children with a deficiency of this hormone. The study was carried out in two phases. Two groups were included in the first phase: group A) children treated with GH; group B) untreated children, prior to starting treatment. In the second phase, group B children were assessed 6 months after starting treatment. In the first phase, groups A and B were compared (case–control study). In the second phase, group B was compared in terms of baseline and final times (before and after study). We analysed: humoral immunity (immunoglobulin (Ig)A, IgG, IgM, C1 inhibitor, C3, and C4) and cell-mediated immunity (CD3+, CD4+, CD8+, CD4+/CD8+, CD19+ lymphocytes, and natural killer (NK) cells). Insulin-like growth factor 1 (IGF-1) and insulin-like growth factor-binding protein 3 (IGFBP-3) were also determined. In the first phase, CD3+, CD4+, CD19+, and NK cells and CD4+/CD8+ were greater in the treated group. CD8+ was lower in this group. No variations were seen in immunoglobulins and the complement between both groups. There were no changes to the complement in either of the two phases. In the second phase, untreated patients were assessed after 6 months of treatment. When comparing the baseline and final immune profiles, a statistically significant decrease in IgG and IgM was observed, and an increase of IGF-1 levels and monocytes. In conclusion, our study shows changes in the cellular and humoral immune profiles in children with GH deficiency who were treated.

Changes in thyroid volume and insulin-like growth factor 1 in pre- and post-pubertal obese children.

There is a mutual dynamic interaction between thyroid volume (TV), insulin-like growth factor-1 (IGF-1), and body mass index (BMI). These covariates undergo a change with the transition into puberty. The heterogeneity of the variates and study populations complicate the evaluation of the role of pure pubertal effect. The purpose of this study was to investigate the effect of puberty on IGF-1 and TV in a predetermined homogenous population such as obese children. Three hundred and eighty children (202 girls and 178 boys) aged between 6 and 18 were enrolled in this prospective study. The children were assigned to two groups according to their pubertal status, i.e., prepubertal (n = 169) and postpubertal (n = 211). According to age and sex, the obese group (n = 222) was made up of children at and above the 95th percentile, and the control group (n = 158) of children under the 85th percentile. The following parameters were evaluated in all children: BMI, pubertal status, TV, and serum IGF-1, IGFBP-3, and IGF-1:IGFBP-3 molar ratio. In comparison to the prepubertal obese group, the obese group at Tanner stage 2 had a larger mean TV (P = 0.008) and higher IGF-1 level (P = 0.033). There was a positive correlation between IGF-1 and TV both in the prepubertal and pubertal group (r169= 0.369, P = 0.001; r211= 0.316, P = 0.004, respectively), whereas there was no correlation between IGF-1 and BMI (r169= 0.99, P = 0.092; r211= 0.094, P = 0.088, respectively). This study showed that the TV and serum IGF-1 levels were increased in obese children in the early stage of puberty and that there was a positive correlation between these two variables in all children, which shows the specific effect of the early stage of puberty on the increase in TV and IGF-1 levels and suggests that increased TV is associated with the increase in IGF-1 levels in a homogenous group such as obese children.

Fermented corn-soybean meal elevated IGF1 levels in grower-finisher pigs1

Fermentation has attracted increasing attention in pig industry, because of low costs and numerous benefits on pig growth and health as well as environmental improvement, although the mechanisms remain largely unknown. In the present study, fermented corn-soybean meal significantly improved average daily gain and gain:food ratio (P < 0.05). Fermented feed (FF) significantly increased insulin-like growth factor 1 (IGF1) transcription in liver (P < 0.05). Meanwhile, fermented meal significantly enhanced the binding of CCAAT/enhancer-binding protein beta (C/EBPβ) to IGF1 promoter and C/EBPβ expression in liver (both P < 0.05). FF tended to increase IGF1 proteins in liver and serum too (both 0.05 < P < 0.10). Meanwhile, FF slightly but significantly increased hepatic and circulating triglyceride and total cholesterol levels, as well as serum ratio of high-density to low-density cholesterol (all P < 0.05). Our data indicated that FF could significantly augment the binding of C/EBPβ to IGF1 promoter and promote hepatic IGF1 expression and production, thus boost pig growth.

A rare challenging case of co-existent craniopharyngioma, acromegaly and squamous cell lung cancer.

