Insulin Resistance and Hormones

Treating high prolactin also lowers insulin resistance, LDL cholesterol and triglycerides

Twenty-two patients with prolactinoma completed 6 months of treatment with dopamine agonist. After 6 months of treatment with dopamine agonist, prolactin levels normalized, but no significant difference in BMI was observed. However, there was a significant decrease on homeostasis model assessment of insulin resistance index, glucose, LDL-cholesterol, and triglyceride levels.

http://www.ncbi.nlm.nih.gov/pubmed/20559294

Insulin resistance is associated with higher free testosterone and estrogen, lower SHBG

Increasing quartiles of bioavailable testosterone and estrogen and decreasing quartiles of SHBG were associated with significantly increased odds of impaired fasting glucose and diabetes. Of 1100 women with normal glucose tolerance, estrogen and DHEA were positively associated, and SHBG was inversely associated with insulin resistance after multivariable adjustment. Bioavailable testosterone was associated with insulin resistance, but not fasting glucose.

http://jcem.endojournals.org/cgi/content/full/92/4/1289

Insulin lowers SHBG

Insulin has been shown in vitro to decrease the synthesis of SHBG.

http://jcem.endojournals.org/cgi/content/abstract/79/4/1173

Insulin increases GnRH and testosterone, while decreasing follicular maturation and SHBG

Hyperinsulinemia increases Gonadotropin-releasing hormone (GnRH) pulse frequency, LH over FSH dominance, increased ovarian androgen production, decreased follicular maturation, and decreased SHBG binding.

http://en.wikipedia.org/wiki/Polycystic_ovary_syndrome

Insulin resistance causes PCOS

Hyperinsulinemia increases GNRH pulse activity leading to disorderly LH and FSH activity, as seen in Polycystic ovary syndrome (PCOS).

http://en.wikipedia.org/wiki/Gonadotropin-releasing_hormone

Estrogen and progesterone are associated with insulin resistance

Significant changes in insulin resistance were observed over the menstrual cycle; from a midfollicular phase level of 1.35, levels rose to 1.59 during the early luteal phase and decreased to 1.55 in the late-luteal phase. Insulin resistance measures primarily reflected changes in insulin and not glucose. After adjustment for age, race, cycle, and other sex hormones, insulin resistance was positively associated with estrogen and progesterone, and inversely associated with FSH and SHBG. LH was not associated with insulin resistance. Further adjustment for BMI weakened the association with SHBG but did not affect other associations. Conclusion: Insulin exhibited minor menstrual cycle variability. Estrogen and progesterone were positively associated with insulin resistance and should be considered in studies of insulin resistance among premenopausal women.

http://www.ncbi.nlm.nih.gov/pubmed/20843950

Pregnancy hormones cause insulin resistance

There is an increased insulin-resistant state during pregnancy mediated by the placental anti-insulin hormones estrogen, progesterone, human somatomammotropin; the pituitary hormone prolactin; and the adrenal hormone, cortisol.

http://www.ncbi.nlm.nih.gov/pubmed/8632110

High insulin is related to low SHBG

There is an inverse relationship between the serum levels of insulin and sex hormone-binding globulin (SHBG) in women.