Prolactin and lactation as modifiers of diabetes risk in gestational diabetes

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Pregnancy and puerperium are periods of intense hormonal changes. Maternal metabolism adapts to spare the mother from harm on behalf of her developing offspring and major alterations maintain normal glucose tolerance. Insulin secretion increases during a normal pregnancy to compensate for pregnancy-induced insulin resistance and maintain euglycemia. Women at risk for gestational diabetes have insulin resistance before conception. Gestational diabetes develops when a woman at risk is unable to meet the insulin secretory demands imposed by the additional insulin resistance characteristic of pregnancy. The lactogens, human placental lactogen and prolactin, are major stimuli for the adaptation of the endocrine pancreas during gestation. This review discusses the role of lactogens on glucose homeostasis during pregnancy and proposes a mechanism by which the hormonal control of lactation, led by prolactin, may regulate adipocyte biology, glucose and lipid metabolism, and guard postpartum women against type 2 diabetes.

Original languageEnglish (US)
Pages (from-to)593-600
Number of pages8
JournalHormone and Metabolic Research
Volume43
Issue number9
DOIs
StatePublished - 2011

Fingerprint

Gestational Diabetes
Medical problems
Lactation
Prolactin
Insulin
Pregnancy
Insulin Resistance
Glucose
Postpartum Period
Placental Lactogen
Mothers
Metabolism
Islets of Langerhans
Lipid Metabolism
Adipocytes
Type 2 Diabetes Mellitus
Homeostasis

Keywords

  • breastfeeding
  • hyperprolactinemia
  • pregnancy
  • puerperium

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism

Cite this

Prolactin and lactation as modifiers of diabetes risk in gestational diabetes. / Ramos-Romn, M. A.

In: Hormone and Metabolic Research, Vol. 43, No. 9, 2011, p. 593-600.

Research output: Contribution to journalArticle

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