Leptin accelerates the onset of puberty in normal female mice

Rexford S Ahima, Jody Dushay, Sarah N. Flier, Daniel Prabakaran, Jeffrey S. Flier

Research output: Contribution to journalArticle

Abstract

The fat-derived hormone, leptin, is proposed to serve as an adipostatic signal to the brain to reduce food intake and body weight. In addition to its effects on body weight, chronic leptin treatment restores puberty and fertility to oblob mice with total leptin deficiency, and acute treatment substantially corrects hypogonadism in mice starved for 2 d without affecting body weight. Leptin may therefore be a critical signal, linking adiposity and reproduction. Since body weight and adiposity appear to play a critical role in the timing of puberty in humans and rodents, and leptin levels rise with increasing adiposity, we studied the effects of once daily injections of recombinant leptin on the onset of puberty in female mice weaned on day 21 and fed ad libitum. There was a linear increase in body weight during the study period, which was not altered by the dose of leptin used. Mice injected with leptin had an earlier onset of three classic pubertal parameters (i.e., vaginal opening, estrus, and cycling) compared with saline-injected controls. Leptin is the first peripheral molecule demonstrated to accelerate the maturation of the reproductive axis in normal rodents. We propose that leptin is the signal that informs the brain that energy stores are sufficient to support the high energy demands of reproduction, and may be a major determinant of the timing of puberty.

Original languageEnglish (US)
Pages (from-to)391-395
Number of pages5
JournalJournal of Clinical Investigation
Volume99
Issue number3
StatePublished - Feb 1 1997
Externally publishedYes

Fingerprint

Puberty
Leptin
Body Weight
Adiposity
Reproduction
Rodentia
Hypogonadism
Estrus
Brain
Fertility
Eating
Fats
Hormones
Injections
Therapeutics

Keywords

  • Cycling
  • Estrus
  • Ob protein
  • Vaginal opening

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Ahima, R. S., Dushay, J., Flier, S. N., Prabakaran, D., & Flier, J. S. (1997). Leptin accelerates the onset of puberty in normal female mice. Journal of Clinical Investigation, 99(3), 391-395.

Leptin accelerates the onset of puberty in normal female mice. / Ahima, Rexford S; Dushay, Jody; Flier, Sarah N.; Prabakaran, Daniel; Flier, Jeffrey S.

In: Journal of Clinical Investigation, Vol. 99, No. 3, 01.02.1997, p. 391-395.

Research output: Contribution to journalArticle

Ahima, RS, Dushay, J, Flier, SN, Prabakaran, D & Flier, JS 1997, 'Leptin accelerates the onset of puberty in normal female mice', Journal of Clinical Investigation, vol. 99, no. 3, pp. 391-395.
Ahima RS, Dushay J, Flier SN, Prabakaran D, Flier JS. Leptin accelerates the onset of puberty in normal female mice. Journal of Clinical Investigation. 1997 Feb 1;99(3):391-395.
Ahima, Rexford S ; Dushay, Jody ; Flier, Sarah N. ; Prabakaran, Daniel ; Flier, Jeffrey S. / Leptin accelerates the onset of puberty in normal female mice. In: Journal of Clinical Investigation. 1997 ; Vol. 99, No. 3. pp. 391-395.
@article{ffb375320fdb437b9af9cb66086e8698,
title = "Leptin accelerates the onset of puberty in normal female mice",
abstract = "The fat-derived hormone, leptin, is proposed to serve as an adipostatic signal to the brain to reduce food intake and body weight. In addition to its effects on body weight, chronic leptin treatment restores puberty and fertility to oblob mice with total leptin deficiency, and acute treatment substantially corrects hypogonadism in mice starved for 2 d without affecting body weight. Leptin may therefore be a critical signal, linking adiposity and reproduction. Since body weight and adiposity appear to play a critical role in the timing of puberty in humans and rodents, and leptin levels rise with increasing adiposity, we studied the effects of once daily injections of recombinant leptin on the onset of puberty in female mice weaned on day 21 and fed ad libitum. There was a linear increase in body weight during the study period, which was not altered by the dose of leptin used. Mice injected with leptin had an earlier onset of three classic pubertal parameters (i.e., vaginal opening, estrus, and cycling) compared with saline-injected controls. Leptin is the first peripheral molecule demonstrated to accelerate the maturation of the reproductive axis in normal rodents. We propose that leptin is the signal that informs the brain that energy stores are sufficient to support the high energy demands of reproduction, and may be a major determinant of the timing of puberty.",
keywords = "Cycling, Estrus, Ob protein, Vaginal opening",
author = "Ahima, {Rexford S} and Jody Dushay and Flier, {Sarah N.} and Daniel Prabakaran and Flier, {Jeffrey S.}",
year = "1997",
month = "2",
day = "1",
language = "English (US)",
volume = "99",
pages = "391--395",
journal = "Journal of Clinical Investigation",
issn = "0021-9738",
publisher = "The American Society for Clinical Investigation",
number = "3",

