Prolactin release by adipose explants, primary adipocytes, and LS14 adipocytes

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Prolactin (PRL) is a multifunctional hormone produced in humans by both pituitary and extrapituitary sites, including adipose tissue. Objectives Our objectives were to: 1) compare PRL secretion by sc and visceral adipose explants and mature adipocytes from obese and nonobese patients; and 2) examine the effects of insulin and selected cytokines on PRL gene expression and release from primary adipocytes and LS14 adipocytes. Design and subjects Adipose tissue was obtained from morbidly obese [body mass index (BMI) > 40 kg/m(2)] and nonobese (BMI Results PRL release from explants and mature adipocytes increased in a time-dependent manner indicating removal from inhibition. Visceral explants from obese patients showed higher PRL release than that from sc explants; both types of explants from nonobese patients released similar amounts of PRL. Analysis of data from 50 patients revealed an inverse relationship between PRL release from sc depots and BMI. Insulin suppressed PRL expression and release from differentiated adipocytes but moderately stimulated PRL release from nondifferentiated cells. The cAMP elevating compound forskolin increased PRL release in both cell types. Conclusions PRL should be recognized as an important adipokine whose release is regulated by insulin and is affected by obesity in a depot-specific manner.

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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