Higher Growth Hormone Concentrations Research Articles

Dietary Palygorskite-Based Antibacterial Agent Supplementation as an Alternative to Antibiotics Improves Growth Performance, Blood Parameters, and Rumen Microbiota in Sheep.

This research aimed to investigate the effects of a palygorskite-based antibacterial agent (PAA) as an alternative to antibiotics on growth performance, blood parameters, and rumen microbiota in sheep. A total of 120 sheep were randomly divided into five groups of six replicates with four sheep each. Sheep were fed a basal diet, an antibiotic diet supplemented with 500 g/t chlortetracycline (CTC), and a basal diet supplemented with 500, 1000, and 2000 g/t PAA for 80 d, respectively. Supplementation with 2000 g/t PAA and 500 g/t CTC increased the average daily gain (ADG) of sheep compared with the control group (p < 0.05). Diets supplemented with 2000 g/t PAA and 500 g/t CTC reduced (p < 0.05) the feed:gain ratio (F/G ratio) in the overall periods. Dietary supplementation with 1000 g/t PAA significantly increased albumin and total protein (p < 0.05). A significant positive correlation was found between growth hormone concentration and PAA supplementation (p < 0.05). In addition, compared to the control group, the CTC group had higher growth hormone concentration and lower lipopolysaccharide concentration (p < 0.05). No difference was observed between the five groups in terms of rumen fermentation characteristics (p > 0.05). At the phylum level, the relative abundance of Proteobacteria was lower in the PAA 2000 and CTC 500 groups than in the control and PAA 500 groups (p < 0.05). At the genus level, a significant decrease (p < 0.05) in the relative abundance of RuminococcaceaeUCG-010 was observed in the PAA 1000, PAA 2000, and CTC 500 groups compared with that in the control group. In addition, the relative abundance of Prevotella1 (p < 0.05) was higher in the PAA 2000 group than in the control group. These findings indicate that dietary supplementation with PAA has ameliorative effects on growth performance, blood parameters, and rumen microbiota, with an optimal dosage of 2000 g/t for sheep.

Mathematical modeling reveals differential dynamics of insulin action models on glycerol and glucose in adolescent girls with obesity.

Under healthy conditions, the pancreas responds to a glucose challenge by releasing insulin. Insulin suppresses lipolysis in adipose tissue, thereby decreasing plasma glycerol concentration, and it regulates plasma glucose concentration through action in muscle and liver. Insulin resistance (IR) occurs when more insulin is required to achieve the same effects, and IR may be tissue-specific. IR emerges during puberty as a result of high concentrations of growth hormone and is worsened by youth-onset obesity. Adipose, liver, and muscle tissue exhibit distinct dose-dependent responses to insulin in multi-phase hyperinsulinemic-euglycemic (HE) clamps, but the HE clamp protocol does not address potential differences in the dynamics of tissue-specific insulin responses. Changes to the dynamics of insulin responses would alter glycemic control in response to a glucose challenge. To investigate the dynamics of insulin acting on adipose tissue, we developed a novel differential-equations based model that describes the coupled dynamics of glycerol concentrations and insulin action during an oral glucose tolerance test in female adolescents with obesity and IR. We compared these dynamics to the dynamics of insulin acting on muscle and liver as assessed with the oral minimal model applied to glucose and insulin data collected under the same protocol. We found that the action of insulin on glycerol peaks approximately 67 min earlier (p < 0.001) and follows the dynamics of plasma insulin more closely compared to insulin action on glucose as assessed by the parameters representing the time constants for insulin action on glucose and glycerol (p < 0.001). These findings suggest that the dynamics of insulin action show tissue-specific differences in our IR adolescent population, with adipose tissue responding to insulin more quickly compared to muscle and liver. Improved understanding of the tissue-specific dynamics of insulin action may provide novel insights into the progression of metabolic disease in patient populations with diverse metabolic phenotypes.