SummaryCo-existence of craniopharyngioma and acromegaly has been very rarely reported. A 65-year-old man presented with visual deterioration, fatigue and frontal headaches. Magnetic resonance imaging revealed a suprasellar heterogeneous, mainly cystic, 1.9 × 2 × 1.9 cm mass compressing the optic chiasm and expanding to the third ventricle; the findings were consistent with a craniopharyngioma. Pituitary hormone profile showed hypogonadotropic hypogonadism, mildly elevated prolactin, increased insulin-like growth factor 1 (IGF-1) and normal thyroid function and cortisol reserve. The patient had transsphenoidal surgery and pathology of the specimen was diagnostic of adamantinomatous craniopharyngioma. Post-operatively, he had diabetes insipidus, hypogonadotropic hypogonadism and adrenocorticotropic hormone and thyroid-stimulating hormone deficiency. Despite the hypopituitarism, his IGF-1 levels remained elevated and subsequent oral glucose tolerance test did not show complete growth hormone (GH) suppression. Further review of the pre-operative imaging revealed a 12 × 4 mm pituitary adenoma close to the right carotid artery and no signs of pituitary hyperplasia. At that time, he was also diagnosed with squamous cell carcinoma of the left upper lung lobe finally managed with radical radiotherapy. Treatment with long-acting somatostatin analogue was initiated leading to biochemical control of the acromegaly. Latest imaging has shown no evidence of craniopharyngioma regrowth and stable adenoma. This is a unique case report of co-existence of craniopharyngioma, acromegaly and squamous lung cell carcinoma that highlights diagnostic and management challenges. Potential effects of the GH hypersecretion on the co-existent tumours of this patient are also briefly discussed.Learning points:Although an extremely rare clinical scenario, craniopharyngioma and acromegaly can co-exist; aetiopathogenic link between these two conditions is unlikely.Meticulous review of unexpected biochemical findings is vital for correct diagnosis of dual pituitary pathology.The potential adverse impact of GH excess due to acromegaly in a patient with craniopharyngioma (and other neoplasm) mandates adequate biochemical control of the GH hypersecretion.

Correlation of Insulin-Like Growth Factor with Acne Severity

Background & Introduction: Insulin-Like Growth Factor-1 (IGF-1) belongs to the growth factor family, structurally resembling pro-insulin, enabling it to bind to insulin receptors. It plays an important role in many tissues including skin, particularly acne pathogenesis by stimulating sebum production and affecting androgen levels. Studies comparing IGF-1 levels in acne patients and controls have found statistically significant differences, proving acne as a sign of insulin resistance. However, no such study has been carried out in Pakistan. Methodology: After approval from the institutional ethical board and informed consent, a case-control study was carried out with 270 acne patients and 80 age and gender- matched controls. Patients belonged to either gender and aged between 15 – 35 years were divided into mild, moderate and severe categories. IGF-1 levels were noted after exclusion of any condition interfering with IGF-1 level and correlated with acne severity and with levels of testosterone, dihydrotestosterone (DHT) and dehydroepiandrosterone sulphate (DHEAS). Quantitative variables were expressed as median and percentiles. Comparisons were done by Mann-WShitney test and correlations by Spearman correlation. A p value of < 0.05 was considered statistically significant. Results: Out of 350 cases and controls, There were 142 (41%) males and 208 (59%) females. In cases, there were 155 females and 115 males, whereas in controls, there were 54 females and 26 males. Median age of the patients was 20 years. Ninety-Seven patients had mild, 108 moderate and 65 had severe disease. Median levels of IGF-1 were 292 ng/m in cases. IGF-1 levels were significantly different between cases and controls and between mild and severe acne, but not between mild and moderate acne. IGF-1 levels were strongly correlated with the levels of androgenic hormones. Conclusion: Increase of IGF-1 levels in acne point to the role of insulin resistance and diet in acne. Future treatments may be targeted to treat IGF-1 levels by dietary interventions reducing glycemic load.

Correlation of Insulin-Like Growth Factor with Acne Severity

Background & Introduction: Insulin-Like Growth Factor-1 (IGF-1) belongs to the growth factor family, structurally resembling pro-insulin, enabling it to bind to insulin receptors. It plays an important role in many tissues including skin, particularly acne pathogenesis by stimulating sebum production and affecting androgen levels. Studies comparing IGF-1 levels in acne patients and controls have found statistically significant differences, proving acne as a sign of insulin resistance. However, no such study has been carried out in Pakistan. Methodology: After approval from the institutional ethical board and informed consent, a case-control study was carried out with 270 acne patients and 80 age and gender- matched controls. Patients belonged to either gender and aged between 15 – 35 years were divided into mild, moderate and severe categories. IGF-1 levels were noted after exclusion of any condition interfering with IGF-1 level and correlated with acne severity and with levels of testosterone, dihydrotestosterone (DHT) and dehydroepiandrosterone sulphate (DHEAS). Quantitative variables were expressed as median and percentiles. Comparisons were done by Mann-WShitney test and correlations by Spearman correlation. A p value of < 0.05 was considered statistically significant. Results: Out of 350 cases and controls, There were 142 (41%) males and 208 (59%) females. In cases, there were 155 females and 115 males, whereas in controls, there were 54 females and 26 males. Median age of the patients was 20 years. Ninety-Seven patients had mild, 108 moderate and 65 had severe disease. Median levels of IGF-1 were 292 ng/m in cases. IGF-1 levels were significantly different between cases and controls and between mild and severe acne, but not between mild and moderate acne. IGF-1 levels were strongly correlated with the levels of androgenic hormones. Conclusion: Increase of IGF-1 levels in acne point to the role of insulin resistance and diet in acne. Future treatments may be targeted to treat IGF-1 levels by dietary interventions reducing glycemic load.