The effects of constant photoperiod on serum prolactin concentrations and sexual behavior of ovariectomized goats was investigated. Fourteen ovariectomized goats were divided into groups of seven goats each and placed in photoperiod-controlled rooms with either 8L:16D or 16L:8D. All goats received six estradiol (E2) treatments in a Latin square design. Following each treatment six 1-h observation periods were conducted. Blood was collected before E2 treatment and at each observation period for prolactin quantification. During the observation periods measures of attractivity, proceptivity, and receptivity were recorded. Goats exposed to 8L:16D displayed sexual behavior in response to doses of E2 lower than those required by goats exposed to 16L:8D. Prolactin concentrations were higher in goats exposed to 16L:8D than in those exposed to 8L:16D. It was concluded that photoperiod affects prolactin concentrations and behavioral sensitivity to E2 in goats. The effect of continued exposure to constant photoperiod on these variables was then investigated. The goats were held in constant photoperiod for 211 d and behavior tests as described for Exp. 1 were repeated. Scores for attractivity, proceptivity, and receptivity did not differ between the two groups after 211 d of exposure to constant photoperiod. Prolactin concentrations did not differ in this study between the two groups. It was concluded that after chronic exposure to 8L:16D ovariectomized goats become refractory to the stimulatory effects of short photoperiod.

Finding therapies that can protect and expand functional β-cell mass is a major goal of diabetes research. Here we generated β-cell-specific conditional knockout and gain-of-function mouse models and used human islet transplant experiments to examine how manipulating Nrf2 levels affects β-cell survival, proliferation and mass. Depletion of Nrf2 in β-cells resulted in decreased glucose-stimulated β-cell proliferation ex vivo and decreased adaptive β-cell proliferation and β-cell mass expansion after a high fat diet in vivo. Nrf2 protects β-cells from apoptosis after a high fat diet. Nrf2 loss-of-function decreases Pdx1 abundance and insulin content. Activating Nrf2 in a β-cell-specific manner increases β-cell proliferation and β-cell mass. Human islets transplanted under the kidney capsule of immunocompromised mice and treated systemically with CDDO-Me, an Nrf2 activator, display increased β-cell proliferation. Thus, Nrf2 regulates β-cell mass and is an exciting therapeutic target for expanding β-cell mass in diabetes.