Growth hormone and periarticular new bone formation--a causal relationship? A preliminary communication

In an attempt to examine the relationship between growth hormone (GH) and periarticular new bone formation (PNBF), we studied eight patients with brain lesions of different origins who were in a prolonged comatose state for 164 to 1320 days. Five of them developed PNBF. The latter reacted to both the specific L-Dopa test and to the non-specific TRH test with an increase in GH serum concentration. Those patients who did not develop PNBF, failed to react significantly to either tests. The difference in GH values between the two groups is statistically significant at the 95% level of confidence. We hypothesize that there may be a causal relationship between high concentrations of GH in serum and PNBF.

Potential applications for rhIGF-I: Bone disease and IGF[sbnd

Growth hormone (GH) and insulin like growth factor-I (IGFI) are key bone trophic hormones, whose rising levels during puberty are critical for pubertal bone accrual. Conditions of GH deficiency and genetic resistance impact cortical and trabecular bone deleteriously with reduced estimates of bone strength. In humans, conditions of undernutrition (as in anorexia nervosa (AN), or subsequent to chronic illnesses) are associated with low IGF-I levels, which correlate with disease severity, and also with lower bone mineral density (BMD), impaired bone structure and lower strength estimates. In adolescents and adults with AN, studies have demonstrated a nutritionally acquired GH resistance with low IGF-I levels despite high concentrations of GH. IGF-I levels go up with increasing body weight, and are associated with rising levels of bone turnover markers. In short-term studies lasting 6–10 days, recombinant human IGF-I (rhIGF-I) administration in physiologic replacement doses normalized IGF-I levels and increased levels of bone formation markers in both adults and adolescents with AN. In a randomized controlled trial in adults with AN in which participants were randomized to one of four arms: (i) rhIGF-I with oral estrogen-progesterone (EP), (ii) rhIGF-I alone, (iii) EP alone, or (iv) neither for 9 months, a significant increase in bone formation markers was noted in the groups that received rhIGF-I, and a significant decrease in bone resorption markers in the groups that received EP. The group that received both rhIGF-I and EP had a significant increase in bone density at the spine and hip compared to the group that received neither. Side effects were minimal, with no documented fingerstick glucose of <50 mg/dl. These data thus suggest a potential role for rhIGF-I administration in optimizing bone accrual in states of undernutrition associated with low IGF-I.

PERTUMBUHAN IKAN BANDENG (Chanos chanos) ANTARA BENIH HATCHERY SKALA RUMAH TANGGA DAN GENERASI KEDUA (G-2) TERSELEKSI

Currently, there is a national concern regarding to the decrease of milkfish production from ponds in North Java due to a low quality of milkfish seed produced by small scale hatcheries in Bali, which is the main producer of milkfish seed. The quality of seed is strongly related to the quality of eggs (fertility), while quality of eggs produced depends on the management of brood stocks carried out by the hatcheries. Growth rate and growth hormone profiles are some of the biological aspects that could be used as a basis/benchmark to evaluate quality level of milkfish seed reared in ponds. The aim of this experiment was to evaluate growth rate and growth hormone profile performance between selected G-2 seed and small scale hatcheries seed as control population the growth rate. Research on grow-out of milkfish seed was conducted at the IMRAD ponds facility in Pejarakan, using milkfish seed produced by small scale hatcheries as well as selected second-generation (G-2) seed, each with the density of 5000 seed/pond (1 pond=0.5 ha). The seeds were fed with dry pellet and reared for 5 – 6 months. The results showed that the seed produced with standard operational procedure (SOP) by small scale hatcheries were having longer (F hit. = 13.68 &gt; F tabel 1%) and heavier body washt (F hit. = 18.98 &gt; F tabel 1%) better than selected G-2 seed and small scale hatcheries seed without SOP with high growth hormone concentration (F hit. = 4.95 &gt; F tabel 5%).

