The Metabolic Profile in Active Acromegaly is Gender-Specific

Ciresi, Alessandro; Amato, Marco; Pivonello, Rosario; Nazzari, Erica; Grasso, Ludovica F. S.; Minuto, Francesco; Ferone, Diego; Colao, A

doi:10.1210/jc.2012-2896

Cited by 59 publications

(47 citation statements)

References 48 publications

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“…as also observed in other endocrine diseases, such as acromegaly, prolactinoma and diabetes (28,29,30,31). However, despite this evidence, the VAI in CS has a strong application limit.…”

Section: Discussionmentioning

confidence: 81%

Is diabetes in Cushing's syndrome only a consequence of hypercortisolism?

Giordano

Guarnotta

Pivonello

et al. 2014

European Journal of Endocrinology

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Objective: Diabetes mellitus (DM) is one of the most frequent complications of Cushing's syndrome (CS). The aim of this study was to define the changes in insulin sensitivity and/or secretion in relation to glucose tolerance categories in newly diagnosed CS patients. Design: Cross-sectional study on 140 patients with CS. Methods: A total of 113 women (80 with pituitary disease and 33 with adrenal disease, aged 41.7G15.7 years) and 27 men (19 with pituitary disease and eight with adrenal disease, aged 38.1G20.01 years) at diagnosis were divided according to glucose tolerance into normal glucose tolerance (CS/NGT), impaired fasting glucose and/or impaired glucose tolerance (CS/prediabetes), and diabetes (CS/DM) groups. Results: Seventy-one patients had CS/NGT (49.3%), 26 (18.5%) had CS/prediabetes and 43 (30.8%) had CS/DM. Significant increasing trends in the prevalence of family history of diabetes (P!0.001), metabolic syndrome (P!0.001), age (P!0.001) and waist circumference (PZ0.043) and decreasing trends in HOMA-b (P!0.001) and oral disposition index (DIo) (P!0.002) were observed among the groups. No significant trends in fasting insulin levels, area under the curve for insulin (AUC INS ), Matsuda index of insulin sensitivity (ISI-Matsuda) and visceral adiposity index were detected. Conclusions: Impairment of glucose tolerance is characterized by the inability of b-cells to adequately compensate for insulin resistance through increased insulin secretion. Age, genetic predisposition and lifestyle, in combination with the duration and degree of hypercortisolism, strongly contribute to the impairment of glucose tolerance in patients with a natural history of CS. A careful phenotypic evaluation of glucose tolerance defects in patients with CS proves useful for the identification of those at a high risk of metabolic complications.

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“…as also observed in other endocrine diseases, such as acromegaly, prolactinoma and diabetes (28,29,30,31). However, despite this evidence, the VAI in CS has a strong application limit.…”

Section: Discussionmentioning

confidence: 81%

Is diabetes in Cushing's syndrome only a consequence of hypercortisolism?

Giordano

Guarnotta

Pivonello

et al. 2014

European Journal of Endocrinology

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“…In addition, in healthy subjects fat distribution and function, represented by the VAI, have been found to be correlated with GH levels [10] and these data confirm the close interrelation between adiposity and the GH axis [11]. The application of the VAI in particular populations of patients with endocrine diseases characterized by a variable degree of cardiometabolic risk, such as acromegaly, polycystic ovary syndrome, type 2 diabetes and prolactinoma, has produced interesting results [12][13][14][15][16]. These have led to the hypothesis that the VAI could be considered as a marker of adipose tissue dysfunction [17].…”

Section: Introductionmentioning

confidence: 66%

The visceral adiposity index is associated with insulin sensitivity and IGF-I levels in adults with growth hormone deficiency

