| Leptin intake during the suckling period improves the metabolic response of adipose tissue to a high-fat diet. | |
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MedLine Citation:
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PMID: 20157325 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: The intake of leptin during the suckling period protects against obesity and improves insulin and central leptin sensitivity in adult rats. OBJECTIVE: We analyzed whether leptin treatment to neonates may also improve later peripheral leptin sensitivity in adipose tissue under high-fat (HF) diet conditions. DESIGN: Male rats were supplemented with a daily oral dose of leptin or the vehicle (controls) during the suckling period. After weaning, animals were fed a normal-fat or an HF diet until the age of 6 months. At this age, mRNA and protein levels of the long-form leptin receptor (OB-Rb) and the expression of other genes related with energy metabolism were measured in various adipose depots (inguinal, mesenteric and retroperitoneal). RESULTS: HF-diet feeding resulted in lower OB-Rb mRNA and protein levels in internal depots in controls but not in leptin-treated animals; these animals maintained OB-Rb mRNA and protein levels under HF-diet conditions in these depots, particularly in the mesenteric one, and this was accompanied by increased expression of genes related with energy uptake (GLUT4, CD36), fatty acid oxidation (peroxisome proliferator activated receptor-alpha (PPARalpha), CPT1, UCP3) and lipogenesis (PPARgamma, GPAT). Leptin-treatment also ameliorated HF-diet-induced hepatic fat accumulation occurring in control animals. CONCLUSION: Leptin treatment during the suckling period may improve the lasting effects of HF-diet feeding on leptin receptor abundance in the adipose tissue and increase its oxidative capacity, resulting in a better handling and partitioning of excess fuel. This, together with the described improvement of central leptin sensitivity, may explain why these animals are more protected against diet-induced obesity and its metabolic-related disorders. |
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Authors:
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T Priego; J Sánchez; A Palou; C Picó |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-02-16 |
Journal Detail:
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Title: International journal of obesity (2005) Volume: 34 ISSN: 1476-5497 ISO Abbreviation: Int J Obes (Lond) Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-05-10 Completed Date: 2010-11-04 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101256108 Medline TA: Int J Obes (Lond) Country: England |
Other Details:
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Languages: eng Pagination: 809-19 Citation Subset: IM |
Affiliation:
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Laboratory of Molecular Biology, University of the Balearic Islands, Palma de Mallorca, Spain. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipose Tissue
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drug effects,
metabolism* Animals Animals, Suckling Antigens, CD36 / metabolism Blotting, Western Body Weight / physiology Dietary Fats / administration & dosage, metabolism* Energy Metabolism / physiology Fatty Acids / metabolism Gene Expression Regulation, Developmental / physiology Glucose Transporter Type 4 / metabolism Ion Channels / metabolism Leptin / administration & dosage*, metabolism Male Mitochondrial Proteins / metabolism PPAR alpha / metabolism PPAR gamma / metabolism RNA, Messenger / metabolism Rats Rats, Wistar Receptors, Leptin / metabolism* Weaning |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD36; 0/Dietary Fats; 0/Fatty Acids; 0/Glucose Transporter Type 4; 0/Ion Channels; 0/Leptin; 0/Mitochondrial Proteins; 0/PPAR alpha; 0/PPAR gamma; 0/RNA, Messenger; 0/Receptors, Leptin; 0/Slc2a4 protein, rat; 0/mitochondrial uncoupling protein 3 |
| Comments/Corrections | |
Comment In:
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Nat Rev Gastroenterol Hepatol. 2010 Jul;7(7):359
[PMID:
20626075
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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