A half-century of studies of growth hormone insensitivity/Laron syndrome: A historical perspective

A growth hormone (GH) dependent substance responsible for sulfate uptake by costal cartilage of hypophysectomized rats, labeled sulfation factor, was reported in 1957. In 1962 the radioimmunoassay for GH was described. The clinical picture of severe GH deficiency but with high serum concentrations of GH was reported in 3 siblings in 1966 and followed by a 1968 report of 22 patients belonging to 14 consanguineous oriental Jewish families in Israel. Defective sulfation factor generation was demonstrated in 15 of these individuals and in a 1971 report; FFA response to IV GH and growth response to GH injections suggested competitive saturation of peripheral tissue receptors by an abnormal GH. However, studies published in 1973 demonstrated normal fractionation of their circulating GH, and normal binding of GH from 22 patients to various antisera used for radioimmunoassay. In 1976, the Israeli investigators reported that circulating GH from 7 patients reacted normally in the recently developed radioreceptor assay for GH. In 1984, using hepatic microsome pellets, they demonstrated that the defect was a failure of GH binding to receptors. Characterization of the human GH receptor (GHR) gene, reported in 1989, included the initial description of a genetic defect of the GHR in 2 of 9 Israeli patients. At about the same time began the identification in Ecuador of what was to become the largest population of GH insensitivity in the world, ~100 individuals, and the only substantial population with a common mutation of the GH receptor. Treatment studies with recombinant IGF-I began in 1990. Growth response was modest compared to that of GH treated GH deficient subjects. The spectrum of GH insensitivity has expanded beyond GH receptor deficiency to include postreceptor abnormalities: IGF-I gene mutation (1996); IGF-I receptor mutation (2003); signal transducer and activator of transcription 5b mutation (2003); and mutation of the GH-dependent acid labile subunit (2004). ConclusionRare conditions of GH insensitivity caused by GH receptor and postreceptor abnormalities have provided insights into the processes of growth, body composition, and metabolism.

Relationship among insulin resistance, growth hormone, and insulin-like growth factor I concentrations in diestrous Swedish Elkhounds.

BackgroundIn the dog, the normal estrous cycle includes a prolonged luteal phase. Progesterone stimulates local canine mammary growth hormone (GH) production, which may act systemically and contribute to insulin resistance. Swedish Elkhounds are predisposed to progesterone‐related diabetes mellitus, and the relationship among insulin resistance, GH, and insulin‐like growth factor I (IGF‐I) is of particular interest.ObjectiveTo study insulin resistance in relation to GH and IGF‐I in nondiabetic Swedish Elkhounds during diestrus. We also assessed whether alterations in these hormones could predict diestrus‐linked diseases and all‐cause mortality.AnimalsEighty‐four privately owned female intact Swedish Elkhounds >4 years of age.MethodsBlood sampling and clinical examination during luteal phase, with a follow‐up questionnaire after 20 months. Insulin resistance was calculated by homeostasis model assessment (HOMA‐IR).ResultsIn multivariable regression analysis, GH was positively associated with HOMA‐IR (P = .009). An increase in GH of 1 ng/mL was associated with a 12.7% increase in HOMA‐IR. Moreover, C‐peptide was positively associated with IGF‐I (P = .04), and an increase in C‐peptide of 0.1 ng/mL was associated with a 6.9% increase in IGF‐I. Structural equation modeling supported these results. Twenty‐three animals were found to have previously unrecognized mammary masses and had higher GH (P < .0001) and IGF‐I (P = .007) than dogs without mammary masses (n = 61). There was no association between high GH and IGF‐I concentrations at sampling and future mammary masses.ConclusionWe showed that GH was strongly associated with insulin resistance in older Swedish Elkhounds during diestrus.