2016

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The visceral adiposity index, based on anthropometric and metabolic parameters, has been shown to be related to adipose tissue function and insulin sensitivity. We aimed to evaluate the performance of the visceral adiposity index in adult patients with growth hormone deficiency. We enrolled 52 patients(mean age 51 ± 13 years) with newly diagnosed growth hormone deficiency and 50 matched healthy subjects as controls at baseline. At baseline and after 12 and 24 months of treatment we evaluated anthropometric measures, lipid profile, glucose and insulin during an oral glucose tolerance test, hemoglobin A1c, homeostasis model assessment estimate of insulin resistance, quantitative insulin sensitivity check index, insulin sensitivity index Matsuda, insulin-like growth factor-I and visceral adiposity index. At baseline growth hormone deficiency patients showed higher waist circumference (p < 0.001), low-density lipoprotein cholesterol (p < 0.001) and visceral adiposity index (p = 0.003) with lower insulin sensitivity index (p = 0.007) and high-density lipoprotein cholesterol (p = 0.001) than controls. During growth hormone treatment we observed a significant increase in insulin-like growth factor-I (p < 0.001), high-density lipoprotein (p < 0.001) with a trend toward increase in insulin sensitivity index (p = 0.055) and a significant decrease in total cholesterol (p < 0.001) and visceral adiposity index (p < 0.001), while no significant changes were observed in other clinical and metabolic parameters. The visceral adiposity index was the only parameter that significantly correlated with growth hormone peak at diagnosis (p < 0.001) and with insulin-like growth factor-I and insulin sensitivity index both at diagnosis (p = 0.009 and p < 0.001) and after 12 (p = 0.026 and p = 0.001) and 24 months (p < 0.001 and p = 0.001) of treatment. The visceral adiposity index, which has shown to be associated with both insulin-like growth factor-I and insulin sensitivity, proved to be the most reliable index of metabolic perturbation, among the most common indexes of adiposity assessment and a marker of benefit during treatment in adult growth hormone deficiency patients.

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“…In this study, as expected, uncontrolled or untreated patients showed a worse metabolic profile, with lower insulin sensitivity, worse lipid profile and higher visceral adiposity index. We already previously demonstrated that active acromegaly is strongly associated with visceral adiposity dysfunction [4,19] and that both SA and SU treatment are able to improve it, as demonstrated by the significant VAI decrease after 12 months of therapy [20]. The alteration in visceral adiposity, both in excess and in deficiency, has been shown to be a main determinant of insulin resistance in non-acromegalic patients [21,22] and this relationship is mediated by adipokine secretion that may modulate insulin sensitivity [23].…”

Section: Discussionmentioning

confidence: 98%

Serum visfatin levels in acromegaly: Correlation with disease activity and metabolic alterations

Ciresi

Amato

Pizzolanti

2015

Growth Hormone & IGF Research

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Objective: The studies that have extensively evaluated the relation between adipokines and metabolic parameters in acromegaly treatment are quite discordant. We aimed to evaluate and correlate a set of selected adipokines, known to have a metabolic role, with the disease activity, metabolic status and treatment modalities. ND patients showed higher VAI, triglycerides, Homa-IR, and visfatin and lower ISI Matsuda, M-value, and leptin compared to other groups (all p b 0.050), while no differences were found among SA, PE and SU patients. IGF-1 (p = 0.048), M-value (p = 0.0029) and VAI (p = 0.010) were independently associated with visfatin, while only ISI Matsuda (p = 0.019) was associated with leptin. Conclusions: In acromegaly visfatin could be considered a useful index of disease activity and metabolic alterations, such as insulin resistance and adipose dysfunction, regardless of the type of treatment.

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The Metabolic Profile in Active Acromegaly is Gender-Specific

Cited by 59 publications

References 48 publications

Is diabetes in Cushing's syndrome only a consequence of hypercortisolism?

Is diabetes in Cushing's syndrome only a consequence of hypercortisolism?

The visceral adiposity index is associated with insulin sensitivity and IGF-I levels in adults with growth hormone deficiency

Serum visfatin levels in acromegaly: Correlation with disease activity and metabolic alterations

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