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title="Dismiss find">✘</a></nav><nav id="jr-fip-info-p"><a id="jr-fip-prev" class="wsprkl btn" title="Jump to previuos match">◀</a><button id="jr-fip-matches">no matches yet</button><a id="jr-fip-next" class="wsprkl btn" title="Jump to next match">▶</a></nav></nav></div><div id="jr-epub-interstitial" class="hidden"></div><div id="jr-content"><article data-type="main"><div class="main-content lit-style" itemscope="itemscope" itemtype="http://schema.org/CreativeWork"><div class="meta-content fm-sec"><div class="fm-sec"><h1 id="_NBK222181_"><span class="title" itemprop="name">Yoda and the fountain of youth?</span></h1><div class="subtitle whole_rhythm">The many hats of IGF-1</div><p class="contribs">Dean L.</p><p class="fm-aai"><a href="#_NBK222181_pubdet_">Publication Details</a></p></div></div><div class="jig-ncbiinpagenav body-content whole_rhythm" data-jigconfig="allHeadingLevels: ['h2'],smoothScroll: false" itemprop="text"><p>Insulin growth factor (IGF-1) is on the World Anti-Doping Agency list of banned
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substances. In children, IGF-1 is important for growth, and in adults, it continues to
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have anabolic effects. Although data are lacking for humans, animal studies have shown
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that IGF-1 can increase muscle mass and speed up healing of injured tendons (<a class="bibr" href="#cb41Yoda.REF.1" rid="cb41Yoda.REF.1 cb41Yoda.REF.2">1, 2</a>).</p><p>IGF-1 also appears to play a part in the aging process. It has long been known that one
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of the causes of short stature, or dwarfism, is a lack of the IGF-1 hormone in
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childhood. And now it appears that IGF-1 deficiency also influences longevity.</p><p>The <i>C. elegans</i> worm can live for twice as long if it is genetically
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engineered to have a mutation in <i>daf-2</i> (equivalent to
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<i>IGF-1</i> receptor in humans) (<a class="bibr" href="#cb41Yoda.REF.3" rid="cb41Yoda.REF.3">3</a>). And Yoda, a dwarf mouse, lived twice as long as
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normal laboratory mouse. With Princess Leia (his cage mate) for company, Yoda lived long
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enough to celebrate his 4<sup>th</sup> birthday (<a class="bibr" href="#cb41Yoda.REF.1" rid="cb41Yoda.REF.1">1</a>).</p><p>
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</p><div id="cb41Yoda.Fa" class="figure bk_fig"><div class="graphic"><img src="/books/NBK222181/bin/cb41Yoda-Image001.jpg" alt="Yoda, a Snell dwarf mouse (left), sniffing his cage-mate, Princess Leia (right)" /></div><div class="caption"><p>Yoda, a Snell dwarf mouse (left), sniffing his cage-mate, Princess Leia (right).
