Serum Adiponectin Is Reduced in Acromegaly and Normalized after Correction of Growth Hormone Excess

Lam, Karen S.L.; Xu, Aimin; Tan, Kathryn Choon Beng; Wong, L. S. Ling; Tiu, Sau Cheung; Tam, Sidney

doi:10.1210/jc.2003-032023

Cited by 52 publications

(38 citation statements)

References 29 publications

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“…They stated that these results may be due to the small sample size, we confirmed their results with a larger sample size. On the other hand, Lam et al stated that the patients in their study were significantly more insulin resistant and had lower adiponectin levels, which are reversible with GH--lowering therapies [22]. The discrepancies in serum insulin and adiponectin levels in acromegaly patients may be due to the therapy that patients were taking for the control of GH.…”

Section: Discussionmentioning

confidence: 87%

“…Data regarding adiponectin levels in active acromegaly available in the literature is variable as lower than [22], higher than [18] or similar to [19,20] those in normal controls. The effect of GH-reducing therapy on serum adiponectin levels has also been studied [21,22].…”

Section: Discussionmentioning

confidence: 97%

“…The effect of GH-reducing therapy on serum adiponectin levels has also been studied [21,22]. Olarescu et al measured adipokines in 37 patients with active acromegaly before and after treatment.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Adiponectin and Cardiac Hypertrophy in Acromegaly

Gurbulak¹,

Akın²,

Yerlikaya³

et al. 2016

Adv Clin Exp Med

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 97%

See 1 more Smart Citation

Adiponectin and Cardiac Hypertrophy in Acromegaly

Gurbulak¹,

Akın²,

Yerlikaya³

et al. 2016

Adv Clin Exp Med

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“…Obesity and insulin resistance are associated with decreased adiponectin levels (Weyer et al 2001). In acromegaly, with raised GH levels and insulin resistance, adiponectin levels have been reported to be decreased (Lam et al 2004). GH supresses adiponectin secretion in cultured human adipose tissue, and in transgenic mice overexpressing GH adiponectin is decreased, while in GHR K/K mice adiponectin is increased (Nilsson et al 2005).…”

Section: External Regulators Of the Central Gh Axismentioning

confidence: 99%

60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-GH axis: the past 60 years

Murray¹,

Higham²,

Clayton³

2015

Journal of Endocrinology

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At the time of the publication of Geoffrey Harris's monograph on 'Neural control of the pituitary gland' 60 years ago, the pituitary was recognised to produce a growth factor, and extracts administered to children with hypopituitarism could accelerate growth. Since then our understanding of the neuroendocrinology of the GH axis has included identification of the key central components of the GH axis: GH-releasing hormone and somatostatin (SST) in the 1970s and 1980s and ghrelin in the 1990s. Characterisation of the physiological control of the axis was significantly advanced by frequent blood sampling studies in the 1980s and 1990s; the pulsatile pattern of GH secretion and the factors that influenced the frequency and amplitude of the pulses have been defined. Over the same time, spontaneously occurring and targeted mutations in the GH axis in rodents combined with the recognition of genetic causes of familial hypopituitarism demonstrated the key factors controlling pituitary development. As the understanding of the control of GH secretion advanced, developments of treatments for GH axis disorders have evolved. Administration of pituitary-derived human GH was followed by the introduction of recombinant human GH in the 1980s, and, more recently, by long-acting GH preparations. For GH excess disorders, dopamine agonists were used first followed by SST analogues, and in 2005 the GH receptor blocker pegvisomant was introduced. This review will cover the evolution of these discoveries and build a picture of our current understanding of the hypothalamo-GH axis.

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“…Conversely, mice lacking the GH receptor or expressing a GH antagonist have increased circulating levels of this hormone (3). Serum adiponectin levels are reduced in patients with acromegaly and normalized after correction of GH excess (29). Also, patients with high circulating PRL due to prolactinomas have hypoadiponectinemia (9,14).…”

mentioning

confidence: 99%

The modulation of adiponectin by STAT5-activating hormones

White

Maier

Zhao

et al. 2016

American Journal of Physiology-Endocrinology and Metabolism

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White UA, Maier J, Zhao P, Richard AJ, Stephens JM. The modulation of adiponectin by STAT5-activating hormones. Am J Physiol Endocrinol Metab 310: E129 -E136, 2016. First published November 25, 2015 doi:10.1152/ajpendo.00068.2015.-Adiponectin is a hormone secreted from adipocytes that plays an important role in insulin sensitivity and protects against metabolic syndrome. Growth hormone (GH) and prolactin (PRL) are potent STAT5 activators that regulate the expression of several genes in adipocytes. Studies have shown that the secretion of adiponectin from adipose tissue is decreased by treatment with PRL and GH. In this study, we demonstrate that 3T3-L1 adipocytes treated with GH or PRL exhibit a reduction in adiponectin protein levels. Furthermore, we identified three putative STAT5 binding sites in the murine adiponectin promoter and show that only one of these, located at Ϫ3,809, binds nuclear protein in a GH-or PRL-dependent manner. Mutation of the STAT5 binding site reduced PRL-dependent protein binding, and supershift analysis revealed that STAT5A and -5B, but not STAT1 and -3, bind to this site in response to PRL. Chromatin immunoprecipitation (IP) analysis demonstrated that only STAT5A, and not STAT1 and -3, bind to the murine adiponectin promoter in a GH-dependent manner in vivo. Adiponectin promoter/reporter constructs were responsive to GH, and chromatin IP analysis reveals that STAT5 binds the adiponectin promoter in vivo following GH stimulation. Overall, these data strongly suggest that STAT5 activators regulate adiponectin transcription through the binding of STAT5 to the Ϫ3,809 site that leads to decreased adiponectin expression and secretion. These mechanistic observations are highly consistent with studies in mice and humans that have high GH or PRL levels that are accompanied by lower circulating levels of adiponectin.signal transducer and activator of transcription 5 GROWTH HORMONE (GH) is known to have profound effects on adipocyte metabolism (reviewed in Ref. 8), such as attenuating lipogenesis and stimulating lipolysis (35,56). The effects of prolactin (PRL) have been well characterized in mammary tissues, and yet there is also evidence suggesting that this hormone can act within adipose tissue in mice and humans (31, 36) to modulate lipolysis (11,32). It is well known that GH and PRL induce signaling via the JAK/STAT pathway, and STAT5 proteins are potently activated by these hormones (reviewed in Ref. 46). However, few direct molecular targets for the actions of GH and PRL in fat cells have been identified.Multiple lines of evidence suggest that STAT5 proteins can modulate adipocyte function. During differentiation of 3T3-L1 adipocytes, the expression levels of STAT5A and -5B are highly induced (50). In addition, GH-dependent adipogenesis of 3T3-F442A cells is attenuated by STAT5 antisense oligonucleotides (58), and constitutively active STAT5 can replace the requirement for GH in adipogenesis of these cells (48). Moreover, ectopic expression of STAT5A has been shown to confer adipogenes...

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Serum Adiponectin Is Reduced in Acromegaly and Normalized after Correction of Growth Hormone Excess

Cited by 52 publications

References 29 publications

Adiponectin and Cardiac Hypertrophy in Acromegaly

Adiponectin and Cardiac Hypertrophy in Acromegaly

60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-GH axis: the past 60 years

The modulation of adiponectin by STAT5-activating hormones

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