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The weight-reducing effect of an intracerebroventricular bolus injection of leptin in genetically obese fa/fa rats. Reduced sensitivity compared with lean animals. (1996)

by I Cusin, F Rohner-Jeanrenaud, A Stricker-Krongrad, B Jeanrenaud
Venue:Diabetes
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Regulation of body weight in humans

by Luc Tappy - Physiology Review , 1999
"... A. Is there a set point for body weight? 452 B. Does metabolic efficiency vary between individuals? 453 II. Nutrient Balance 455 A. Why macronutrients can be considered separately 455 ..."
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A. Is there a set point for body weight? 452 B. Does metabolic efficiency vary between individuals? 453 II. Nutrient Balance 455 A. Why macronutrients can be considered separately 455
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...the hypothalamus (270). This mechanism could explain the reduction in appetite and the increase in energy expenditure induced by leptin administration in ob/ob and DIO mice. Furthermore, Cusin et al. =-=(64)-=- reported that intracerebroventricular bolus injection of leptin in lean rats resulted in a decrease in NPY levels in its sites of synthesis (arcuate nucleus) of the hypothalamus; this effect was asso...

MAYUMI TAKASAKI,1 AND HIROSHI KANNAN2 Departments of 1Anesthesiology and 2Physiology and 3Internal Medicine,

by Masamitsu Nakazato, Mayumi Takasaki, Hiroshi Kannan
"... rapid communication Sympathetic and cardiovascular actions of orexins in conscious rats ..."
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rapid communication Sympathetic and cardiovascular actions of orexins in conscious rats
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...se relationship between obesity, hypertension, and altered cardiovascular responses (10). In this regard, leptin, the peptide product of the obese gene (25), has been reported to decrease food intake =-=(3)-=- and to produce an increase in MAP (5, 16) and RSNA (5). Therefore, these neuropeptides, leptin and orexin, which are involved in the control of energy balance, may be chemical mediators in the brain ...

effects of brain leptin administration in the rat Metabolic, gastrointestinal, and CNS neuropeptide Melanocortin Signaling in Rats Hypothalamic, Metabolic, and Behavioral Responses to Pharmacological Inhibition of CNS

by G Baskin , Stephen C Woods , Michael W Schwartz , Charles W Wilkinson , Paul Burn , L Arthur Campfield , Renata Tenenbaum , Denis Gertjan Van Dijk , Randy J Seeley , Todd E Thiele , Mark I Friedman , Hong Ji , Jill E Schneider , Dan Zhou , Folkert Kuipers , Roger A H Adan , Denis G Baskin , Michael W Schwartz , Gertjan Van Dijk , Tiziana Adage , Anton J W Scheurink , Sietse F De Boer , Koert De Vries , Jan Pieter Konsman , Gertjan Van Dijk , Marie-Pierre Ruffin , Tiziana Adage , Folkert Kuipers , Jan H Strubbe , Anton J W Scheurink
"... ..."
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Nashville, TN Approved:

by Kelly Ann Posey, Alan D. Cherrington, Richard M. O’brien, Owen P. Mcguinness, Larry L. Swift, Maureen A. Gannon, Phd Acknowledgements , 2009
"... This work would not be possible without the help of so many others. Although I cannot begin to thank all of those involved or even express in words my gratitude, I would like to acknowledge the following. First of all the Molecular Physiology and Biophysics department deserves a thank you for their ..."
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This work would not be possible without the help of so many others. Although I cannot begin to thank all of those involved or even express in words my gratitude, I would like to acknowledge the following. First of all the Molecular Physiology and Biophysics department deserves a thank you for their continued support of all the graduate students. We have the privilege to work with wonderful faculty members and staff that always place the best interest of the student first. In particular, I would like to acknowledge Angie Pernell, Dr. Chuck Cobb, and Dr. Danny Winder for their support and guidance in navigating the maze that is graduate school. A special thanks to Angie for being an advocate and a friend, and for going above and beyond to make our graduate school experience as painless as possible. I am also grateful for my dissertation committee members Dr. Alan Cherrington,
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...icates leptin transport is decreased in obesity [10]. However, resistance to the food lowering effects of centrally administered leptin is also observed in genetically obese and HF fed, obese rodents =-=[51, 105]-=-, unpublished observations). Thus, inadequate transport does not fully explain the CNS leptin resistance seen in obesity, but appears to be a contributing factor. In addition, the ability of leptin to...

