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Cited by 144Regulation of Appetite and ObesityHypothalamic control of reproductive hormonesAdipokines, Inflammation, and Metabolic Diseases

The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.

Region-Specific Reduction in Leptin-Induced Phosphorylation of Signal Transducer and Activator of Transcription-3 (STAT3) in the Rat Hypothalamus Is Associated with Leptin Resistance during Pregnancy

Ladyman, S. R., Grattan, D. R.·2004·Endocrinology
DOI 10.1210/en.2004-0338
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Abstract

Leptin concentrations increase during pregnancy, but this does not prevent the pregnancy-induced increase in food intake, suggesting a state of leptin resistance. This study investigated the response to intracerebroventricular leptin administration in pregnant rats. After fasting, nonpregnant, d-7 and d-14 pregnant rats received leptin (4 μg) or vehicle, then food intake was measured. Serial blood samples were collected in another group of rats to determine plasma leptin concentrations. Further groups of d-14 pregnant and nonpregnant rats were killed after leptin or vehicle treatment, and brains were collected. Hypothalamic nuclei were microdissected, and levels of signal transducer and activator of transcription (STAT)3 phosphorylation were measured using Western blot analysis. Fasting decreased leptin concentrations in both pregnant and nonpregnant rats. Leptin treatment significantly reduced food intake in nonpregnant and d-7 pregnant rats but not in d-14 pregnant rats. In addition, there was no postfasting hyperphagic response in the pregnant rats. In the pregnant rats, leptin-induced STAT3 phosphorylation was suppressed in the arcuate nucleus and, to a lesser extent, in the ventromedial hypothalamus (VMH), compared with nonpregnant rats. Unstimulated STAT3 levels were also decreased in the VMH during pregnancy. Leptin-induced phosphorylation of STAT3 in the dorsomedial and lateral hypothalamus was not different between pregnant and nonpregnant rats. These data indicate that pregnant rats become resistant to the satiety action of leptin. Furthermore, leptin-induced activation of the STAT3 is impaired during pregnancy, specifically in the arcuate nucleus and VMH. These data support the hypothesis that pregnancy is a state of hypothalamic leptin resistance.

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Metadata

Authors
Ladyman, S. R., & Grattan, D. R.
Affiliations
University of Otago (NZ)
Corresponding author
Grattan, D. R.
ORCID
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2004-08-01
Volume
145
Issue
8
Pages
3704-3711
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
DOI
10.1210/en.2004-0338
OpenAlex
W2015900343
Cited by
144
References
52
Citations by year
2026: 4 · 2025: 3 · 2024: 2 · 2023: 2 · 2022: 6 · 2021: 5 · 2020: 7 · 2019: 12 · 2018: 5 · 2017: 7 · 2016: 9 · 2015: 3 · 2014: 9 · 2013: 8 · 2012: 5
FWCI
2.77
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Keywords
leptin resistance, pregnancy, STAT3 phosphorylation, hypothalamus, arcuate nucleus, ventromedial hypothalamus, dietary intake, satiety, fasting, leptin, hypothalamic nuclei
MeSH terms
Animals, Arcuate Nucleus of Hypothalamus, DNA-Binding Proteins, Eating, Female, Hypothalamus, Injections, Intraventricular, Phosphorylation, Pregnancy, Pregnancy, Animal, Ventromedial Hypothalamic Nucleus, Signal Transduction, Trans-Activators, Rats, Sprague-Dawley, Leptin, STAT3 Transcription Factor, Rats

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