The hepatic expression of GH/IGF1 axis components is impaired with fibrosis progression in patients with HCV-related chronic hepatitis

Background and aim: Resistance to the action of growth hormone (GH), characterized by low serum levels of insulin-like growth factor-1 (IGF1) in the face of high concentrations of GH, frequently complicates cirrhosis (Assy et al., 2008). Physiologically, the activation of GH receptor (GHR) determines phosphorylation of signal transducer and activator of transcription (STAT)-5 and the consequent induction of IGF-1 expression. The suppressor of cytokine signalling (SOCS)-3 negatively regulates this intracellular cascade. Since, to date, the hepatic expression of the GH/IGF1 axis components has been studied mainly in animal models (Blaas L et al., 2010), we aimed to evaluate their expression in the liver of patients with HCV-related chronic hepatitis. Methods: Fifty HCV patients were studied and liver samples were histologically re-evaluated for grading and staging. The expression of GH/IGF1 axis components was assessed by immunohistochemistry. Results: At the hepatocyte level, IGF-1 and phospho-STAT5 showed a negative correlation with fibrosis stage, while SOCS3 a positive one (p<0,05 for all). Furthermore, the hepatocyte expression of IGF1 was negatively correlated with its expression by hepatic stellate cells (p<0,05). Conclusions: IGF1 expression by hepatocytes was reduced with fibrosis progression, probably due to the impairment of GHR intracellular cascade. The inverse correlation between IGF1 expressed by hepatocytes and hepatic stellate cells suggests specific roles for IGF-I produced by different hepatic cells.

Effect of hypothyroidism on insulin sensitivity and glucose tolerance in dogs

To determine the effects of hypothyroidism on insulin sensitivity, glucose tolerance, and concentrations of hormones counter-regulatory to insulin in dogs. 8 anestrous mixed-breed bitches with experimentally induced hypothyroidism and 8 euthyroid control dogs. The insulin-modified frequently sampled IV glucose tolerance test and minimal model analysis were used to determine basal plasma insulin and glucose concentrations, acute insulin response to glucose, insulin sensitivity, glucose effectiveness, and disposition index. Growth hormone response was assessed by stimulation and suppression tests. Additionally, basal serum growth hormone (GH) and insulin-like growth factor-1 (IGF-1) concentrations and urine cortisol-to-creatinine concentration ratios were measured and dual energy x-ray absorptiometry was performed to evaluate body composition. Insulin sensitivity was lower in the hypothyroid group than in the euthyroid group, whereas acute insulin response to glucose was higher. Glucose effectiveness and disposition index were not different between groups. Basal serum GH and IGF-1 concentrations as well as abdominal fat content were high in hypothyroid dogs, but urine cortisol-to-creatinine concentration ratios were unchanged. Hypothyroidism appeared to negatively affect glucose homeostasis by inducing insulin resistance, but overall glucose tolerance was maintained by increased insulin secretion in hypothyroid dogs. Possible factors affecting insulin sensitivity are high serum GH and IGF-1 concentrations and an increase in abdominal fat. In dogs with diseases involving impaired insulin secretion such as diabetes mellitus, concurrent hypothyroidism can have important clinical implications.

Existe-t-il une relation entre la dose d'hormone de croissance et d'éventuelles complications tumorales ou cardiovasculaires ?

Growth hormone (GH) affects protein (anabolism), lipid (lipolysis) and carbohydrate (hyperglycemia) metabolism and stimulates hepatic synthesis of insulin-like growth factor 1 (IGF1). IGF1 is believed to act as a postnatal growth factor. In addition to its effects on growth, IGF1 affects cell proliferation, differentiation and survival, and has anabolic effects on proteins, and also lipogenic and glucose-lowering effects. The increasing availability of biosynthetic pituitary GH has made it feasible to treat GH-deficient children and adults, and patients of short stature due to a variety of other causes (Turner's syndrome, anomalies of SHOX, intrauterine growth retardation (IUGR), chronic renal failure, Prader-Willi syndrome, or idiopathic short stature). The therapeutic dose has been increased in some situations in which the response is inadequate, particularly in patients with certain conditions such as IUGR. However, it has been reported that cancers and cardiovascular diseases are associated with high plasma concentrations of GH and IGF1, particularly in patients with acromegaly but also in large epidemiological studies of apparently healthy populations. These findings raise questions as to the safety of GH treatment. Some long-term follow-up studies have shown an increase in the risk of some kinds of cancer or cerebrovascular disease, but these findings have not been replicated by others. The results of these studies remain debatable, due to their small sample sizes, methodological weaknesses, nonexhaustive data collection and problems involved in comparing these patients with an appropriate control group. Finally, GH and IGF1 deficiencies are themselves associated with an increased risk of cardiovascular diseases, as is small stature/low weight at birth (due to IUGR). Recent studies have demonstrated a higher risk of cardiovascular disease in patients with both low and high plasma concentrations of GH and IGF1, these risks disappearing at average values. These findings suggest that the GH dose should be adjusted during treatment to ensure that plasma IGF1 concentrations remain within the physiological range.