Journal of Clinical Endocrinology and Metabolism Printed in U.S.A. Copyright © 1998 by The Endocrine Society Evidence for Leptin Regulation of Food Intake in Humans*

by Hillevi Larsson, Sölve Elmståhl, Göran Berglund, Bo Ahrén
"... The adipocyte hormone leptin regulates body weight in mice by decreasing food intake and increasing energy expenditure. Whether leptin is of physiological importance for these processes in humans is, however, not clear. We therefore studied the relation between leptin and habitual food intake in 64 ..."
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The adipocyte hormone leptin regulates body weight in mice by decreasing food intake and increasing energy expenditure. Whether leptin is of physiological importance for these processes in humans is, however, not clear. We therefore studied the relation between leptin and habitual food intake in 64 healthy postmenopausal women. Dietary habits were assessed with a modified diet history method. Body fat content was measured using bioelectrical impedance. In the 64 women, aged 58.6 � 0.4 yr (mean � SD), serum leptin was 19.3 � 12.7 ng/mL, body mass index was 25.0 � 3.5 kg/m 2, body fat content was 31.6 � 4.3%, fasting glucose was 4.6 � 0.5 mmol/L, and fasting insulin LEPTIN is produced in adipose tissue and is known to regulate body weight in mice. Thus, leptin administration inhibits food intake (1, 2) through a central effect on leptin receptors in the hypothalamus (3, 4), and increases
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...leptin is related to the quantity rather than the quality of habitual food intake. (J Clin Endocrinol Metab 83: 4382–4385, 1998) As leptin has been demonstrated to inhibit NPY in the rat hypothalamus =-=(4, 21, 22)-=-, it is conceivable that leptin, in addition to regulating total energy intake, is related to qualitative aspects of food intake. Our aim was to determine whether leptin levels are associated with hab...

Journal of Clinical Endocrinology and Metabolism Printed in U.S.A. Copyright © 1999 by The Endocrine Society Central Administration of Leptin Inhibits Food Intake and Activates the Sympathetic Nervous System in Rhesus Macaques*

by Mads Tang-christensen, Peter J. Havel, Rebecca R. Jacobs, Philip J. Larsen, Judy, L. Cameron
"... The present study was performed to determine the effects of central administration of leptin on food intake and sympathetic nervous system activity in a nonrodent species, the rhesus monkey. Peripheral administration of leptin at doses (1 and 3 �g/kg, sc) that produced increments of circulating lept ..."
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The present study was performed to determine the effects of central administration of leptin on food intake and sympathetic nervous system activity in a nonrodent species, the rhesus monkey. Peripheral administration of leptin at doses (1 and 3 �g/kg, sc) that produced increments of circulating leptin concentrations within a physiological range did not inhibit food intake over the subsequent 3 days. In contrast, leptin (1 �g/kg, intracerebroventricularly) had no acute effect on food intake, but caused a significant and sustained suppression (40–50%) of food intake during the entire following day (P � 0.01). In addition, circulating norepinephrine levels increased by 55 � 16% (P � 0.02) 1 h after intracerebroventricular leptin administration, but LEPTIN, a hormone produced by adipocytes, is believed to play an important role in the regulation of body adiposity by acting at the level of the central nervous system
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...n leptin’s action on food intake in rodents (21, 22). Although the icv dose of leptin employed, based on body weight, was substantially lower than the doses used in studies with icv leptin in rodents =-=(20, 25, 32, 33)-=-, it may have been a pharmacological dose. Average concentrations of leptin in the CSF of healthy human subjects are approximately 0.2–0.3 ng/mL (50, 51). It is very likely that central administration...

The Journal of Clinical Endocrinology & Metabolism Printed in U.S.A. Copyright © 1999 by The Endocrine Society Liver Pathology and the Metabolic Syndrome X in