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Dwarf mice are usually caged with normal-sized mice to help them to keep warm. <br />Photo credit: Richard Miller, University of Michigan Medical School</p></div></div><p>Dwarf mice, like the long-living worms, lack IGF-1. These mice are commonly used to study
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the effects of aging and there are three main types. The Snell and Ames dwarf mice have
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been bred to inherit mutations in <i>Pit-1</i> and <i>Prop1</i>
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genes, respectively, which disrupt the embryonic development of the pituitary gland. As
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a result, both types of mice lack multiple hormones, including growth hormone,
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prolactin, and thyroid stimulating hormone.</p><p>The third type of dwarf mouse, the Laron dwarf, is a knock-out mouse model. This mouse
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has a targeted gene deletion of either the growth hormone receptor (GHR-KO) or the
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growth hormone binding protein (GHBP-KO). So even though this mouse produces growth
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hormone, it is still growth-restricted because it is unable to respond to it (<a class="bibr" href="#cb41Yoda.REF.4" rid="cb41Yoda.REF.4">4</a>). </p><p>Dwarf mice all share non-detectable levels of IGF-1 because one of the main actions of
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growth hormone is to stimulate the production of IGF-1. Interestingly, in addition to
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their small size, these mice also have reduced glucose and insulin levels, a lower
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incidence of tumors, and a longer average and maximum lifespan. In fact, their lifespan
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is increased by about 40% (<a class="bibr" href="#cb41Yoda.REF.4" rid="cb41Yoda.REF.4 cb41Yoda.REF.5">4,
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5</a>).</p><div class="figure"><div class="mp-outer"><div class="ncbimedia" id="_bk_plyr_cb41tutorial"><video preload="none" poster="/books/NBK222181/bin/cb41slide.jpg" height="360" width="428"><source src="/books/NBK222181/bin/cb41tutorial-pmcvs_normal.flv" type="video/flash"></source><source src="/books/NBK222181/bin/cb41tutorial-pmcvs_normal.mp4" type="video/mp4"></source><source src="/books/NBK222181/bin/cb41tutorial-pmcvs_normal.webm" type="video/webm"></source></video></div></div><div class="half_rhythm"><a href="/books/NBK222181/bin/cb41tutorial.mp4">Download</a> video file.<sup>(196M, mp4)</sup></div></div><p>Such mouse models are useful, but is there a similar link between IGF-1 deficiency and
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long-life seen in humans? Individuals with Laron syndrome have been helping to provide
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this answer. Laron syndrome, also known as primary growth hormone insufficiency, is
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caused by a mutation in the growth hormone receptor gene. A variety of different
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mutations have been identified, and most affect the extracellular region of the receptor
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that contains the growth hormone binding site. Affected individuals are typically less
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than 4 feet tall, but if they are given IGF-1 before puberty, they may grow taller
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(<a class="bibr" href="#cb41Yoda.REF.6" rid="cb41Yoda.REF.6 cb41Yoda.REF.7">6, 7</a>). </p><p>In southern Ecuador, there is a village where more than 250 individuals are thought to
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have Laron syndrome, and this community has been well-studied. The results have been
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surprising. For example, Laron patients appear to be protected against developing
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cancer, a disease that is associated with aging (<a class="bibr" href="#cb41Yoda.REF.8" rid="cb41Yoda.REF.8">8</a>). Unfortunately, this apparent protection by IGF-1
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deficiency does not translate to a longer life span compared to the general population
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(<a class="bibr" href="#cb41Yoda.REF.9" rid="cb41Yoda.REF.9">9</a>). One factor may be a higher
|
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death rate from causes of death that are not related to age, such as trauma and
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alcoholism (<a class="bibr" href="#cb41Yoda.REF.10" rid="cb41Yoda.REF.10">10</a>). </p><p>So, could targeting IGF-1 be a pathway to the elixir of youth? We know that a certain
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level of GH and IGF-1 is required for the functioning of the heart and other organs, and
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the level of these hormones declines with age. However, GH and IGF-1 are oncogenes, and
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using IGF-1 as a treatment for individuals who do not have a genetic deficiency might
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lead to unexpected and harmful outcomes (<a class="bibr" href="#cb41Yoda.REF.11" rid="cb41Yoda.REF.11">11</a>). </p><p>What is clear is that extending the life of any organism, from worm to human, is an
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incredibly complex process, involving many pathways, and potentially many drug targets.
