The Involvement of Growth Hormone-Binding Protein in Altered GH-IGF Axis in IDDM

Kobayashi, Kenichi; Amemiya, Shin; Kobayashi, Koji; Sawanobori, Emi; Mochizuki, M.; Ishihara, Tsukasa; Higashida, Kosuke; Miura, Masaichi; Nakazawa, Shinpei

doi:10.1507/endocrj.46.suppl_s67

Cited by 3 publications

(1 citation statement)

References 10 publications

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“…Some studies showed that tissue IGF-1 gene expression might be affected by systemic or local factors or both in diabetes, i.e. decrease of GH receptors in target cells and its binding affinity [13] , and by reduced or absent pulsatile pattern secretion of GH, metabolic abnormality of insulin like growth factor binding proteins (IGFBPs) [6,14] , negative nitrogen balance [15,16] etc. All these may probably lead to a decline of IGF-1.…”

Section: Discussionmentioning

confidence: 99%

Expression of liver insulin-like growth factor 1 gene and its serum level in rats with diabetes

Wang²,

Chen³

et al. 2004

WJG

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Section: Discussionmentioning

confidence: 99%

Expression of liver insulin-like growth factor 1 gene and its serum level in rats with diabetes

Wang²,

Chen³

et al. 2004

WJG

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Modulation of the growth hormone–insulin-like growth factor (GH–IGF) axis by pharmaceutical, nutraceutical and environmental xenobiotics: An emerging role for xenobiotic-metabolizing enzymes and the transcription factors regulating their expression. A review

Scarth¹

2006

Xenobiotica

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The growth hormone-insulin-like growth factor (GH-IGF) axis has gained considerable focus over recent years. One cause of this increased interest is due to a correlation of age-related decline in plasma GH/IGF levels with age-related degenerative processes, and it has led to the prescribing of GH replacement therapy by some practitioners. On the other hand, however, research has also focused on the pro-carcinogenic effects of high GH-IGF levels, providing strong impetus for finding regimes that reduce its activity. Whereas the effects of GH/IGF activity on the action of xenobiotic-metabolizing enzyme systems is reasonably well appreciated, the effects of xenobiotic exposure on the GH-IGF axis has not received substantial review. Relevant xenobiotics are derived from pharmaceutical, nutraceutical and environmental exposure, and many of the mechanisms involved are highly complex in nature, not easily predictable from existing in vitro tests and do not always predict well from in vivo animal models. After a review of the human and animal in vivo and in vitro literature, a framework for considering the different levels of direct and indirect modulation by xenobiotics is developed herein, and areas that still require further investigation are highlighted, i.e. the actions of common endocrine disruptors such as pesticides and phytoestrogens, as well as the role of xenobiotic-metabolizing enzymes and the transcription factors regulating their expression. It is anticipated that a fuller appreciation of the existing human paradigms for GH-IGF axis modulation gained through this review may help explain some of the variation in levels of plasma IGF-1 and its binding proteins in the population, aid in the prescription of particular dietary regimens to certain individuals such as those with particular medical conditions, guide the direction of long-term drug/nutraceutical safety trials, and stimulate ideas for future research. It also serves to warn athletes that using compounds touted as performance enhancing because they promote short-term GH release could in fact be detrimental to performance in the long-run.

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Transient outward potassium channel regulation in healthy and diabetic heartsThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 1 of a 2-part Special Issue).

Gallego

Alday

Urrutia

et al. 2009

Can. J. Physiol. Pharmacol.

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Diabetic patients have a higher incidence of cardiac arrhythmias, including ventricular fibrillation and sudden death, and show important alterations in the electrocardiogram, most of these related to the repolarization. In myocytes isolated from diabetic hearts, the transient outward K+ current (Ito) is the repolarizing current that is mainly affected. Type 1 diabetes alters Ito at 3 levels: the recovery of inactivation, the responsiveness to physiologic regulators, and the functional expression of the channel. Diabetes slows down Ito recovery of inactivation because it triggers the switching from fast-recovering Kv4.x channels to the slow-recovering Kv1.4. Diabetic animals also have decreased responsiveness of Ito towards the sympathetic nervous system; thus, the diabetic heart develops a resistance to its physiologic regulator. Finally, diabetes impairs support of various trophic factors required for the functional expression of the channel and reduces Ito amplitude by decreasing the amount of Kv4.2 and Kv4.3 proteins.

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The Involvement of Growth Hormone-Binding Protein in Altered GH-IGF Axis in IDDM

Cited by 3 publications

References 10 publications

Expression of liver insulin-like growth factor 1 gene and its serum level in rats with diabetes

Expression of liver insulin-like growth factor 1 gene and its serum level in rats with diabetes

Modulation of the growth hormone–insulin-like growth factor (GH–IGF) axis by pharmaceutical, nutraceutical and environmental xenobiotics: An emerging role for xenobiotic-metabolizing enzymes and the transcription factors regulating their expression. A review

Transient outward potassium channel regulation in healthy and diabetic heartsThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 1 of a 2-part Special Issue).

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