MONDAY, Nov. 21 (HealthDay News) -- In female mice with diet-induced obesity (DIO), insulin sensitivity is maintained in the pituitary and ovary, according to an experimental study published online Nov. 10 in Diabetes.
Sheng Wu, Ph.D., from Johns Hopkins University School of Medicine in Baltimore, and colleagues investigated whether reproductive dysfunction was caused by differential insulin signaling. Insulin signaling in reproductive tissues was compared with that in energy storage tissues of lean and DIO female mice, and pituitary-specific insulin receptor knockout control mice. Macrophage infiltration and phosphorylated Jun NH2-terminal kinase (pJNK) signaling was assayed to investigate insulin resistance due to high-fat diet-induced stress.
The investigators found that, in lean mice, there was reduced insulin sensitivity in the reproductive tissues compared with the peripheral metabolic tissues. In obese mice, insulin sensitivity was maintained in the pituitary and ovary, whereas metabolic tissues exhibited insulin resistance. Insulin activated both insulin receptor substrates (IRS), IRS1 and IRS2, in the ovary but only activated IRS2 in the pituitary. Relative to DIO mice, in the pituitary and ovary of lean mice, there was no increase in macrophage infiltration or pJNK signaling.
"The lack of inflammation and cytokine signaling in the pituitary and ovary in DIO mice compared with lean mice may be one of the reasons that these tissues remained insulin sensitive. Retained sensitivity of the pituitary and ovary to insulin may contribute to the pathophysiology of polycystic ovary syndrome," the authors write.
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