Growth Hormone Is a Modulator of Lymphocyte Migration

Cell migration is crucial for intrathymic T cell differentiation and export of mature T lymphocytes to the peripheral lymphoid organs. The intrinsic regulation of T cell migration, mediated by adhesion molecules and chemokines, can be influenced by a number of endogenous factors, such as hormones, as for instance growth hormone (GH). Laminin deposition was enhanced in GH-treated mice and in GH-transgenic animals, compared with corresponding controls, and thymocyte adhesion to laminin was increased by in vivoGH treatment. An enhancing effect was also observed ex vivo in relation to the number of migrating cells in laminin-coated transwell chambers. Additionally, we found that the chemokine CXCL12, in conjunction with laminin, further enhanced the migration of thymocytes previously exposed to high concentrations of GH in vivo. Moreover, an increase in CXCL12 production has been detected in the thymus of GH-transgenic mice as well as in primary thymic epithelial cell cultures derived from these animals, as compared to age-matched wild-type counterparts. In keeping with these data, in vivo experiments showed that GH favors the trafficking of naive CD4+CD8– recent thymic emigrants to the peripheral lymph nodes. In addition, we found that migration of lymphocytes from mesenteric lymph nodes of GH-transgenic mice, triggered by the chemokine CXCL12, in conjunction with laminin or fibronectin, was enhanced, when compared to lymphocytes from control mice. Since GH-based therapy has been used in human and experimental infectious diseases, this hormone can be envisioned as an additional therapeutic tool in situations in which increasing lymphocyte numbers and migration are required for correcting a given pathological state.

Effects of nutrient restriction on mammary cell turnover and mammary gland remodeling in lactating dairy cows

The aim of this study was to investigate the effects of a severe nutrient restriction on mammary tissue morphology and remodeling, mammary epithelial cell (MEC) turnover and activity, and hormonal status in lactating dairy cows. We used 16 Holstein × Normande crossbred dairy cows, divided into 2 groups submitted to different feeding levels (basal and restricted) from 2 wk before calving to wk 11 postpartum. Restricted-diet cows had lower 11-wk average daily milk yield from calving to slaughter than did basal-diet cows (20.5 vs. 33.5kg/d). Feed restriction decreased milk fat, protein, and lactose yields. Restriction also led to lower plasma insulin-like growth factor 1 and higher growth hormone concentrations. Restricted-diet cows had lighter mammary glands than did basal-diet cows. The total amount of DNA in the mammary gland and the size of the mammary acini were smaller in the restricted-diet group. Feed restriction had no significant effect on MEC proliferation at the time of slaughter but led to a higher level of apoptosis in the mammary gland. Gelatin zymography highlighted remodeling of the mammary extracellular matrix in restricted-diet cows. Udders from restricted-diet cows showed lower transcript expression of α-lactalbumin and kappa-casein. In conclusion, nutrient restriction resulted in lower milk yield in lactating dairy cows, partly due to modulation of MEC activity and a lower number of mammary cells. An association was found between feed restriction-induced changes in the growth hormone–insulin-like growth factor-1 axis and mammary epithelial cell dynamics.