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And although IGF-1 may be one of these targets, knowing how to use this treatment safely
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and effectively remains a long way away.</p><div id="cb41Yoda.Acknowledgments"><h2 id="_cb41Yoda_Acknowledgments_">Acknowledgments</h2><p>The author would like to thank Zvi Laron, Professor Emeritus of Pediatric
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Endocrinology, Tel Aviv University, for reviewing this summary.</p></div><div id="cb41Yoda.References"><h2 id="_cb41Yoda_References_">References</h2><dl class="temp-labeled-list"><dl class="bkr_refwrap"><dt>1.</dt><dd><div class="bk_ref" id="cb41Yoda.REF.1">Pobojewski, S. <em>World's
|
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oldest mouse reaches milestone birthday</em>. The University Record
|
|
[Online ] May 1, 2014]; Available from: <a href="http://www.ur.umich.edu/0304/Apr19_04/26.shtml" ref="pagearea=cite-ref&targetsite=external&targetcat=link&targettype=uri">http://www<wbr style="display:inline-block"></wbr>​.ur.umich.edu<wbr style="display:inline-block"></wbr>​/0304/Apr19_04/26.shtml</a>.</div></dd></dl><dl class="bkr_refwrap"><dt>2.</dt><dd><div class="bk_ref" id="cb41Yoda.REF.2">Kurtz C.A., et al. Insulin-like growth factor I accelerates
|
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functional recovery from Achilles tendon injury in a rat
|
|
model. <span><span class="ref-journal">Am J Sports
|
|
Med. </span>1999;<span class="ref-vol">27</span>(3):363–9.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/10352775" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 10352775</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>3.</dt><dd><div class="bk_ref" id="cb41Yoda.REF.3">Chen D., et al. Germline signaling mediates the
|
|
synergistically prolonged longevity produced by double mutations in
|
|
daf-2 and rsks-1 in C. elegans. <span><span class="ref-journal">Cell
|
|
Rep. </span>2013;<span class="ref-vol">5</span>(6):1600–10.</span> [<a href="/pmc/articles/PMC3904953/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC3904953</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/24332851" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 24332851</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>4.</dt><dd><div class="bk_ref" id="cb41Yoda.REF.4">Bartke A., Brown-Borg H. Life extension in the dwarf
|
|
mouse. <span><span class="ref-journal">Curr Top Dev
|
|
Biol. </span>2004;<span class="ref-vol">63</span>:189–225.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/15536017" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 15536017</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>5.</dt><dd><div class="bk_ref" id="cb41Yoda.REF.5">Flurkey K., et al. Lifespan extension and delayed immune and
|
|
collagen aging in mutant mice with defects in growth hormone
|
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production. <span><span class="ref-journal">Proc Natl Acad Sci U S
|
|
A. </span>2001;<span class="ref-vol">98</span>(12):6736–41.</span> [<a href="/pmc/articles/PMC34422/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC34422</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/11371619" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 11371619</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>6.</dt><dd><div class="bk_ref" id="cb41Yoda.REF.6">Savage M.O., et al. Endocrine assessment, molecular
|
|
characterization and treatment of growth hormone insensitivity
|
|
disorders. <span><span class="ref-journal">Nat Clin Pract Endocrinol
|
|
Metab. </span>2006;<span class="ref-vol">2</span>(7):395–407.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/16932322" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 16932322</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>7.</dt><dd><div class="bk_ref" id="cb41Yoda.REF.7">Laron, Z., Kopchick, J.
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(Eds.), <em>Laron Syndrome - From Man to Mouse. Lessons from Clinical
|
|
and Experimental Experience</em>. 2011: Springer.</div></dd></dl><dl class="bkr_refwrap"><dt>8.</dt><dd><div class="bk_ref" id="cb41Yoda.REF.8">Steuerman R., Shevah O., Laron Z. Congenital IGF1 deficiency tends to confer
|
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protection against post-natal development of
|
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malignancies. <span><span class="ref-journal">Eur J
|
|
Endocrinol. </span>2011;<span class="ref-vol">164</span>(4):485–9.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/21292919" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 21292919</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>9.</dt><dd><div class="bk_ref" id="cb41Yoda.REF.9">Aguiar-Oliveira M.H., et al. Longevity in untreated congenital growth
