Cited by 336Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and Metabolism

The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.

Leptin selectively decreases visceral adiposity and enhances insulin action

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Barzilai, N, Wang, J, Massilon, D, Vuguin, P, Hawkins, M, Rossetti, L·1997·Journal of Clinical Investigation

Abstract

Intraabdominal adiposity and insulin resistance are risk factors for diabetes mellitus, dyslipidemia, arteriosclerosis, and mortality. Leptin, a fat-derived protein encoded by the ob gene, has been postulated to be a sensor of energy storage in adipose tissue capable of mediating a feedback signal to sites involved in the regulation of energy homeostasis. Here, we provide evidence for specific effects of leptin on fat distribution and in vivo insulin action. Leptin (LEP) or vehicle (CON) was administered by osmotic minipumps for 8 d to pair-fed adult rats. During the 8 d of the study, body weight and total fat mass decreased similarly in LEP and in CON. However, while moderate calorie restriction (CON) resulted in similar decreases in whole body (by 20%) and visceral (by 21%) fat, leptin administration led to a specific and marked decrease (by 62%) in visceral adiposity. During physiologic hyperinsulinemia (insulin clamp), leptin markedly enhanced insulin action on both inhibition of hepatic glucose production and stimulation of glucose uptake. Finally, leptin exerted complex effects on the hepatic gene expression of key metabolic enzymes and on the intrahepatic partitioning of metabolic fluxes, which are likely to represent a defense against excessive storage of energy in adipose depots. These studies demonstrate novel actions of circulating leptin in the regulation of fat distribution, insulin action, and hepatic gene expression and suggest that it may play a role in the pathophysiology of abdominal obesity and insulin resistance.

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Metadata

Authors
Barzilai, N., Wang, J., Massilon, D., Vuguin, P., Hawkins, M., & Rossetti, L.
Affiliations
Albert Einstein College of Medicine (US)
Corresponding author
Rossetti, L
Venue
Journal of Clinical Investigation
Published
1997-12-15
Volume
100
Issue
12
Pages
3105-3110
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2152760501
Cited by
335
References
34
Citations by year
2026: 1 · 2025: 3 · 2024: 2 · 2022: 2 · 2021: 7 · 2020: 8 · 2019: 3 · 2018: 4 · 2017: 7 · 2016: 5 · 2015: 12 · 2014: 10 · 2013: 6 · 2012: 11
FWCI
6.31
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Amgen
  • Medical Research Council Canada
  • National Institutes of Health
  • Medical Research Council
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK-48321, DK20541, DK-45024)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Keywords
leptin, visceral fat, intra-abdominal fat, insulin action, insulin resistance, abdominal obesity, body fat distribution, hepatic glucose production, hepatic glucose uptake, hepatic gene expression, energy homeostasis, caloric restriction, hyperinsulinemia
MeSH terms
Adipose Tissue, Animals, Blood Glucose, Body Weight, Eating, Glucose, Insulin, Liver, Male, Proteins, Recombinant Proteins, Viscera, Gene Expression, Rats, Sprague-Dawley, Leptin, Mice, Rats

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