Abstract:
:Single-minded 1 (SIM1) mutations are associated with obesity in mice and humans. Haploinsufficiency of mouse Sim1 causes hyperphagic obesity with increased linear growth and enhanced sensitivity to a high-fat diet, a phenotype similar to that of agouti yellow and melanocortin 4 receptor knockout mice. To investigate the effects of increased Sim1 dosage, we generated transgenic mice that overexpress human SIM1 and examined their phenotype. Compared with wild-type mice, SIM1 transgenic mice had no obvious phenotype on a low-fat chow diet but were resistant to diet-induced obesity on a high-fat diet due to reduced food intake with no change in energy expenditure. The SIM1 transgene also completely rescued the hyperphagia and partially rescued the obesity of agouti yellow mice, in which melanocortin signaling is abrogated. Our results indicate that the melanocortin 4 receptor signals through Sim1 or its transcriptional targets in controlling food intake but not energy expenditure.
journal_name
Endocrinologyjournal_title
Endocrinologyauthors
Kublaoui BM,Holder JL Jr,Tolson KP,Gemelli T,Zinn ARdoi
10.1210/en.2006-0453subject
Has Abstractpub_date
2006-10-01 00:00:00pages
4542-9issue
10eissn
0013-7227issn
1945-7170pii
en.2006-0453journal_volume
147pub_type
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