![]() It acts by blocking the AR sites and prevents translocation of the hormone receptor complex to the nucleus. It has no androgenic, estrogenic, antiestrogenic or progestogenic activity. A selective antagonist of the AR is flutamide (Flu), which is a synthetic non-steroidal antiandrogen. Antiandrogens or AR antagonists block the receptor and prevent androgens from expressing their function. However, DHT has a higher affinity to the receptor than testosterone. Both testosterone and DHT bind to the androgen receptor (AR) and activate it. It is metabolized from testosterone by the enzyme 5-alpha-reductase. Dihydrotestosterone (DHT) is the main metabolite of testosterone. It controls the masculinization of the genital and the brain. Testosterone is the major male sex hormone and the dominant androgen. However, there are strong surges during prenatal development and puberty, which are critical periods for the sexual differentiation of the brain. Sex hormones are produced throughout the whole life. Based on their exposure time prenatal and postnatal sex hormone effects can be distinguished. Sex hormones comprise androgens, estrogens and progestogens. The constitution of the brain and an individual’s behavior are strongly influenced by sex hormones. These findings demonstrate that prenatal androgen activity is involved in the development of body morphology and might be a useful marker for prenatal androgen exposure. We tested mice for handedness, but did not find a significant effect of the prenatal treatment. Another factor that is thought to be influenced by early androgens is handedness. We also measured other parameters, such as head size, body length and tail length and demonstrate that body morphology is affected by prenatal androgen exposure with more prominent effects in females. In males treated with DHT, the 2D:4D ratio was increased, while flutamide-treatment in females led to a reduced 2D:4D ratio. In addition to that, also total paw length and the 2D:4D ratio was affected. ![]() Here we show in a mouse model that experimental manipulation of the prenatal androgen level, by blocking the androgen receptor with flutamide or activating the androgen receptor with dihydrotestosterone (DHT), leads to changes in the length of the fingers of all paws in males and females. ![]() Especially the second-to-fourth finger length (2D:4D) ratio has been implicated to be modified when exposed to higher androgen levels in utero. It has been suggested that prenatal sex hormones affect adult morphological parameters, such as the finger length. ![]() Based on this evidence, we suggest that the digit ratio can predict adult penile size and that the effects of prenatal testosterone may in part explain the differences in adult penile length.Prenatal sex hormones exert organizational effects. Univariate and multivariate analysis using linear regression models showed that only height was a significant predictive factor for flaccid penile length (univariate analysis: r=0.185, P=0.026 multivariate analysis: r=0.172, P=0.038) and that only digit ratio was a significant predictive factor for stretched penile length (univariate analysis:r=-0.216, P=0.009 multivariate analysis: r=-0.201, P=0.024 stretched penile length=-9.201×digit ratio + 20.577). Under anaesthesia, flaccid and stretched penile lengths were measured by another investigator who did not measure nor have any the information regarding the digit lengths. Right-hand second- and fourth-digit lengths were measured by a single investigator prior to measurement of penile length. Korean men who were hospitalized for urological surgery at a single tertiary academic centre were examined in this study, and 144 men aged 20 years or older who gave informed consent were prospectively enrolled. In this study, we investigated the relationship between digit ratio and penile length. Both prenatal testosterone and the AR play a central role in penile growth. The second to fourth digit ratio (2D:4D) has been proposed as a putative biomarker for prenatal testosterone and covaries with the sensitivity of the androgen receptor (AR).
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