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  • mice
  • OLETF rats have a deficit in their ability to limit the size of meals and in contrast to CCK-1 receptor knockout mice, do not compensate for this increase in the size of their spontaneous meals, resulting in hyperphagia. (frontiersin.org)
  • Study of the OLETF rats has revealed important differences in the organization of the DMH in rats and mice and elucidated previously unappreciated roles for DMH NPY in energy balance and glucose homeostasis. (frontiersin.org)
  • function
  • Characterization of overall pancreatic function in OLETF rats demonstrated the absence of a pancreatic amylase response to administration of the brain gut peptide cholecystokinin (CCK) ( 2 ). (frontiersin.org)
  • expression
  • Prior to becoming obese and in response to pair feeding, OLETF rats have increased expression of neuropeptide Y (NPY) in the compact region of the dorsomedial hypothalamus (DMH), and this overexpression contributes to their overall hyperphagia. (frontiersin.org)
  • model
  • OLETF rats were initially studied primarily as a model of late onset type 2 diabetes, as older OLETF rats were not only obese but also hyperglycemic and insulin resistant ( 1 ). (frontiersin.org)