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 <30 kg/m(2)) patients. Explants and isolated mature adipocytes were incubated for 10 d. Primary adipocytes or LS14 cells were used before or after differentiation and incubated with the test compounds for 24 h. PRL release was analyzed by a bioassay, and PRL expression was determined by real-time PCR. 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.
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 <30 kg/m(2)) patients. Explants and isolated mature adipocytes were incubated for 10 d. Primary adipocytes or LS14 cells were used before or after differentiation and incubated with the test compounds for 24 h. PRL release was analyzed by a bioassay, and PRL expression was determined by real-time PCR. RESULTS:PRL release from explants and mature adipocytes increased in a time-dependent manner indicating removal from inhibition. Visceral explants from obesepatients 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.
Authors: Petra Kok; Ferdinand Roelfsema; Marijke Frölich; A Edo Meinders; Hanno Pijl Journal: J Clin Endocrinol Metab Date: 2004-09 Impact factor: 5.958
Authors: William C Stewart; James E Baugh; Z Elizabeth Floyd; Jacqueline M Stephens Journal: Biochem Biophys Res Commun Date: 2004-11-05 Impact factor: 3.575
Authors: Heather R Christensen; Michael K Murawsky; Nelson D Horseman; Tara A Willson; Karen A Gregerson Journal: Endocrinology Date: 2013-09-12 Impact factor: 4.736
Authors: Antonio J Ponce; Tomás Galván-Salas; Ricardo M Lerma-Alvarado; Xarubet Ruiz-Herrera; Tomás Hernández-Cortés; Rodrigo Valencia-Jiménez; Laura E Cárdenas-Rodríguez; Gonzalo Martínez de la Escalera; Carmen Clapp; Yazmín Macotela Journal: Endocrine Date: 2020-01-09 Impact factor: 3.633