Cited by 210Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesLipid metabolism and biosynthesis

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Site and mechanism of leptin action in a rodent form of congenital lipodystrophy

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Asilmaz, Esra, Cohen, Paul, Miyazaki, Makoto, Dobrzyn, Pawel, Ueki, Kohjiro, Fayzikhodjaeva, Gulnorakhon, Soukas, Alexander A., Kahn, C. Ronald, Ntambi, James M., Socci, Nicholas D., Friedman, Jeffrey M.·2004·Journal of Clinical Investigation

DOI 10.1172/jci200419511

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Abstract

Lipodystrophy is characterized by the complete or partial absence of adipose tissue, insulin resistance, hepatic steatosis, and leptin deficiency. Here, we show that low-dose central leptin corrects the insulin resistance and fatty liver of lipodystrophic aP2-nSREBP-1c mice, while the same dose given peripherally does not. Central leptin also repressed stearoyl-CoA desaturase-1 (SCD-1) RNA and enzymatic activity, which were increased in livers of lipodystrophic mice. aP2-nSREBP-1c mice homozygous for an SCD-1 deletion had markedly reduced hepatic steatosis, increased saturated fatty acids, decreased acetyl-CoA carboxylase activity, and decreased malonyl-CoA levels in the liver. Despite the reduction in hepatic steatosis, these mice remained diabetic. A leptin dose-response curve showed that subcutaneous leptin improved hyperglycemia and hyperinsulinemia in aP2-nSREBP-1c mice at doses that did not substantially alter hepatic steatosis or hepatic SCD enzymatic activity. Leptin treatment at this dose improved insulin-stimulated insulin receptor and insulin receptor substrate 2 (IRS-2) phosphorylation, IRS-2–associated PI3K activity, and Akt activity in liver. Together, these data suggest that CNS-mediated repression of SCD-1 contributes to leptin's antisteatotic actions. Intracerebroventricular leptin improves glucose homeostasis by improving insulin signal transduction in liver, but in this case the effect appears to be independent of SCD-1.

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Authors: Asilmaz, E., Cohen, P., Miyazaki, M., Dobrzyn, P., Ueki, K., Fayzikhodjaeva, G., Soukas, A. A., Kahn, C. R., Ntambi, J. M., Socci, N. D., & Friedman, J. M.
Affiliations: Rockefeller University (US)
University of Wisconsin System (US)
Joslin Diabetes Center (US)
Albert Einstein College of Medicine (US)
Howard Hughes Medical Institute (US)
Corresponding author: Friedman, Jeffrey M.
ORCID: Cohen, Paul
Miyazaki, Makoto
Ueki, Kohjiro
Soukas, Alexander A.
Kahn, C. Ronald
Ntambi, James M.
Socci, Nicholas D.
Friedman, Jeffrey M.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2004-02-01
Volume: 113
Issue: 3
Pages: 414-424
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci200419511
OpenAlex: W2104945088
Cited by: 210
References: 51
Citations by year: 2025: 1 · 2024: 2 · 2023: 9 · 2022: 2 · 2021: 5 · 2020: 6 · 2019: 8 · 2018: 3 · 2017: 9 · 2016: 13 · 2015: 8 · 2014: 13 · 2013: 12 · 2012: 5
FWCI: 6.74
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (GM07739, MSTPGM07739)
National Institute of General Medical Sciences (GM 07739, T32GM007739)
National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK-41096, R01DK062388, R01-DK-62388, R01DK041096)
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
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords: leptin, congenital lipodystrophy, insulin resistance, hepatic steatosis, stearoyl-CoA desaturase 1, glucose homeostasis, insulin receptor substrate 2, PI3K/Akt signaling, acetyl-CoA carboxylase, malonyl-CoA
MeSH terms: Animals, Disease Models, Animal, Female, Lipodystrophy, Liver, Male, Mice, Inbred C57BL, Phylogeny, Stearoyl-CoA Desaturase, Muscle, Skeletal, Leptin, Gene Expression Profiling, Mice

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Site and mechanism of leptin action in a rodent form of congenital lipodystrophy

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