Cited by 212Regulation of Appetite and ObesityPeroxisome Proliferator-Activated ReceptorsAdipokines, Inflammation, and Metabolic Diseases

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Restoration of hypothalamic lipid sensing normalizes energy and glucose homeostasis in overfed rats

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Pocai, A.·2006·Journal of Clinical Investigation

DOI 10.1172/jci26640PMC PMC1395479

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Abstract

Short-term overfeeding blunts the central effects of fatty acids on food intake and glucose production. This acquired defect in nutrient sensing could contribute to the rapid onset of hyperphagia and insulin resistance in this model. Here we examined whether central inhibition of lipid oxidation is sufficient to restore the hypothalamic levels of long-chain fatty acyl-CoAs (LCFA-CoAs) and to normalize food intake and glucose homeostasis in overfed rats. To this end, we targeted the liver isoform of carnitine palmitoyltransferase-1 (encoded by the CPT1A gene) by infusing either a sequence-specific ribozyme against CPT1A or an isoform-selective inhibitor of CPT1A activity in the third cerebral ventricle or in the mediobasal hypothalamus (MBH). Inhibition of CPT1A activity normalized the hypothalamic levels of LCFA-CoAs and markedly inhibited feeding behavior and hepatic glucose fluxes in overfed rats. Thus central inhibition of lipid oxidation is sufficient to restore hypothalamic lipid sensing as well as glucose and energy homeostasis in this model and may be an effective approach to the treatment of diet-induced obesity and insulin resistance.

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Authors: Pocai, A.
Affiliations: Albert Einstein College of Medicine (US)
Corresponding author: Pocai, A.
ORCID: Pocai, A.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2006-03-23
Volume: 116
Issue: 4
Pages: 1081-1091
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci26640
PMC: PMC1395479
OpenAlex: W2156594005
Cited by: 211
References: 52
Citations by year: 2026: 4 · 2025: 3 · 2024: 4 · 2023: 5 · 2022: 2 · 2021: 8 · 2020: 6 · 2019: 4 · 2018: 3 · 2017: 9 · 2016: 15 · 2015: 9 · 2014: 6 · 2013: 17 · 2012: 23
FWCI: 8.68
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: American Diabetes Association
Skirball Foundation
National Institutes of Health
Albert Einstein College of Medicine, Yeshiva University
National Institute on Aging (P01AG021654, AG 21654, T32AG023475)
National Institute of Diabetes and Digestive and Kidney Diseases (DK-48321, R01DK045024, R01DK048321, R37DK048321, DK20541, P60DK020541, DK-45024, P30DK020541)
Topics: Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Keywords: overfeeding, CPT1A, carnitine palmitoyltransferase 1, long-chain fatty acyl-CoA, lipid oxidation, hyperphagia, insulin resistance, diet-induced obesity, glucose homeostasis, energy homeostasis, hepatic glucose production, ribozymes, mediobasal hypothalamus, fatty acid signaling
MeSH terms: Animals, Carnitine O-Palmitoyltransferase, Energy Metabolism, Glucose, Homeostasis, Hyperphagia, Hypothalamus, Liver, Male, Models, Biological, Oxidation-Reduction, Rats, Sprague-Dawley, Lipid Metabolism, Rats

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Restoration of hypothalamic lipid sensing normalizes energy and glucose homeostasis in overfed rats

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