Human growth hormone (GH) immunoassay: standardization and clinical implications

The poor comparability of growth hormone (GH) results obtained using commercially available methods, is partly due to standard preparations used in calibration. The system relies on the use of the International Reference Preparation (IRP) international standard (IS) 80/505, of human pituitary origin, containing all GH isoforms. Recently, a 22K recombinant GH isoform IRP IS 98/574 was commercialized. Our aim was to evaluate the influence of both calibrators on GH results. GH concentration in 97 serum samples from children undergoing a growth hormone releasing hormone+arginine stimulation test was measured using Siemens IMMULITE electro-chemiluminescence method, calibrated with both IS 80/505 and IS 98/574 (GRH Growth hormone-Recombinant 98/574-kit). Comparison of our results obtained with the two sets of calibrators showed good correlation, although we found higher percentage variation (var%) than that stated by Siemens. The mean var% value was confirmed when all results were sub-divided into subgroups based on both high and low GH concentrations. Since the GH assay is influenced by a variety of binding proteins, isoforms and conversion factors, standardization of the assay is strongly required. In Italy, the Agenzia Italiana del Farmaco 39 note provides GH laboratory values which are useful for therapy. On the basis of our results, we therefore propose to adjourn these GH values in order to ensure better management of patients with GH-related disorders.

Diabetes Mellitus in Elkhounds Is Associated with Diestrus and Pregnancy

Female Elkhounds are shown to be at increased risk for diabetes mellitus, and occurrence of diabetes during pregnancy has been described in several cases. Onset of diabetes mellitus in Elkhounds is associated with diestrus. Sixty-three Elkhounds with diabetes mellitus and 26 healthy controls. Medical records from 63 Elkhounds with diabetes were reviewed and owners were contacted for follow-up information. Blood samples from the day of diagnosis were available for 26 dogs. Glucose, fructosamine, C-peptide, growth hormone (GH), insulin-like growth factor-1, progesterone, and glutamate decarboxylase isoform 65-autoantibodies were analyzed and compared with 26 healthy dogs. Logistic models were used to evaluate the association of clinical variables with the probability of diabetes and with permanent diabetes mellitus after ovariohysterectomy (OHE). All dogs in the study were intact females and 7 dogs (11%) were pregnant at diagnosis. The 1st clinical signs of diabetes mellitus occurred at a median of 30 days (interquartile range [IQR], 3-45) after estrus, and diagnosis was made at a median of 46 days (IQR, 27-62) after estrus. Diabetes was associated with higher concentrations of GH and lower concentrations of progesterone compared with controls matched for time after estrus. Forty-six percent of dogs that underwent OHE recovered from diabetes with a lower probability of remission in dogs with higher glucose concentrations (odds ratio [OR], 1.2; P=.03) at diagnosis and longer time (weeks) from diagnosis to surgery (OR, 1.5; P=.05). Diabetes mellitus in Elkhounds develops mainly during diestrus and pregnancy. Immediate OHE improves the prognosis for remission of diabetes.

Interaction between sleep and growth hormone

The relation between nightly growth hormone (GH) secretion and sleep is poorly understood. To examine whether disturbances in GH secretion are reflected in abnormal sleep patterns 8 subjects with isolated GH deficiency and 9 subjects with excess of GH (acromegalics) underwent all night sleep studies, polysomnography. Moreover, the effect of correcting GH concentration on sleep patterns were examined in the same subjects. The results showed that all subjects with GH disturbances had abnormal REM and delta sleep and normalization of GH concentration was followed by correction of the sleep stages. By power spectrum analysis of the sleep EEG it was showed that during low GH concentration the sleep energy was low, and high GH concentration was associated with high sleep energy, and correction of abnormal plasma GH levels resulted in normalization of REM and delta sleep energy per time unit.