by Severe Obesity, P. Marceau, S. Biron, F. -s. Hould, S. Marceau, S. Simard, S. N. Thung
"... The metabolic syndrome X, characterized by insulin resistance, dyslipidemia, hypertension, and a male, visceral distribution of adipose tissue, is associated with increased morbidity and mortality from several prevalent diseases, such as diabetes, cancers, myocardial infarction, and stroke. Because ..."
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The metabolic syndrome X, characterized by insulin resistance, dyslipidemia, hypertension, and a male, visceral distribution of adipose tissue, is associated with increased morbidity and mortality from several prevalent diseases, such as diabetes, cancers, myocardial infarction, and stroke. Because the liver has a central role in carbohydrate, lipid, and steroid metabolism, we investigated the relationships between liver pathology and the metabolic syndrome. Blood chemistry, anthropometry (waist/hip circumference ratio), and intraoperative routine knife biopsies of the liver were obtained in 551 (112 men) severely obese patients (body mass index, 47 � 9; mean � SD) undergoing antiobesity surgery. Steatosis was found in 86%, fibrosis in 74%, mild inflammation or steatohepatitis in 24%, and unexpected FATTY infiltration is a typical response of the liver to a wide array of noxious stimuli, including hypoxia, toxins,
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...sults in a receptor protein lacking the intracellular signaling domain (33–35). The fa/fa rat, but not the db/db mouse, will respond to exogenous leptin when it is delivered intracerebroventricularly =-=(39)-=-. The fa mutation may either impair transport of leptin or reduce the number of receptors that are localized in the plasma membrane. The biological effects of leptin are thought to result from the act...

Biochemical and Molecular Roles of Nutrients Phenotypic Consequences of a Nonsense Mutation in the Leptin Receptor Gene (fa k) in Obese Spontaneously Hypertensive Koletsky Rats (SHROB) 1,2,3

by Tatsuya Ishizuka, Paul Ernsberger, Sha Liu, David Bedol, Timothy M. Lehman, Richard J. Koletsky, Jacob E. Friedman
"... ABSTRACT The genetically obese Koletsky rat (SHROB, fa k) has a novel point mutation of the leptin receptor at amino acid �763, resulting in a premature stop codon in the leptin receptor extracellular domain. This implies that all leptin receptor isoforms should be absent in this model. We examined ..."
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ABSTRACT The genetically obese Koletsky rat (SHROB, fa k) has a novel point mutation of the leptin receptor at amino acid �763, resulting in a premature stop codon in the leptin receptor extracellular domain. This implies that all leptin receptor isoforms should be absent in this model. We examined the phenotypic consequences of this mutation on leptin and leptin receptor mRNA in hypothalamus and peripheral tissues from SHROB and their lean SHR littermates. Despite the mutation, mRNA for both the long (ObRa) and the short (ObRb) form were expressed at comparable levels in SHROB and SHR in brain and throughout peripheral tissues. Adipose tissue mRNA for leptin was two to three times greater in SHROB compared to SHR (P � 0.01), while circulating leptin concentration was 170 times greater than SHR littermates (P � 0.01), suggesting extreme leptin resistance in SHROB. Leptin was also detected in the cerebrospinal fluid (CSF) of SHR and SHROB (13.8 and 27.2 pmol/L, respectively); however, the CSF/plasma ratio for leptin was 32-fold greater in SHR than in SHROB. To assess the putative action of leptin and leptin receptors on insulin-mediated glucose transport, muscles from SHR and SHROB were incubated in vitro with recombinant human leptin. Leptin directly suppressed insulin-mediated glucose transport by 50 % in skeletal muscle from SHR but not in obese SHROB rats lacking all forms of the leptin receptor. These results suggest that the natural leptin receptor knockout in the SHROB represents a unique rat model to define the functional role(s) of leptin in central and peripheral energy metabolism. J. Nutr. 128: 2299–2306, 1998.
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.... 1996b). The fa mutation reduced binding affinity of the leptin receptor (Yamashita et al. 1997), reduced its receptor density, and impaired responsiveness to exogenous leptin in fa/fa rats in vivo (=-=Cusin et al. 1996-=-). The obesity mutation fa k is predicted to truncate all forms of the leptin receptor, leaving the SHROB incapable of signaling central and peripheral responses mediated by leptin. The highest levels...

©2004 FASEB The FASEB Journal express article 10.1096/fj.04-2295fje. Published online September 23, 2004.

by unknown authors
"... A new function of the leptin receptor: mediation of the recovery from lipopolysaccharide-induced hypothermia ..."
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A new function of the leptin receptor: mediation of the recovery from lipopolysaccharide-induced hypothermia

RESEARCH ARTICLE Leptin Is Required for Glucose Homeostasis after Roux-en-Y Gastric Bypass in Mice

by unknown authors
"... ☯ These authors contributed equally to this work. ..."
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☯ These authors contributed equally to this work.
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