Adipokine Profile and Urinary Albumin Excretion in Isolated Growth Hormone Deficiency

Oliveira, Carla R. P.; Salvatori, Roberto; Meneguz‐Moreno, Rafael Alexandre; Aguiar‐Oliveira, Manuel H.; Pereira, Rossana M. C.; Valença, Eugênia H. A.; Araújo, Vanessa P.; Farias, Natália T.; Silveira, Débora Consuelo Rocha; Vieira, José Gilberto H.; Barreto‐Filho, José Augusto

doi:10.1210/jc.2009-1919

Cited by 35 publications

(24 citation statements)

References 40 publications

(20 reference statements)

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“…ADP could be a potential new target drug for curing fat metabolism disorders (Krakoff et al, 2003). This study demonstrated that ADP levels in adult GHD patients are higher than those in healthy individuals, which corresponds to the conclusion drawn by Oliveira et al (2010). Currently, there is little research on ADP levels in adult GHD patients owing to the small number of subjects, the absence of reference hypophysis hormone levels, and different methods.…”

Section: Discussionsupporting

confidence: 79%

Study of the correlation between growth hormone deficiency and serum leptin, adiponectin, and visfatin levels in adults

Zhang

Gao

et al. 2014

Genet. Mol. Res.

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ABSTRACT. We aimed to determine the significance and changes in leptin, adiponectin (ADP), and visfatin levels in adults with growth hormone deficiency (GHD). Forty adults (19 men, 21 women) who had been diagnosed with GHD comprised the observation group, while 36 healthy adults (18 men, 18 women) were used as the control group. Fasting venous blood was collected to detect leptin, ADP, and visfatin levels. There was no statistically significant difference (P > 0.05) between the GHD group and the control group in terms of gender ratio, age, and body mass index. The waist-to-hip ratio (0.894 ± 0.061 vs 0.830 ± 0.481), cholesterol (4.99 ± 1.046 vs 4.18 ± 0.683), triglyceride (1.97 ± 1.428 vs 1.08 ± 0.403), LDL (2.91 ± 0.980 vs 2.29 ± 0.540), leptin (3.00 ± 1.233 vs 1.89 ± 1.554), ADP (15.26 ± 6.449 vs 10.24 ± 7.608), and visfatin levels (10.42 ± 3.715 vs 5.87 ± 3.90) in the GHD group were significantly higher than those in the control 4051 GHD and leptin, adiponectin, and visfatin ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (2): 4050-4056 (2014) group (all P < 0.05). The levels of growth hormone (1.68 ± 1.67 vs 15.53 ± 6.23), insulin-like growth factor-1 (IGF-1, 22.64 ± 16.41 vs 61.85 ± 28.48), IGF-binding protein-3 (4889 ± 2962 vs 6866 ± 3823), and dehydroepiandrosterone sulfate (1.466 ± 1.804 vs 6.000 ± 2.767) in the GHD group were significantly lower than those in the control group (all P < 0.05). Correlation analysis demonstrated that leptin level was positively correlated to ADP and visfatin in both the GHD and control groups and negatively correlated to IGF-1 (r = 0.332, P < 0.05). Logistic regression analysis demonstrated that leptin, ADP, and visfatin were independent risk factors for adults with GHD.

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Section: Discussionsupporting

confidence: 79%

Study of the correlation between growth hormone deficiency and serum leptin, adiponectin, and visfatin levels in adults

Zhang

Gao

et al. 2014

Genet. Mol. Res.

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“…It has been suggested that a very low level of IGF-I might have a protective role, whereas a milder decrease (as seen in adult-onset GH deficiency) might be noxious (48). In addition, the increase in serum adiponectin (protein influenced by GH level) may contribute to such a beneficial outcome (52). They also exhibit normal urinary albumin excretion.…”

Section: Metabolic and Cardiovascular Consequencesmentioning

confidence: 99%

“…These features have been published in 42 different publications (2,19,22,25,27,29,30,31,32,33,36,37,38,40,41,44,45,46,47,48,49,50,51,52,53,54,56,57,61,62,63,64,66,67,68,74,75,76,77,78,79,80). We have used this experiment of nature to discover 'usual laws of nature' as suggested by William Harvey, and to understand some aspects of more common conditions such as short stature, insulin resistance, diabetes, atherosclerosis, osteoporosis, cancer and ultimately longevity.…”

Section: Introductionmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: The multiple facets of GHRH/GH/IGF-I axis: lessons from lifetime, untreated, isolated GH deficiency due to a GHRH receptor gene mutation