Growth Hormone and Insulin-Like Growth Factor-I as an Endocrine Axis in Alzheimers Disease

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment with insidious onset. Neuropathological analysis of AD-affected brains reveals extensive atrophy and an accumulation of neurofibrillary tangles. Taken together, the neurochemical changes in the brain in patients with AD indicate multiple disturbances, and it seems likely that the changes are secondary to more fundamental changes in the brain. The IGF-I is a potent neurotrophic as well as a neuroprotective factor found in the brain, with a wide range of actions in both the central and the peripheral nervous systems. There is a physiological decline of the growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis with ageing, and the possibility that the GH/IGF-I axis is involved in cognitive deficits has been recognized for several years. IGF-I is a critical promoter of brain development and neuronal survival, and plays a role in neuronal rescue during degenerative diseases. The investigations of GH-releasing stimulation tests, and especially of GHRH in AD, are equivocal and in some cases contradictory. The results of several studies addressing this point show varied results: superimposable response of GH to GHRH than response of GH to GHRH in controls; blunted GH to GHRH response in AD patients; higher GH concentrations in the morning; greater increase of GH to GHRH in AD patients than in controls. When an acetylcholinesterase inhibitor, such as rivastigmine, a drug for AD, is acutely administered, the area under the curve of the GH response to GHRH doubles, showing that rivastigmine is a powerful drug in the enhancement of GH release. Consequently, an emerging clinical target for improving the clinical manifestations of AD may be the activation of GH/IGF-I, which rejuvenates the axis, so resulting in an overall physiological benefit.

Exercise and humoral mediators of peripheral energy balance: ghrelin and adiponectin.

Ghrelin and adiponectin are recently discovered peptides that are both associated with energy homeostasis and insulin action. In addition, circulating levels of both peptides are altered in obese populations and are associated with poor health. Moreover, expression of ghrelin and adiponectin returns to normal levels following weight loss in obese patients. Because exercise training improves the health status of obese individuals and is associated with reduction of body weight, there is interest in the effects of exercise on adiponectin and ghrelin and whether these peptides may provide better understanding of how exercise improves health. Ghrelin levels do not increase in response to acute running and cycling in humans, and therefore ghrelin does not appear to regulate growth hormone (GH) release during exercise. There is some evidence that ghrelin levels are suppressed following resistance exercise of moderate intensity and are lower with higher GH concentrations during aerobic exercise. It has been suggested that negative feedback from elevated GH produces the reductions, but why these responses have not been consistently found in other studies and whether postexercise reduction in ghrelin affects appetite warrants further investigation. There are a few studies (but not all) that suggest long-term chronic exercise produces increases in ghrelin levels when weight loss is produced. Ghrelin levels are much higher in amenorrheic athletes than in ovulating exercisers or in female exercisers with a luteal phase defect, suggesting an association with reproductive function. Adiponectin concentrations do not change in response to moderate and strenuous running or low- and moderate- intensity cycling. Most studies have revealed that chronic exercise that improves fitness levels, increases insulin sensitivity, and reduces body weight, will increase resting adiponectin levels. However, it does not appear that changes in insulin sensitivity brought about by moderate exercise training are attributable to adiponectin.

Feed intake, body composition, and plasma metabolic hormones in Merino sheep that differ genetically in fleece weight or fibre diameter

