The effect of Type 1 diabetes on the reproductive endocrine axis can be conceptualized as anorexia-like hypothalamic anovulation. Diabetic women with low BMI are most likely to have menstrual irregularities. There are katabolic procedures in young diabetic girls and dietary constraint leads to intracellular starvation, particularly before the diagnosis and starting insulin treatment. This may consequently cause disruption in hypothalamic pulsetile secretion of gonadotrophin-releasing hormonal agent (GnRH), with a resultant decline in gonadotropins secretion.
In diabetic animal studies conducted by Johnson and Sidman in 1979, it appeared that the main etiologic elements associated with impaired hypothalamus– pituitary function were certainly insufficient release of GnRH and/or decrease in the level of sensitivity of the pituitary gland to GnRH. Studies in women by Djursing et al. in 1983 and 1985 found lower basal levels of luteinizing hormone (LH) in Type 1 diabetic patients with amenorrhea, and revealed different reactions of LH to exogenous GnRH, thus recommending that menstrual disturbances in Type 1 diabetic patients are generally of hypothalamic origin instead of primary pituitary dysfunction.
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Neuroendocrine control needs to also be thought about when translating disruptions in the HPO axis. It was reported by Djursing that Type 1 diabetic women had lower basal prolactin levels, unassociated to the presence of menstrual disorders. However, only diabetic amenorrheic patients had a reduced prolactin reaction to dopamine villains. These outcomes suggest that diabetic patients with menstrual conditions may have increased main dopaminergic activity, which in turn inhibits GnRH secretion. Endogenous opium-like peptides– endorphins– likewise have an inhibitory result on GnRH release. It is believed that gonadotrophin secretion is regulated by an interaction in between dopamine and endogenous opioids. However, a previous study by O’Hare et al. in 1987 cannot show a change in gonadotophic levels or initiation of menstruation after administration of the opioid inhibitor naloxon in hypogonadotrophic amenorrheic Type 1 diabetic women. Lastly, an association in between Type 1 diabetes and polycystic ovary syndrome (PCOS) was reported in a current study by Codner et al. These authors discovered that energetic treatment with insulin, often used in Type 1 diabetes in order to prevent diabetic complications, might cause supraphysiolgical dosages of insulin, consequently starting hyperandrogenism and PCOS. In addition to exogenous hyperinsulinism, insulin resistance is also possible in women with Type 1 diabetes, owing to reduced glucose uptake by the muscle. That also adds to the development of androgen excess in women with Type 1 diabetes. Codner et al. spotted increased levels of overall and totally free testosterone, increased LH to follicle-stimulating hormone ratio, bigger ovarian volumes and irregularities in ovarian morphology. This was specifically popular amongst women with the beginning of Type 1 diabetes before menarche. PCOS prevalence of 31 and 40% were reported using the Androgen excess society requirements and Rotterdam criteria, respectively, among Type 1 diabetic women in Codner’s research study.