blacktail

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Currently on a cycle and added igf1 a month ago and I have noticed an increase in the size of my testicles. They where pretty small do to current cycle. Anyone else ever notice this happening to them?
 
Some others have said that here and on other sites I’ve read it , I think we might even have posted a study on this but not positive it’s posted here or if I read it but here it is


<header class="fm-sec" style="font-size: 0.9375em; line-height: 1.8667; font-family: "Archivo Narrow", "Arial Narrow", "Trebuchet MS", ArialMT, Arial, sans-serif; margin-bottom: 0px; color: rgb(0, 0, 0); -webkit-text-size-adjust: 100%;">[h=1]effects of Insulin-like Growth Factor-I on testicular atrophy induced by hypoxia[/h]Fernando Diez-Caballero, Inma Castilla-Cortázar, [...], and Salvador Gonzalez-Barón
Additional article information
</header>[FONT=&quot][h=2]Abstract[/h][h=2]Background[/h]Insulin-like Growth Factor-I (IGF-I) supplementation restores testicular atrophy associated with advanced liver cirrhosis that is a condition of IGF-I deficiency. The aim of this work was to evaluate the effect of IGF-I in rats with ischemia-induced testicular atrophy (AT) without liver disease and consequently with normal serum level of IGF-I.

[h=2]Methods[/h]Testicular atrophy was induced by epinephrine (1, 2 mg/Kg intra-scrotal injection five times per week) during 11 weeks. Then, rats with testicular atrophy (AT) were divided into two groups (n = 10 each): untreated rats (AT) receiving saline sc, and AT+IGF, which were treated with IGF-I (2 μg.100 g b.w.-1.day-1, sc.) for 28d. Healthy controls (CO, n = 10) were studied in parallel. Animals were sacrificed on day 29th. Hypophyso-gonadal axis, IGF-I and IGFBPs levels, testicular morphometry and histopathology, immuno-histochemical studies and antioxidant enzyme activity phospholipid hydroperoxide glutathione peroxidase (PHGPx) were assessed.

[h=2]Results[/h]Compared to controls, AT rats displayed a reduction in testicular size and weight, with histological testicular atrophy, decreased cellular proliferation and transferrin expression, and all of these alterations were slightly improved by IGF-I at low doses. IGF-I therapy increased signifincantly steroidogenesis and PHGPx activity (p < 0.05). Interestingly, plasma IGF-I did not augment in rats with testicular atrophy treated with IGF-I, while IGFBP3 levels, that reduces IGF-I availability, was increased in this group (p < 0.05).

[h=2]Conclusion[/h]In testicular atrophy by hypoxia, condition without IGF-I deficiency, IGF-treatment induces only partial effects. These findings suggest that IGF-I therapy appears as an appropriate treatment in hypogonadism only when this is associated to conditions of IGF-I deficiency (such as Laron Syndrom or liver cirrhosis).


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[FONT=&quot][h=2]Background[/h]Insulin-Like Growth Factor-I (IGF-I) is an anabolic hormone, produced mainly in the liver by GH stimulation [1]. In advanced liver cirrhosis plasma levels of IGF-I are reduced [1] because liver biosynthesis and GH receptor expression in hepatocytes are decreased. Testicular atrophy is a common complication in advanced cirrhosis. Previous results have shown that IGF-I supplementation recovers testicular atrophy associated to experimental cirrhosis [1]. Since advanced cirrhosis is a condition of "IGF-I deficiency" and IGF-I therapy was able to revert testicular atrophy in cirrhotic rats in only three weeks, a direct effect of IGF-I on testes seems to be the most important factor to explain our findings. This idea is supported by the existence of receptors for IGF-I in Sertoli cells, germ cells and Leydig cells [2,3]. Following treatment with exogenous IGF-I patients with Laron dwarfism, a condition of IGF-I deficiency due to the absence of receptors for growth hormone, show an increase in testicular size and serum testosterone levels [4]. Stopping IGF-I administration led to a return of both parameters to the pretreatment situation indicating a specific effect of IGF-I [4].
On the other hand, since IGF-I therapy was also able to improve nutritional status, intestinal absorption and liver function tests [5-9], other factors could contribute to the gonadal improvement observed in these rats with cirrhosis treated with IGF-I.
The aims of the present study were: 1) to go more into the beneficial effects of the mechanisms mediated by IGF-I; and 2) investigate if IGF-I therapy could be an adequate treatment to improve testicular function in other conditions without liver disorder and consequently with normal serum levels of IGF-I.
With these objectives, the present work was carried out using an experimental model of hypoxia-induced testicular atrophy including three groups: healthy controls, untreated rats with testicular atrophy and rats with testicular atrophy treated with low doses of IGF-I during 28 days. Testes histopathology and function, pituitary-gonadal axis and IGF-I and IGFBPs plasma levels were assessed in the three experimental groups.
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[FONT=&quot][h=2]Methods[/h][h=3]Induction of testicular atrophy[/h]Testicular atrophy was induced as previously described [10]. Briefly, male Wistar rats (4 weeks old, 150–160 g) were subjected to 1.2 mg/Kg b.w. five times/week intra-scrotal injections of epinephrine in sterile saline (Sigma), for 11 weeks. Rats were housed in cages placed in a room with 12-hour light-dark cycle and constant humidity and temperature (20°C). Both, food (standard semipurified diet for rodents; B.K. Universal, Sant Vicent del Horts, Spain) and water were given ad libitum. Healthy age-matched control rats were studied in parallel. All experimental procedures were performed in conformity with The Guiding Principles for Research Involving Animals.

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There’s actually another study out there but I haven’t found it yet , but it shows that igf is effective in reversing raisin nuts
 
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