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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcitonin is an endogenous regulator of calcium homeostasis, which acts principally on bone. At present, the principal indications for the therapeutic use of calcitonin are disorders involving hypercalcemia Paget's disease, acute pancreatitis, high-bone-turnover osteoporosis, pain associated with osteoporosis or bone metastases, and Sudeck's atrophy. The aim of this study was to compare the analgesic effects on postoperative pain of salmon calcitonin versus opioids administered epidurally. Our prospective study included 53 ASA I-II patients who were scheduled for total hip arthoplasty under epidural anaesthesia and who did not fulfill 1 or more of the exclusion criteria: a history of pituitary gland dysfunction; diabetes mellitus; obesity; contraindications to performing an epidural block and/or an allergy to calcitonin. These patients were randomly allocated into 3 groups (A, B, and C), each of which received postoperatively a different analgesic epidural mixture of 10 mL to control postoperative pain. Group A was given bupivacaine 0.5% (5 mL) + fentanyl 100 (2 mL) + NaCl 0.9% (3 mL). Group B was given bupivacaine 0.5% (5 mL) + salmon calcitonin 100IU (1 mL) + NaCl 0.9% (4 mL). Group C was given salmon calcitonin 100IU (1 mL) + NaCl 0.9% (9 mL). Perioperatively, 4 blood samples were taken from each patient at the following specific times: 1. Before the induction of anesthesia; 2. At the end of the operation and before the epidural administration of the analgesic mixture; 3. At the end of the first postoperative hour (1 hour after the administration of the analgesic mixture); and 4. At the end of the second postoperative hour (2 hours after the administration of the mixture). In each blood sample, glucose, cortisol, growth hormone, and prolactin plasma levels were determined in order to investigate the changes of these parameters as a result of the endocrine reaction to stress, and to pain relief. The analgesic solution was administered immediately after the second blood sample was taken. At the same time as the 4 blood samples were taken, haemodynamic parameters and pain scores were recorded. Epidural salmon calcitonin in combination with local anaesthetic produces an analgesic effect similar to fentanyl and with stable hemodynamic results. It also eliminates postoperative hyperglycaemia. The cortisol plasma level does not increase during the first postoperative hour, but increases significantly during the second postoperative hour. Growth hormone and prolactin plasma levels were stable in all patients in all 3 groups. This study shows that calcitonin is a suitable alternative for the treatment of acute postoperative pain.
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PMID:Epidural calcitonin: does it provide better postoperative analgesia? An analysis of the haemodynamic, endocrine, and nociceptive responses of salmon calcitonin and opioids in epidural anesthesia for hip arthroplasty surgery. 1715 40

Growth hormone's (GH) lipolytic activity in white adipose tissue (WAT) results in decreased body fat in giant GH transgenic mice and increased subcutaneous fat in dwarf growth hormone receptor/binding protein gene-disrupted mice (GHR -/-). We therefore hypothesized that GH action would affect expression of CIDE-A (cell-death-inducing DFF45-like effector-A), a protein found in white adipose tissue (WAT) and involved in lipid metabolism. CIDE-A RNA levels were determined in subcutaneous, retroperitoneal and epididymal adipose tissue isolated from wild-type and GHR -/- mice. The adipose tissue was also analyzed for adipocyte size. We determined that the lack of GH action has depot-specific effects on the levels of CIDE-A RNA and affected adipocyte cell size. CIDE-A expression is significantly reduced in GHR -/- subcutaneous fat compared to wild-type but is not altered in retroperitoneal or epididymal fat. Likewise, adipocytes are significantly enlarged in GHR -/- subcutaneous adipose tissue relative wild-type mice. A high-fat diet also influenced the level of CIDE-A RNA in mouse adipose tissue. The high-fat diet significantly reduced CIDE-A expression in wild-type subcutaneous fat but did not alter CIDE-A expression in subcutaneous fat of GHR -/- mice. The diet also reduced CIDE-A expression in wild-type retroperitoneal fat but the levels of CIDE-A in epididymal fat were unchanged. In contrast, the high-fat diet reduced CIDE-A expression in both retroperitoneal and epididymal fat of GHR -/- mice. These data demonstrate that CIDE-A levels are reduced in two different mouse models of obesity and this reduction may contribute to altered lipid metabolism.
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PMID:CIDE-A gene expression is decreased in white adipose tissue of growth hormone receptor/binding protein gene disrupted mice and with high-fat feeding of normal mice. 1754 97