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hormone deficiency due to a homozygous mutation in the GHRH receptor
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gene. <span><span class="ref-journal">J Clin Endocrinol
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Metab. </span>2010;<span class="ref-vol">95</span>(2):714–21.</span> [<a href="/pmc/articles/PMC2840870/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC2840870</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/19965916" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 19965916</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>10.</dt><dd><div class="bk_ref" id="cb41Yoda.REF.10">Laron Z. The GH-IGF1 axis and longevity. The paradigm
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of IGF1 deficiency. <span><span class="ref-journal">Hormones
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(Athens). </span>2008;<span class="ref-vol">7</span>(1):24–7.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/18359741" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 18359741</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>11.</dt><dd><div class="bk_ref" id="cb41Yoda.REF.11">Werner, H., Attias-Geva, Z.,
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Bentov, I., Sarfstein, R., Schayek, H., Weinstein, D., Bruchim, I.,
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<em>Cancer Genes, Tumor Suppressors, and Regulation of IGF1-R Gene
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Expression in Cancer</em>, in <em>Insulin-like Growth Factors
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and Cancer: From Basic Biology to Therapeutics</em>, D.E. LeRoith,
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Editor. 2012, Springer Science. p. p159-177.</div></dd></dl></dl></div><div style="display:none"><div style="display:none" id="figcb41YodaFa"><img alt="Image cb41Yoda-Image001" src-large="/books/NBK222181/bin/cb41Yoda-Image001.jpg" /></div></div><div id="bk_toc_contnr"></div></div></div><div class="fm-sec"><h2 id="_NBK222181_pubdet_">Publication Details</h2><h3>Author Information and Affiliations</h3><p class="contrib-group"><h4>Authors</h4><span itemprop="author">Laura Dean</span>, MD<sup>1</sup>.</p><h4>Affiliations</h4><div class="affiliation"><sup>1</sup> NCBI<div><span class="email-label">Email: </span><a href="mailto:dev@null" data-email="vog.hin.mln.ibcn@naed" class="oemail">vog.hin.mln.ibcn@naed</a></div></div><h3>Publication History</h3><p class="small">Created: <span itemprop="datePublished">July 21, 2014</span>.</p><h3>Copyright</h3><div><div class="half_rhythm"><a href="/books/about/copyright/">Copyright Notice</a></div></div><h3>Publisher</h3><p><a href="http://www.ncbi.nlm.nih.gov/" ref="pagearea=page-banner&targetsite=external&targetcat=link&targettype=publisher">National Center for Biotechnology Information (US)</a>, Bethesda (MD)</p><h3>NLM Citation</h3><p>Dean L. Yoda and the fountain of youth?The many hats of IGF-1. 2014 Jul 21. In: Dean L, McEntyre J, editors. Coffee Break: Tutorials for NCBI Tools [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 1999-. <span class="bk_cite_avail"></span></p></div><div class="small-screen-prev"><a href="/books/n/coffeebrk/cb42_copper/?report=reader"><svg xmlns="http://www.w3.org/2000/svg" viewBox="0 0 100 100" preserveAspectRatio="none"><path d="M75,30 c-80,60 -80,0 0,60 c-30,-60 -30,0 0,-60"></path><text x="20" y="28" textLength="60" style="font-size:25px">Prev</text></svg></a></div><div class="small-screen-next"><a href="/books/n/coffeebrk/cb40LDL/?report=reader"><svg xmlns="http://www.w3.org/2000/svg" viewBox="0 0 100 100" preserveAspectRatio="none"><path d="M25,30c80,60 80,0 0,60 c30,-60 30,0 0,-60"></path><text x="20" y="28" textLength="60" style="font-size:25px">Next</text></svg></a></div></article><article data-type="fig" id="figobcb41YodaFa"><div id="cb41Yoda.Fa" class="figure bk_fig"><div class="graphic"><img data-src="/books/NBK222181/bin/cb41Yoda-Image001.jpg" alt="Yoda, a Snell dwarf mouse (left), sniffing his cage-mate, Princess Leia (right)" /></div><div class="caption"><p>Yoda, a Snell dwarf mouse (left), sniffing his cage-mate, Princess Leia (right).
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Dwarf mice are usually caged with normal-sized mice to help them to keep warm. <br />Photo credit: Richard Miller, University of Michigan Medical School</p></div></div></article></div><div id="jr-scripts"><script src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/libs.min.js"> </script><script src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/jr.min.js"> </script><script type="text/javascript">
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