Aguiar‐Oliveira

Souza

Oliveira

et al. 2017

European Journal of Endocrinology

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Twenty years ago, we described kindred of 105 individuals with isolated GH deficiency (IGHD) in Itabaianinha County, in northeast Brazil, carrying a homozygous mutation in the GH-releasing hormone receptor gene. These subjects exhibit markedly reduced GH responsiveness to stimulatory tests, and anterior pituitary hypoplasia. Serum concentrations of IGF-I, IGF binding protein type 3 and the acid-labile subunit are markedly reduced, with a lesser reduction of IGF-II. The most striking physical findings of these IGHD individuals are the proportionate short stature, doll facies, high-pitched voice and visceral obesity with reduced fat-free mass. There is neither microphallus, nor neonatal hypoglycemia. Puberty is delayed, menopause anticipated, but fertility is preserved in both genders. The reduction in bone sizes is not even, with mean standard deviation scores for height of −7.2, total maxillary length of −6.5, total facial height of −4.3 and cephalic perimeter of −2.7. In addition, the non-osseous growth is not uniform, preserving some organs, like pancreas, liver, kidney, brain and eyes, and compromising others such as thyroid, heart, uterus and spleen. These subjects present higher prevalence of dizziness, mild high-tones sensorineural hearing loss, reduction of vascular retinal branching points, increase of optic disk, genu valgum and increased systolic blood pressure. Biochemically, they have high low density lipoprotein cholesterol and C-reactive protein levels, but maintain increased insulin sensitivity, and do not show premature atherosclerosis. Finally, they have normal immune function, and normal longevity. This review details the findings and summarizes 20 years of clinical research carried out in this unique population.

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“…We also found that the number of individuals with atherosclerosis plaques did not further increase with longer follow-up, but in one individual the plaque disappeared, showing that despite some conflicting data (19,20), it is possible not only to reduce vascular wall volume but also to decrease plaques' volume as shown with some lipid-lowering agents (21,22). This occurred despite atherogenic conditions, such as abdominal obesity, increased SBP, LDL, and CRP (8,9,10).…”

Section: Discussionmentioning

confidence: 68%

“…These individuals have very low serum GH and insulin-like growth factor 1 (IGF1), reduced fat-free mass, increased percentage of fat mass, total and LDL, CRP levels, systolic blood pressure (SBP), and waist:hip ratio. Despite these cardiovascular risk factors, they have no premature atherosclerosis, no insulin resistance, and normal longevity (7,8,9,10,11).…”

Section: Introductionmentioning

confidence: 99%

Arrest of atherosclerosis progression after interruption of GH replacement in adults with congenital isolated GH deficiency

Araújo

Aguiar‐Oliveira

Oliveira

et al. 2012

European Journal of Endocrinology

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Objective: GH replacement therapy (GHRT) in adult-onset GH deficiency (AOGHD) reduces carotid intima-media thickness (IMT) and increases myocardial mass, with improvement of systolic and diastolic function. These observations have reinforced the use of GHRT on AOGHD. Conversely, we have previously reported that in adults with lifetime congenital and severe isolated GH deficiency (IGHD) due to a mutation in GHRH receptor gene (GHRHR), a 6-month treatment with depot GH increased carotid IMT, caused the development of atherosclerotic plaques, and an increase in left ventricular mass index (LVMI), posterior wall, and septal thickness and ejection fraction. Such effects persisted 12 months after treatment (12-month washout -12mo). Methods: We have studied the cardiovascular status (by echocardiography and carotid ultrasonography) of these subjects 60 months after completion of therapy (60-month washout -60mo). Results: Carotid IMT reduced significantly from 12 to 60mo, returning to baseline (pre-therapy) value. The number of individuals with plaques was similar at 12 and 60mo, remaining higher than pretherapy. LVMI, relative posterior wall thickness, and septum thickness did not change between 12 and 60mo, but absolute posterior wall increased from 12 to 60mo. Systolic function, evaluated by ejection fraction and shortening fraction, was reduced at 60mo in comparison with 12mo returning to baseline levels. The E/A wave ratio (expression of diastolic function) decreased at 60mo compared with both 12mo and baseline. Conclusions: In adults with lifetime congenital IGHD, the increase in carotid IMT elicited by GHRT was transitory and returned to baseline 5 years after therapy discontinuation. Despite this, the number of subjects with plaques remained stable at 60mo and higher than at baseline. 166 977-982 European Journal of Endocrinology

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Adipokine Profile and Urinary Albumin Excretion in Isolated Growth Hormone Deficiency

Cited by 35 publications

References 40 publications

Study of the correlation between growth hormone deficiency and serum leptin, adiponectin, and visfatin levels in adults

Study of the correlation between growth hormone deficiency and serum leptin, adiponectin, and visfatin levels in adults

MECHANISMS IN ENDOCRINOLOGY: The multiple facets of GHRH/GH/IGF-I axis: lessons from lifetime, untreated, isolated GH deficiency due to a GHRH receptor gene mutation

Arrest of atherosclerosis progression after interruption of GH replacement in adults with congenital isolated GH deficiency

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