Growth hormone (GH) is licensed for treatment for Prader-Willi syndrome (PWS) for improvement of body composition,1(-)3 height velocity, mobility, behaviour and quality of life.4 Recent case reports, however, have pointed out the occurrence of sudden death during initiation of GH, mainly during sleep and possibly related to severe obesity and sleep-disordered breathing (SDB).5(-)15 Concerns for an increased mortality in PWS children starting GH therapy led to a call for cessation of its use. Children with PWS are at risk of developing SDB secondary to both deficient autonomic sleep control and upper airway obstruction (UAO). It has been suggested that GH exacerbates pre-existing gas-exchange deficiencies in three ways: (a) by stimulation of adenotonsillar hypertrophy;16 17 (b) by a rise in basal metabolic rate with a resultant rise in oxygen demand;18 and (c) by normalisation of previously decreased hydration with augmentation of volume load.19 Are we withholding GH therapy, a treatment known to be of benefit in PWS, without adequate evidence to justify our actions? We consider it safe to treat severely obese children with GH once SDB is addressed using respiratory support such as continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP). In this paper, we evaluate the current evidence for the use of GH in PWS from a respiratory bias and propose a pathway for the identification and monitoring of these "at risk" patients.
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PMID:Prader-Willi syndrome: who can have growth hormone? 1808 32

Growth hormone (GH)-deficiency is usually associated with elevated adiposity, hyperleptinemia, and increased fracture risk. Since leptin is thought to enhance cortical bone formation, we have investigated the contribution of elevated adiposity and hyperleptinemia on femoral strength in rodent models of GH deficiency. Quantification of the transpubertal development of femoral strength in the moderately GH-deficient/hyperleptinemic Tgr rat and the profoundly GH-deficient/hypoleptinemic dw/dw rat revealed that the mechanical properties of cortical bone in these two models were similarly compromised, a 25-30% reduction in failure load being entirely due to impairment of geometric variables. In contrast, murine models of partial (GH antagonist transgenic) and complete (GH receptor-null) loss of GH signaling and elevated adiposity showed an impairment of femoral cortical strength proportionate to the reduction of GH signaling. To determine whether impaired femoral strength is exacerbated by obesity/hyperleptinemia, femoral strength was assessed in dw/dw rats following two developmental manipulations that elevate abdominal adiposity and circulating leptin, neonatal monosodium glutamate (MSG) treatment, and maintenance on an elevated fat diet. The additional impairment of femoral strength following MSG treatment is likely to have resulted from a reduction in residual activity of the hypothalamo-pituitary-GH-IGF-I axis, but consumption of elevated dietary fat, which did not reduce circulating IGF-I, failed to exacerbate the compromised femoral strength in dw/dw rats. Taken together, our data indicate that the obesity and hyperleptinemia usually associated with GH deficiency do not exert a significant influence over the strength of cortical bone.
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PMID:Does adiposity status influence femoral cortical strength in rodent models of growth hormone deficiency? 1900 45

Growth hormone (GH) is an endocrine regulator of glucose and lipid metabolism as well as body growth. GH levels are decreased and a unique pulsatile secretory pattern becomes obvious after puberty particularly in males. Coincidentally with this, males tend to deposit body fat. Experimental and clinical evidence has accumulated that obesity is associated with a decrease in GH levels. A strain of transgenic rats has been generated with severe obesity but normal nose-to-tail length, which has low circulating GH levels without pulsatility (human growth hormone (hGH) transgenic rats). The present review mainly focuses on recent and current work analysing the relationship between the occurrence of obesity and low GH levels and/or the absence of GH pulsatility in this transgenic animal model. This model has elevated blood glucose, non-esterified fatty acid, insulin and leptin levels associated with hyperphagia, suggesting that these rats also carry insulin- and leptin-resistant characteristics. hGH transgenic rats were subjected to a pair-feeding treatment to normalize food intake and chronic GH replacement to normalize GH levels. While the pair-feeding for 8 weeks successfully suppressed body-weight gain, the fat pad : body weight ratio remained very similar to freely-eating control hGH transgenic rats, which indicates the hyperphagia is not the sole contributor to the excess fat accumulation in this model. However, continuous elevation of peripheral hGH levels (approximately 2-fold) for 8 weeks by means of a slow-release vehicle resulted in a significant decrease in the fat mass : body weight ratios by 30 %. This GH treatment altered neither food intake nor body-weight gain. Thus, two characteristic phenotypes observed in the hGH transgenic rats, hyperphagia and obesity, seem to be closely related to GH levels and GH secretory pattern. This relationship might be working in the regulation of changes in seasonal body composition in wild animals.
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PMID:Effects of pulsatile secretion of growth hormone (GH) on fat deposition in human GH transgenic rats. 1908 6