}

TY - JOUR

T1 - Leptin accelerates the onset of puberty in normal female mice

AU - Ahima, Rexford S

AU - Dushay, Jody

AU - Flier, Sarah N.

AU - Prabakaran, Daniel

AU - Flier, Jeffrey S.

PY - 1997/2/1

Y1 - 1997/2/1

N2 - The fat-derived hormone, leptin, is proposed to serve as an adipostatic signal to the brain to reduce food intake and body weight. In addition to its effects on body weight, chronic leptin treatment restores puberty and fertility to oblob mice with total leptin deficiency, and acute treatment substantially corrects hypogonadism in mice starved for 2 d without affecting body weight. Leptin may therefore be a critical signal, linking adiposity and reproduction. Since body weight and adiposity appear to play a critical role in the timing of puberty in humans and rodents, and leptin levels rise with increasing adiposity, we studied the effects of once daily injections of recombinant leptin on the onset of puberty in female mice weaned on day 21 and fed ad libitum. There was a linear increase in body weight during the study period, which was not altered by the dose of leptin used. Mice injected with leptin had an earlier onset of three classic pubertal parameters (i.e., vaginal opening, estrus, and cycling) compared with saline-injected controls. Leptin is the first peripheral molecule demonstrated to accelerate the maturation of the reproductive axis in normal rodents. We propose that leptin is the signal that informs the brain that energy stores are sufficient to support the high energy demands of reproduction, and may be a major determinant of the timing of puberty.

AB - The fat-derived hormone, leptin, is proposed to serve as an adipostatic signal to the brain to reduce food intake and body weight. In addition to its effects on body weight, chronic leptin treatment restores puberty and fertility to oblob mice with total leptin deficiency, and acute treatment substantially corrects hypogonadism in mice starved for 2 d without affecting body weight. Leptin may therefore be a critical signal, linking adiposity and reproduction. Since body weight and adiposity appear to play a critical role in the timing of puberty in humans and rodents, and leptin levels rise with increasing adiposity, we studied the effects of once daily injections of recombinant leptin on the onset of puberty in female mice weaned on day 21 and fed ad libitum. There was a linear increase in body weight during the study period, which was not altered by the dose of leptin used. Mice injected with leptin had an earlier onset of three classic pubertal parameters (i.e., vaginal opening, estrus, and cycling) compared with saline-injected controls. Leptin is the first peripheral molecule demonstrated to accelerate the maturation of the reproductive axis in normal rodents. We propose that leptin is the signal that informs the brain that energy stores are sufficient to support the high energy demands of reproduction, and may be a major determinant of the timing of puberty.

KW - Cycling

KW - Estrus

KW - Ob protein

KW - Vaginal opening

UR - http://www.scopus.com/inward/record.url?scp=0030868077&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030868077&partnerID=8YFLogxK

M3 - Article

C2 - 9022071

AN - SCOPUS:0030868077

VL - 99

SP - 391

EP - 395

JO - Journal of Clinical Investigation

JF - Journal of Clinical Investigation

SN - 0021-9738

IS - 3

ER -