Document Detail


Leptin and insulin modulate nutrient partitioning and weight loss in ob/ob mice through regulation of long-chain fatty acid uptake by adipocytes.
MedLine Citation:
PMID:  12949354     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Leptin treatment of ob/ob mice leads to weight loss appreciably greater than that in pair-fed mice. To test whether this "extra" weight loss is mediated by leptin-induced alterations in nutrient partitioning, the effects in ob/ob mice of subcutaneous leptin infusion (500 ng/h for <or=21 d) on adipocyte fatty acid uptake and transporter gene expression were examined. Mice were initially hyperinsulinemic (5.25 +/- 1.57 nmol/L). Plasma insulin decreased by 55 +/- 10% within 8 h of leptin infusion, declining progressively to normal by d 14. The V(max) for saturable adipocyte fatty acid uptake fell from 31.1 +/- 5.6 to 25.2 +/- 4.0 pmol/(s. 50000 cells) (P < 0.05) by 24 h, and to a normal rate (8.0 +/- 0.8 pmol/(s. 50000 cells) by d 21 (P > 0.5 vs. normal C57BL/6J controls). Adipocyte mRNA levels for plasma membrane fatty acid binding protein and fatty acid translocase, putative fatty acid transporters that are up-regulated three- to fourfold in adipocytes from ob/ob mice, had also normalized by d 21. The initial changes in V(max) preceded decreases in food intake and body weight by at least 24 h. In pair-fed mice, insulin levels, V(max) and body weight all declined more slowly than in leptin-treated mice, and all remained significantly elevated compared with normal values at d 21. The data suggest that insulin up-regulates and leptin down-regulates adipocyte fatty acid uptake, leading to alterations in fatty acid partitioning that affect adiposity.
Authors:
Xinqing Fan; Michael W Bradbury; Paul D Berk
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of nutrition     Volume:  133     ISSN:  0022-3166     ISO Abbreviation:  J. Nutr.     Publication Date:  2003 Sep 
Date Detail:
Created Date:  2003-09-01     Completed Date:  2003-10-28     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0404243     Medline TA:  J Nutr     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2707-15     Citation Subset:  IM    
Affiliation:
Departments of Medicine, The Mount Sinai School of Medicine, New York, NY 10029, USA.
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MeSH Terms
Descriptor/Qualifier:
Adipocytes / metabolism*,  pathology
Animal Nutritional Physiological Phenomena*
Animals
Antigens, CD36
Aspartate Aminotransferases / genetics
Body Weight / drug effects
Cell Size
Eating / drug effects
Fatty Acids / chemistry,  metabolism*
Insulin / blood,  pharmacology,  physiology*
Kinetics
Leptin / blood,  pharmacology,  physiology*
Male
Membrane Glycoproteins / genetics
Mice
Mice, Inbred C57BL
Mice, Inbred Strains
Mitochondria / enzymology
Obesity / genetics,  pathology,  physiopathology*
Organic Anion Transporters / genetics
Osmolar Concentration
RNA, Messenger / metabolism
Receptors, Leptin
Weight Loss / physiology*
Grant Support
ID/Acronym/Agency:
DK26438/DK/NIDDK NIH HHS; DK52401/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD36; 0/Fatty Acids; 0/Leptin; 0/Membrane Glycoproteins; 0/Organic Anion Transporters; 0/RNA, Messenger; 0/Receptors, Leptin; 0/leptin receptor, mouse; 11061-68-0/Insulin; EC 2.6.1.1/Aspartate Aminotransferases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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