Immune and neuroendocrine systems have bidirectional communications. Growth hormone (GH) and an orexigenic hormone ghrelin are expressed in various immune cells such as T lymphocytes, B lymphocytes, monocytes and neutrophils. These immune cells also bear receptors for hormones: growth hormone receptor (GHR) for GH and growth hormone secretagogue receptor (GHS-R) for ghrelin. The expression of GH in immune cells is stimulated by ghrelin as in anterior pituitary cells, whereas the regulation of GH secretion in the immune system by other peptides seems to be different from that in the anterior pituitary gland. Cytokines and mitogens enhance GH secretion from immune cells. GH has several biological actions in the immune system: enhancing thymopoiesis and T cell development, modulating cytokine production, enhancing B cell development and antibody production, priming neutrophils and monocytes for superoxide anion secretion, enhancing neutrophil adhesion and monocyte migration and anti-apoptotic action. Biological actions of ghrelin include attenuation of septic shock and anti-inflammatory actions, modulating phagocytosis, and enhancing thymopoiesis. The effect of ghrelin may be direct or through GH production, and that of GH may be direct or through insulin like growth factor-I (IGF-I) production. Elucidation of the roles of GH and ghrelin in the immune system may shed light on the treatment and prevention of immunological disorders such as AIDS and organ damages due to obesity/ageing-related chronic inflammation.
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PMID:Expression, regulation and biological actions of growth hormone (GH) and ghrelin in the immune system. 1914 54

Adult survivors of childhood cancer, particularly brain tumours and acute lymphoblastic leukaemia demonstrate evidence of increased rates of metabolic complications and cardiovascular disease in later life. Evidence is accumulating that risk factors for these complications include obesity, physical inactivity, lipid abnormalities, insulin resistance and development of the metabolic syndrome. Cranial radiotherapy-induced growth hormone deficiency, other direct adverse effects of radiotherapy and anthracycline-induced left ventricular dysfunction are clearly identified risk factors for developing these complications. Growth hormone replacement, where appropriate, has been of some benefit in reducing the prevalence of metabolic complications in some long-term survivors. In others, it is clear that multidisciplinary interventions will need to be developed which focus on modifying aspects of lifestyle including increasing levels of habitual physical activity, improving diet and prevention of smoking along with the use of lipid-lowering medication.
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PMID:Metabolic disorders. 1929 4

Growth hormone (GH) is the most important hormonal regulator of postnatal longitudinal growth in man. In adults GH is no longer needed for longitudinal growth. Adults with growth hormone deficiency (GHD) are characterised by perturbations in body composition, lipid metabolism, cardiovascular risk profile and bone mineral density. It is well established that adult GHD usually is accompanied by an increase in fat accumulation and GH replacement in adult patients with GHD results in reduction of fat mass and abdominal fat mass in particular. It is also recognized that obesity and abdominal obesity in particular results in a secondary reduction in GH secretion and subnormal insulin-like growth factor-I (IGF-I) levels. The recovery of the GH IGF-I axis after weight loss suggest an acquired defect, however, the pathophysiologic role of GH in obesity is yet to be fully understood. In clinical studies examining the efficacy of GH in obese subjects very little or no effect are observed with respect to weight loss, whereas GH seems to reduce total and abdominal fat mass in obese subjects. The observed reductions in abdominal fat mass are modest and similar to what can be achieved by diet or exercise interventions.
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PMID:Obesity, growth hormone and weight loss. 1972 58

Skeletal muscle is the major constituent of lean body mass and a major determinant of energy expenditure both at rest and during physical activity. Growth hormone, in turn, influences muscle mass as well as energy expenditure. Growth hormone substitution in adults increases muscle mass by 5-10%, but part of the effect is attributed to rehydration rather than protein accretion. In addition, GH regulates substrate metabolism in muscle and in particular antagonizes insulin-stimulated glucose disposal. This effect is linked to increased free fatty acid (FFA) flux but the molecular mechanisms remain unclear. During fasting, GH-induced insulin resistance may be favorable by reducing the demand of gluconeogenesis from protein. But in the postprandial phase, GH exposure may compromise glucose tolerance via the same mechanisms. Understanding the mechanisms whereby GH antagonizes insulin-stimulated glucose disposal in muscle is an important future research field with implications for a variety of clinical conditions ranging from malnutrition to obesity and type 2 diabetes.
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PMID:Effects of GH in human muscle and fat. 1990 70

Growth hormone (GH) secretion in children and adults is profoundly, but reversibly, suppressed in obesity. Since GH deficiency leads to increased fat mass, differentiation of both conditions remains challenging. Here we review the known and still speculative mechanisms underlying the inhibitory effects of obesity on GH secretion including peripheral factors like IGF-I and insulin, as well as central hypothalamic/pituitary modulators. We further discuss the basis of current testing for GH deficiency in obesity and the validity of the various provocative tests in overweight subjects.
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PMID:GH/IGF-I regulation in obesity--mechanisms and practical consequences in children and adults. 2019 66


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