Attenuation of the obesity syndrome of ob/ob mice by the loss of neuropeptide Y.
The obesity syndrome of ob/ob mice results from lack of leptin, a hormone released by fat cells that acts in the brain to suppress feeding and stimulate metabolism. Neuropeptide Y (NPY) is a neuromodulator implicated in the control of energy balance and is overproduced in the hypothalamus of ob/ob mice. To determine the role of NPY in the response to leptin deficiency, ob/ob mice deficient for NPY were generated. In the absence of NPY, ob/ob mice are less obese because of reduced food intake and increased energy expenditure, and are less severely affected by diabetes, sterility, and somatotropic defects. These results suggest that NPY is a central effector of leptin deficiency.
Erickson
J C
JC
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195-7370, USA.
Hollopeter
G
G
Palmiter
R D
RD
D000273:Adipose Tissue / Q000473:pathology; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001823:Body Composition; D001827:Body Height; D001835:Body Weight; D003920:Diabetes Mellitus / Q000209:etiology; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology; D004435:Eating; D004734:Energy Metabolism; D005260:Female; D005298:Fertility; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D020738:Leptin; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D008820:Mice, Obese; D009478:Neuropeptide Y / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D009765:Obesity / Q000473:pathology / Q000503:physiopathology*; D010101:Oxygen Consumption; D011506:Proteins / Q000235:genetics / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism
D001786:Blood Glucose; D020738:Leptin; D009478:Neuropeptide Y; D011506:Proteins; D012333:RNA, Messenger; D007334:Insulin-Like Growth Factor I