Abstract：
:Leptin activates the long form of the leptin receptor (LRb) to control feeding and neuroendocrine function and thus regulate adiposity. While adiposity influences insulin sensitivity, leptin also regulates glucose homeostasis independently of energy balance. Disruption of the LRb/STAT3 signal in s/s mice results in hyperphagia, neuroendocrine dysfunction, and obesity similar to LRb null db/db mice. Insulin resistance and glucose intolerance are improved in s/s compared to db/db animals, however, suggesting that LRb/STAT3-independent signals may contribute to the regulation of glucose homeostasis by leptin. Indeed, caloric restriction normalized glycemic control in s/s animals, but db/db mice of similar weight and adiposity remained hyperglycemic. These differences in glucose homeostasis were not attributable to differences in insulin production between s/s and db/db animals but rather to decreased insulin resistance in s/s mice. Thus, in addition to LRb/STAT3-mediated adiposity signals, non-LRb/STAT3 leptin signals mediate an important adiposity-independent role in promoting glycemic control.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Bates SH,Kulkarni RN,Seifert M,Myers MG Jrdoi
10.1016/j.cmet.2005.02.001keywords:
subject
Has Abstractpub_date
2005-03-01 00:00:00pages
169-78issue
3eissn
1550-4131issn
1932-7420pii
S1550-4131(05)00054-9journal_volume
1pub_type
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