Document Detail

Obesity of TallyHO/JngJ Mouse Is Due to Increased Food Intake with Early Development of Leptin Resistance.
MedLine Citation:
PMID:  21031339     Owner:  NLM     Status:  In-Data-Review    
TALLYHO/JngJ (TallyHo) mouse is a recently established animal model for type 2 diabetes mellitus (T2DM) with phenotypes of mild obesity and male-limited hyperglycemia. In this study, we investigated how obesity develops in TallyHo mice by measuring parameters of food intake and energy expenditure. At 4 weeks of age, TallyHo mice were heavier than control C57BL/6 mice with increased food intake but comparable energy expenditure parameters, such as body temperature, cold-induced thermogenesis, oxygen consumption rate (VO (2)) and spontaneous locomotor activity. Furthermore, pair-fed TallyHo mice, which were fed the same amount of food as C57BL/6 mice, showed similar patterns of body weight gain to C57BL/6 mice at all ages, implying that obesity in TallyHo mice may develop by increased food intake but not by decreased energy consumption. TallyHo mice appear to have hypothalamic leptin resistance at 4 weeks of age, as indicated by the increased expression of orexigenic neuropeptides in the hypothalamus and no alteration of food intake and neuropeptide expression upon intravenous leptin treatment. Leptin injection to TallyHo mice, however, increased the phosphorylation of STAT3 and Akt, an important signaling mediator of leptin, in a pattern similar to that in C57BL/6 mice. In conclusion, increased food intake is a crucial component in the development of obesity in TallyHo mice, in which central leptin resistance, possibly caused by uncoupling between activation of leptin signaling and neuropeptide expression, might be involved.
S D Rhee; Y Y Sung; Y S Lee; J Y Kim; W H Jung; M J Kim; M-S Lee; M K Lee; S-D Yang; H G Cheon
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Publication Detail:
Type:  Journal Article     Date:  2010-10-28
Journal Detail:
Title:  Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association     Volume:  119     ISSN:  1439-3646     ISO Abbreviation:  Exp. Clin. Endocrinol. Diabetes     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-04-05     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9505926     Medline TA:  Exp Clin Endocrinol Diabetes     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  243-51     Citation Subset:  IM    
Copyright Information:
© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York.
Center for Metabolic Syndrome Therapeutics, Korea Research Institute of Chemical Technology, Daejon, Korea.
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