Prolactin Promotes Adipose Tissue Fitness and Insulin Sensitivity in Obese Males.

Abstract:

:Excessive accumulation of body fat triggers insulin resistance and features of the metabolic syndrome. Recently, evidence has accumulated that obesity, type 2 diabetes, and metabolic syndrome are associated with reduced levels of serum prolactin (PRL) in humans and rodents, raising the question of whether low PRL levels contribute to metabolic dysfunction. Here, we have addressed this question by investigating the role of PRL in insulin sensitivity and adipose tissue fitness in obese rodents and humans. In diet-induced obese rats, treatment with PRL delivered via osmotic mini-pumps, improved insulin sensitivity, prevented adipocyte hypertrophy, and reduced inflammatory cytokine expression in visceral fat. PRL also induced increased expression of Pparg and Xbp1s in visceral adipose tissue and elevated circulating adiponectin levels. Conversely, PRL receptor null mice challenged with a high-fat diet developed greater insulin resistance, glucose intolerance, and increased adipocyte hypertrophy compared with wild-type mice. In humans, serum PRL values correlated positively with systemic adiponectin levels and were reduced in insulin-resistant patients. Furthermore, PRL circulating levels and PRL produced by adipose tissue correlated directly with the expression of PPARG, ADIPOQ, and GLUT4 in human visceral and sc adipose tissue. Thus, PRL, acting through its cognate receptors, promotes healthy adipose tissue function and systemic insulin sensitivity. Increasing the levels of PRL in the circulation may have therapeutic potential against obesity-induced metabolic diseases.

journal_name

Endocrinology

journal_title

Endocrinology

authors

Ruiz-Herrera X,de Los Ríos EA,Díaz JM,Lerma-Alvarado RM,Martínez de la Escalera L,López-Barrera F,Lemini M,Arnold E,Martínez de la Escalera G,Clapp C,Macotela Y

doi

10.1210/en.2016-1444

subject

Has Abstract

pub_date

2017-01-01 00:00:00

pages

56-68

issue

1

eissn

0013-7227

issn

1945-7170

journal_volume

158

pub_type

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