title: The prolactin-deficient mouse has an unaltered metabolic phenotype.
abstract: Prolactin (PRL), best recognized for its lactogenic activity, is also involved in the regulation of metabolic homeostasis in both mammalian and nonmammalian species. Although several mouse models have been used to study the metabolic functions of PRL, a clear-cut consensus has not emerged given the limited and often conflicting data. To clarify the role of PRL in metabolic homeostasis in males and nonlactating females, we used the PRL-deficient mouse. Our objectives were to compare: 1) weight gain, 2) body composition, 3) serum lipid profile, 4) circulating leptin and adiponectin levels, and 5) glucose tolerance in PRL knockout, heterozygous, and wild-type mice maintained on standard chow, high-fat, or low-fat diets. In addition, we compared the lipolytic actions of PRL using adipose tissue explants from mice, rats, and humans. We are reporting that PRL deficiency does not affect the rate of weight gain, body composition, serum lipids, or adiponectin levels in either sex on any diet. Glucose tolerance was slightly impaired in very young PRL knockout male pups but not in adults or in females at any age. Leptin was elevated in male, but not female, PRL knockout mice maintained on a low-fat diet. PRL did not affect lipolysis in adipose tissue explants from mice but significantly inhibited glycerol release from both rat and human adipose explants in a dose-dependent manner. We conclude that PRL deficiency has negligible gross metabolic effects in mice.
authors.affiliation: Department of Cell Biology, University of Cincinnati, 3125 Eden Avenue, Ohio 45267-0521, USA.
authors.forename: Christopher R
authors.initials: CR
authors.lastname: LaPensee
authors.forename: Nelson D
authors.initials: ND
authors.lastname: Horseman
authors.forename: Patrick
authors.initials: P
authors.lastname: Tso
authors.forename: Terry D
authors.initials: TD
authors.lastname: Brandebourg
authors.forename: Eric R
authors.initials: ER
authors.lastname: Hugo
authors.forename: Nira
authors.initials: N
authors.lastname: Ben-Jonathan
mesh_terms: D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D001823:Body Composition / Q000235:genetics / Q000502:physiology; D018752:Diet, Fat-Restricted; D004041:Dietary Fats; D005260:Female; D018149:Glucose Intolerance / Q000235:genetics; D005951:Glucose Tolerance Test; D006801:Humans; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000097:blood; D008066:Lipolysis / Q000187:drug effects; D008214:Lymphocytes / Q000378:metabolism; D008297:Male; D008660:Metabolism / Q000235:genetics / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D010641:Phenotype; D011388:Prolactin / Q000172:deficiency / Q000502:physiology*; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012727:Sex Characteristics; D015430:Weight Gain / Q000502:physiology
chemical_list: D052242:Adiponectin; D004041:Dietary Fats; D020738:Leptin; D008055:Lipids; D011388:Prolactin