6 results match your criteria: "764 Clinical Research Building[Affiliation]"
Diabetes
December 2006
University of Pennsylvania School of Medicine, Division of Endocrinology, Diabetes and Metabolism, 764 Clinical Research Building, 415 Curie Blvd., Philadelphia, PA 19104, USA.
Adipose tissue secretes factors that control various physiological systems. The fall in leptin during fasting mediates hyperphagia and suppresses thermogenesis, thyroid and reproductive hormones, and immune system. On the other hand, rising leptin levels in the fed state stimulate fatty acid oxidation, decrease appetite, and limit weight gain.
View Article and Find Full Text PDFDiabetes
November 2006
University of Pennsylvania School of Medicine, Division of Endocrinology, Diabetes and Metabolism, 764 Clinical Research Building, 415 Curie Blvd., Philadelphia, PA 19104, USA.
Neuropeptide Y (NPY) stimulates feeding and weight gain, but deletion of the NPY gene does not affect food intake and body weight in mice bred on a mixed genetic background. We reasoned that the orexigenic action of NPY would be evident in C57Bl/6J mice susceptible to obesity. NPY deficiency has no significant effect in mice fed a normal rodent diet.
View Article and Find Full Text PDFDiabetes
November 2006
University of Pennsylvania School of Medicine, Division of Endocrinology, DiabetesMetabolism, 764 Clinical Research Building, 415 Curie Blvd., Philadelphia, PA 19104, USA.
Resistin levels are increased in obesity, and hyperresistinemia impairs glucose homeostasis in rodents. Here, we have determined the role of resistin in ob/ob mice that are obese and insulin resistant because of genetic deficiency of leptin. Loss of resistin increased obesity in ob/ob mice by further lowering the metabolic rate without affecting food intake.
View Article and Find Full Text PDFPhysiol Behav
April 2004
Department of Medicine, Division of Endocrinology, Diabetes & Metabolism, University of Pennsylvania School of Medicine, 415 Curie Boulevard, 764 Clinical Research Building, Philadelphia, PA 19104, USA.
The discovery of leptin was a major breakthrough in our understanding of the role of adipose tissue as a storage and secretory organ. Leptin was initially thought to act mainly to prevent obesity; however, studies have demonstrated profound effects of leptin in the response to fasting, regulation of neuroendocrine and immune systems, hematopoiesis, bone and brain development. This review will focus on the signaling pathways which mediate these diverse effects of leptin in the brain and other physiologic systems.
View Article and Find Full Text PDFDiabetes
July 2002
Division of Endocrinology, Diabetes and Metabolism, University of Pennsylvania School of Medicine, 764 Clinical Research Building, 415 Curie Boulevard, Philadelphia, PA 19104, USA.
The rise in obesity and its complications has generated enormous interest in the regulation of feeding and body weight. We show that a spermine metabolite of cholesterol (MSI-1436) decreases body weight, specifically fat, by suppressing feeding and preventing the reduction in energy expenditure, hormonal changes, and patterns of neuropeptide expression normally associated with weight loss. MSI-1436 enters the brain after peripheral injection and is more potent when injected into the cerebral ventricle (intracerebroventricular [ICV]).
View Article and Find Full Text PDFRegul Pept
August 2000
Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Pennsylvania School of Medicine, 764 Clinical Research Building, 415 Curie Blvd., 19104, Philadelphia, PA, USA.
Leptin is produced mainly by adipose tissue and has been shown to regulate feeding, energy balance and neuroendocrine function. Regulation of energy homeostasis by leptin is thought to be mediated by hypothalamic neuropeptides, at least in adult rodents. The neonatal period is a critical stage of development during which mammals have to optimize caloric intake to support growth and development, as well as maintain body temperature.
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