Negative genetic correlations result in sheep selected for fleece weight having reduced fatness and reproductive turnoff. Both of these characteristics depend mainly on energy metabolism, but the links between wool growth and energy metabolism are poorly defined. The present study examined aspects of energy metabolism (body composition, feed intake, and metabolic hormones) in Merino sheep with high or low estimated breeding values for clean fleece weight (CFW) or fibre diameter (FD). The groups were selected to have similar mean liveweights. High CFW sheep had a lower proportion of fat (P &lt; 0.01) and more lean tissue (P &lt; 0.05) in their body, and ate more of a medium-quality diet (P &lt; 0.05). Intake of a straw diet with low digestibility that imposed a physical constraint on feed intake was not associated with CFW. When fed at the same level (1.2 × calculated maintenance), high CFW sheep had lower plasma concentrations of glucose (P &lt; 0.01), insulin (P &lt; 0.05), and insulin-like growth factor-1 (P &lt; 0.05), and higher concentrations of growth hormone (P &lt; 0.001). Responses of plasma insulin or glucose to treatment with insulin, adrenaline, or propranolol were independent of CFW. No differences were found between the high and low FD groups, except that the plasma cortisol response to adrenocorticotrophic hormone (ACTH) was higher in sheep with low FD. Calculations indicate that the lower fat reserves and plasma insulin and glucose concentrations in the high CFW sheep are sufficient to account for previous reports of reduced number of lambs weaned in high CFW sheep. Furthermore, the results indicate that high CFW sheep have smaller metabolic energy reserves to withstand unfavourable feed conditions, and so may be less able to thrive and reproduce successfully in harsh feed environments.

Secretory dynamics of leptin in adolescent girls with anorexia nervosa and healthy adolescents

Leptin, an adipocytokine that suppresses appetite and may regulate neuroendocrine pathways, is low in undernourished states like anorexia nervosa (AN). Although leptin exhibits pulsatility, secretory characteristics have not been well described in adolescents and in AN, and the contribution of hypoleptinemia to increased growth hormone (GH) and cortisol in AN has not been explored. We hypothesized that hypoleptinemia in AN reflects decreased basal and pulsatile secretion and may predict increased GH and cortisol levels. Sampling for leptin, GH, cortisol, and ghrelin was performed every 30 min (from 2000 to 0800) in 23 AN and 21 controls 12-18 yr old, and data were analyzed using Cluster and deconvolution methods. Estradiol, thyroid hormones, and body composition were measured. AN girls had lower pulsatile and total leptin secretion than controls (P < 0.0001) subsequent to decreased burst mass (P < 0.0001) and basal secretion (P = 0.02). Nutritional markers predicted leptin characteristics. In a regression model including BMI, body fat, and ghrelin, leptin independently predicted GH burst interval and frequency. Valley leptin contributed to 56% of the variability in GH burst interval, and basal leptin and fasting ghrelin contributed to 42% of variability in burst frequency. Pulsatile leptin independently predicted urine free cortisol/creatinine (15% of variability). Valley leptin predicted cortisol half-life (22% of variability). Leptin predicted estradiol and thyroid hormone levels. In conclusion, hypoleptinemia in AN is subsequent to decreased basal and pulsatile secretion and nutritionally regulated. Leptin predicts GH and cortisol parameters and with ghrelin predicts GH burst frequency. Low leptin and high ghrelin may be dual stimuli for high GH concentrations in undernutrition.

Improvement of delivery and live birth rates after ICSI in women aged &gt;40 years by ovarian co-stimulation with growth hormone

Growth hormone (GH) is required for ovarian follicular development, and its administration during ovarian stimulation improves pregnancy rate in cow and sheep. Data on the use of exogenous GH in human assisted reproduction treatment are inconsistent. This prospective randomized study evaluates the usefulness of GH administration in women of >40 years undergoing ovarian stimulation for assisted reproduction treatment. One hundred women of >40 years undergoing assisted reproduction treatment were randomized between a GH treatment group and a placebo group. Assisted reproduction treatment outcomes were evaluated. In patients of the GH treatment group, a similar number of oocytes, embryos and pregnancies was achieved as compared with the placebo group. However, the patients treated with GH suffered fewer pregnancy losses, resulting in higher delivery and live birth rates. These patients also showed higher peak serum estradiol concentration and higher concentrations of GH and estradiol in pre-ovulatory follicular fluid as compared with the placebo group. Administration of GH during ovarian stimulation alleviates age-related decrease in assisted reproduction treatment efficiency. This effect appears to be mainly due to an improvement of oocyte developmental potential, but GH action on the uterus cannot be excluded.