Effects of 22K or 20K Human Growth Hormone on Lipolysis, Leptin Production in Adipocytes in the Presence and Absence of Human Growth Hormone Binding Protein

Asada, Nobuhiko; Takahashi, Yuka; Honjo, Masaru

doi:10.1159/000053260

Cited by 12 publications

(9 citation statements)

References 16 publications

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“…Of interest, this increase in leptin synthesis can be reversed by TZD treatment in humans [123]. Furthermore, potent down-regulation of leptin secretion by growth hormone in 3T3-L1 adipocytes overexpressing the human growth hormone receptor has been shown (Table 1) [124]. In a clinical context, leptin concentrations are increased in subjects with growthhormone deficiency [125,126] and are lower in acromegaly [127,128].…”

Section: Leptinmentioning

confidence: 99%

Regulation of adipocytokines and insulin resistance

2003

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It has long been known that obesity and insulin resistance are linked. Recently, it has been shown that adipocytes secrete several proteins including tumour necrosis factor-α, interleukin-6, resistin, and adiponectin. Since several of these so-called adipocytokines influence insulin sensitivity and glucose metabolism profoundly, they might provide a molecular link between increased adiposity and impaired insulin sensitivity. Thiazolidinediones which decrease insulin resistance and are used in the treatment of Type 2 diabetes seem to mediate part of their insulin-sensitising effects via modulation of adipocytokine expression.Furthermore, hormones such as β-adrenergic agonists, insulin, glucocorticoids, and growth hormone might impair insulin sensitivity at least in part via up-regulation or down-regulation of adipocytokine synthesis. We summarise the current knowledge on how major adipocyte-secreted proteins are regulated by hormones and drugs influencing insulin sensitivity and discuss its implications for insulin resistance and obesity. [Diabetologia (2003[Diabetologia ( ) 46:1594[Diabetologia ( -1603

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Section: Leptinmentioning

confidence: 99%

Regulation of adipocytokines and insulin resistance

2003

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“…The following morning, fresh low-serum (0.1%) medium was added, and experiments were performed by treating cells for 120 min with 20 ml of PBS (CON), 100 ng/ml IL-6 (IL-6), or 100 ng/ml IL-6 with the addition of 0.1 ug/ml dexamethasone (SigmaAldrich, Castle Hill, Australia) and 10 ng/ml growth hormone (Genotropin; Pharmacia). The concentrations of these latter treatments were based on previous studies (1,31). Medium was collected from triplicate cell incubations and frozen for subsequent glycerol analysis, using an enzymatic assay linked to NADH with fluorometric detection.…”

Section: Cell Culture Experimentsmentioning

confidence: 99%

Acute IL-6 treatment increases fatty acid turnover in elderly humans in vivo and in tissue culture in vitro

Petersen¹,

Carey²,

Sacchetti³

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

265

229

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. Acute IL-6 treatment increases fatty acid turnover in elderly humans in vivo and in tissue culture in vitro. Am J Physiol Endocrinol Metab 288: E155-E162, 2005. First published September 21, 2004; doi:10.1152/ ajpendo.00257.2004.-To determine whether IL-6 increases lipolysis and fat oxidation in patients with type 2 diabetes and/or whether it exerts this effect independently of changes to the hormonal milieu, patients with type 2 diabetes (D) and healthy control subjects (CON) underwent recombinant human (rh)IL-6 infusion for 3 h. Rates of appearance (Ra) and disappearance (Rd) of [U-13 C]palmitate and [6,6-2 H2]glucose were determined. rhIL-6 infusion increased (P Ͻ 0.05) palmitate Ra and Rd in a similar fashion in both groups. Neither plasma glucose concentration nor glucose Ra/Rd was affected by rhIL-6 infusion in either group, whereas rhIL-6 infusion resulted in a reduction (P Ͻ 0.05) in circulating insulin in D. Plasma growth hormone (GH) was increased (P Ͻ 0.05) by IL-6 in CON, and cortisol increased (P Ͻ 0.05) in response to IL-6 in both groups. To determine whether IL-6 was exerting its effect directly or through activation of these hormones, we performed cell culture experiments. Fully differentiated 3T3-L1 adipocytes were treated with PBS (control) IL-6, or IL-6 plus dexamethasone and GH. IL-6 treatment alone increased (P Ͻ 0.05) lipolysis, but this effect was reduced by the addition of dexamethasone and GH such that IL-6 plus dexamethasone and GH had blunted (P Ͻ 0.05) lipolysis compared with IL-6 alone. To assess whether IL-6 increases fat oxidation, L6 myotubes were treated with PBS (Control), IL-6, or AICAR, a compound known to increase lipid oxidation. Both IL-6 and AICAR markedly increased (P Ͻ 0.05) oxidation of [ 14 C]palmitate compared with Control. Acute IL-6 treatment increased fatty acid turnover in D patients as well as healthy CON subjects. Moreover, IL-6 appears to be activating lipolysis independently of elevations in GH and/or cortisol and appears to be a potent catalyst for fat oxidation in muscle cells. cytokines; metabolism; insulin sensitivity THE CYTOKINE INTERLEUKIN-6 (IL-6) has traditionally been known for its immunomodulatory effects, but recent research has focused on its metabolic role in the etiology of obesity and type 2 diabetes. Studies have demonstrated that acute IL-6 administration can alter fat metabolism and lipolysis. We (28) and others (13) have demonstrated that the infusion of recombinant human (rh)IL-6 into healthy humans increases whole body lipolysis and free fatty acid (FFA) oxidation. In addition, Wallenius et al. (30) recently demonstrated that an IL-6 knockout mouse became obese, a phenotype which was partially reduced with IL-6 treatment. Hence, it has been suggested that IL-6 is a possible target therapy for obesity-related disorders (30). In line with altered fatty acid metabolism, the effect of IL-6 on insulin sensitivity is not completely clear, since a number of both in vitro and in vivo studies have demonstrated that IL-6 decreases (3,10,11,18,2...

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“…In vitro studies have shown that GHBP inhibits GH effects, regarding GH binding to GHR, as well as lipolysis, cell proliferation and IGF-I generation [81][82][83][84][85][86]. In contrast GHBP regulates GHR gene transcription in a human hepatoma cell line in a bidirectional manner: with low GHBP concentrations (50 pM) GH receptor gene transcription was increased, whereas high concentrations (500 pM) reduced GHR gene expression [87].…”

Section: Functional Roles Of Ghbpmentioning

confidence: 99%

“…In adult GHD patients a negative correlation has been described between GH responsiveness (as measured by increase in lean body mass) and levels of GHBP [233]. The underlying mechanism could be an inverse correlation between GH receptor availability in visceral fat and GHBP levels, or an inhibitory effect of GHBP on GH action as suggested from in vitro studies [81][82][83][84]86]. In GHD children GHBP levels have been shown to correlate positively to growth velocity during GH treatment [139], whereas in healthy children growth correlated inversely with GHBP levels [137].…”

Section: Adipose Tissuementioning

confidence: 99%

Physiology and pathophysiology of growth hormone-binding protein: Methodological and clinical aspects

Fisker

2006

Growth Hormone & IGF Research

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Effects of 22K or 20K Human Growth Hormone on Lipolysis, Leptin Production in Adipocytes in the Presence and Absence of Human Growth Hormone Binding Protein

Cited by 12 publications

References 16 publications

Regulation of adipocytokines and insulin resistance

Regulation of adipocytokines and insulin resistance

Acute IL-6 treatment increases fatty acid turnover in elderly humans in vivo and in tissue culture in vitro

Physiology and pathophysiology of growth hormone-binding protein: Methodological and clinical aspects

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