The Link Between Polycystic Ovary Syndrome and Both Type 1 and Type 2 Diabetes Mellitus

What Do We Know Today?

Thomas M Barber; Stephen Franks

Disclosures

Women's Health. 2012;8(2):147-154. 

In This Article

Link Between PCOS & T1D

Epidemiology

There are relatively few studies reported in the literature on the prevalence of PCOS in women with T1D. The prevalence reported is influenced by the population studied and the diagnostic criteria employed. In one study from Spain on 85 women with T1D, hyperandrogenic disorders were demonstrated in 33 women (38.8%). Of those with hyperandrogenic disorders, 16 (18.8%) had PCOS (NIH diagnostic criteria[8]) and 17 (20%) had hirsutism without menstrual dysfunction.[62] For comparison, the prevalence of PCOS (NIH criteria[8]) was shown to be much lower at 6.5% within the Spanish general adult female population.[1] In a Chilean study by Codner and colleagues on 42 women with T1D, the prevalence of PCOS was 12% using NIH criteria, 40.5% using the Rotterdam diagnostic criteria, and just 2.6% in the female control group.[63] Using Rotterdam diagnostic criteria, the relative risk of PCOS in T1D versus female controls was 15.4 (p < 0.0001).[63] In the studies outlined by Escobar-Morreale and Codner, up to 30% of women with T1D also have hirsutism, compared with rates of hirsutism of 7.1 and 3% in the Spanish and Chilean general female populations, respectively.[62,63] Chronic oligo-amenorrhea was reported in approximately 20% of women with T1D,[62,63] compared with a prevalence of just 8% in nondiabetic women.[14] Oligo-amenorrhea has been shown to be particularly prevalent in young women with T1D.[64]

Pathogenesis

While insulin resistance plays a central role in the pathogenesis of PCOS,[2] the key pathogenic factors implicated in the development of T1D are β-cell dysfunction and insulin deficiency.[65] The increased prevalence of PCOS in women with T1D therefore requires further discussion and explanation. Although obesity, insulin resistance and endogenous hyperinsulinemia are not prerequisites for the development of T1D, the treatment of T1D does involve exogenous insulin administration. Endogenous insulin, following release into the portal circulation, has direct effects on hepatic glucose production and undergoes some hepatic extraction prior to release into the systemic circulation. Conversely, exogenous insulin therapy is absorbed directly into the systemic circulation (without direct effects on the liver). For portal insulin concentrations to reach sufficient levels to suppress hepatic glucose generation, supraphysiological concentrations of insulin must be reached in the systemic circulation.[66] Supraphysiological concentrations of insulin in the systemic circulation have direct effects on the peripheral tissues, including the ovarian theca cells, with consequent stimulation of ovarian steroidogenesis.[67]

Consistent with the hypothesis that implicates iatrogenic insulin excess as a causal factor, is the observation that the proportion of women with T1D who also manifest features of PCOS is influenced by the intensity of the insulin regimen. Codner and colleagues showed that 75% of women with T1D on intensive insulin therapy had either PCOS or asymptomatic polycystic ovarian morphology, in contrast to just 33% of women with T1D on conservative conventional therapy (twice-daily insulin injections).[63,66] In addition to the adverse effects of supraphysiological systemic concentrations of insulin, a further explanation for the development of PCOS in adolescent girls with T1D is likely to be the increased fat mass, weight gain and insulin resistance demonstrated during the pubertal transition.[68]

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