okay, so basically I'm just so confused how you can be non-ir and still have elevated testosterone?! I've always been under the impression that its elevated insulin that causes the increase in testosterone production, but what does that mean if youre non-ir and still making too much testosterone?I'm basically just wanting to know how much insulin plays a role in pcos with non-ir cysters? It seems like it has to effect us some, because we wouldn't be prescribed metformin if not right? Sometimes I feel like such a freak! I really just want to understand what the heck is wrong with me! Can anyone else relate?
The effects of metformin on metabolic and cardiovascular risk factors in nonobese women with polycystic ovary syndrome.
Sahin Y, Unluhizarci K, Yilmazsoy A, Yikilmaz A, Aygen E, Kelestimur F.
Department of Obstetrics and Gynecology, Erciyes University Medical School, Kayseri, Turkey.
OBJECTIVE: There are conflicting data regarding the effects of metformin in lean women with polycystic ovary syndrome (PCOS). Thus, our aim was to evaluate the effects of 6 months of metformin therapy on various metabolic and cardiovascular risk factors in lean women with PCOS.
DESIGN: This was a prospective clinical study performed in a University hospital.
PATIENTS: Twenty nonobese PCOS women and 20 age- and BMI-matched healthy women were included in the study. Metformin (2550 mg/day) was administered for 6 months in women with PCOS. The hormonal and metabolic parameters were evaluated before and after metformin treatment.
MEASUREMENTS: The main outcome measures were serum androgens, FSH, LH, oestradiol, 17-hydroxyprogesterone, glucose, insulin, lipid profile, lipoprotein(a) [Lp(a)] and homocysteine levels. In addition 24-h ambulatory blood pressure monitoring (ABPM) and carotid intima-media thickness (IMT) were taken.
RESULTS: After 6 months of metformin therapy, women with PCOS had decreased LH, total testosterone, free androgen index and slightly increased SHBG levels. Metformin treatment resulted in resumption of regular menses in 12 (60%) patients, and in 8 (40%) of them serum progesterone level was compatible with ovulation. Glucose and insulin responses to oral glucose tolerance test (OGTT) and homeostasis model assessment of insulin resistance (HOMA-IR) did not improve after the metformin therapy. There were no significant changes in terms of cardiovascular risk factors such as lipids and homocysteine, IMT and ABPM.
CONCLUSION: Metformin may have beneficial effects in lean PCOS women in terms of resumption of menses without any remarkable effect on metabolic and cardiovascular risk factors.
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Role of insulin in the hyperandrogenemia of lean women with polycystic ovary syndrome and normal insulin sensitivity.
Baillargeon JP, Carpentier A.
Department of Medicine, Division of Endocrinology, Université de Sherbrooke, Sherbrooke, Quebec, Canada. jp.baillargeon@usherbrooke.ca
OBJECTIVE:To determine the effect of reducing insulin secretion on hyperandrogenemia in lean normoinsulinemic women with polycystic ovary syndrome (PCOS) and normal metabolic insulin sensitivity.
DESIGN: Transversal assessment at baseline and prospective follow-up of lean PCOS group after 8 days of diazoxide, which reduces insulin secretion, and 1 month of leuprolide, which suppresses LH.
SETTING: Clinical research center of an academic hospital.
PATIENT(S): Nine lean women (body mass index <or=25 kg/m(2)) with PCOS and normal insulin levels, as well as 17 lean healthy women.
INTERVENTION(S): Lean PCOS women were reassessed after 8 days of diazoxide and after 1 month of leuprolide, which suppresses LH. MAIN
OUTCOME MEASURE(S): Androgen levels and insulin-stimulated glucose disposal (metabolic insulin sensitivity), determined by euglycemic-hyperinsulinemic clamp (M-value).
RESULT(S): Mean M-value of lean PCOS women (48.5 micromol/kg.min) was similar to lean control subjects (52.9 micromol/kg.min). They also had comparable anthropometric measures, lipids, fibrinogen, and plasminogen activator inhibitor 1. The LH did not change significantly after diazoxide, but was almost suppressed after leuprolide in the PCOS group. Androstenedione decreased significantly after diazoxide and even more after leuprolide. However, free T significantly decreased only after diazoxide in lean PCOS women. Diazoxide also increased SHBG significantly in this group.
CONCLUSION(S): In women with typical PCOS and normal insulin levels and metabolic insulin sensitivity, reducing insulin secretion significantly decreased androgen and increased SHBG levels. These results suggest that insulin contributes to hyperandrogenemia even in PCOS women with normal metabolic insulin sensitivity, which might be due to increased sensitivity of their androgenic insulin pathway.
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CONCLUSION(S): In women with typical PCOS and normal insulin levels and metabolic insulin sensitivity, reducing insulin secretion significantly decreased androgen and increased SHBG levels. These results suggest that insulin contributes to hyperandrogenemia even in PCOS women with normal metabolic insulin sensitivity, which might be due to increased sensitivity of their androgenic insulin pathway.[/quote]
So is this article saying that thin cysters have more of a problem with increased insulin production rather than IR?
okay, so basically I'm just so confused how you can be non-ir and still have elevated testosterone?! I've always been under the impression that its elevated insulin that causes the increase in testosterone production, but what does that mean if youre non-ir and still making too much testosterone?I'm basically just wanting to know how much insulin plays a role in pcos with non-ir cysters? It seems like it has to effect us some, because we wouldn't be prescribed metformin if not right? Sometimes I feel like such a freak! I really just want to understand what the heck is wrong with me! Can anyone else relate?
There is a piece to Thin PCOS that is missing and I think you just put it into words. This is the exact issue that I fight with my PCOS specialist about. Why are some PCOSers overweight and some not. It just doesn't make any sense when you are looking are IR or even over-production of insulin.
So frustrated!! 
