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Species | Barry LevinSummaryAffiliation: New Jersey Country: USA Publications
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Publications
Effect of streptozotocin-induced diabetes on rat brain sulfonylurea binding sitesB E Levin
Neurology Service 127C, VA Medical Center, East Orange, NJ 07018 1095, USA
Brain Res Bull 46:513-8. 1998..These and other data suggest that this combination of abnormalities in diabetes should have an adverse effect on the glucose sensing capacity of the brain...
Let the sensor fit the dietBarry E Levin
Neurology Service, Veterans Administration Medical Center, East Orange, NJ 07019, USA Department of Neurology and Neurosciences, New Jersey Medical School University of Medicine and Dentistry of New Jersey, Newark, NJ 07101, USA Electronic address
Cell Metab 16:689-90. 2012..Miyamoto et al. (2012) describe fly neurons that are highly tuned to fructose availability and are critical determinants of ingestive behavior on a diet of simple sugars...- Factors promoting and ameliorating the development of obesityBarry E Levin
385 Tremont Avenue, VA Medical Center, Neurology Service 127C E Orange, NJ 07018 1095, United States
Physiol Behav 86:633-9. 2005.... 
Epigenetic influences on food intake and physical activity level: review of animal studiesBarry E Levin
Neurology Service, VA Medical Center, East Orange, New Jersey, USA
Obesity (Silver Spring) 16:S51-4. 2008..Because perinatal manipulations can permanently alter the systems which regulate energy homeostasis, it behooves us to identify the responsible factors as a means of stemming the tide of the emerging worldwide obesity epidemic...- Chronic exercise lowers the defended body weight gain and adiposity in diet-induced obese ratsBarry E Levin
Neurology Service 127C VA Medical Center, 385 Tremont Ave, E Orange, NJ 07018 1095, USA
Am J Physiol Regul Integr Comp Physiol 286:R771-8. 2004..This may be due to exercise-related factors other than plasma insulin and leptin... - Obesity-prone rats have normal blood-brain barrier transport but defective central leptin signaling before obesity onsetBarry E Levin
Neurology Service, Veterans Affairs Memorial Center, E Orange, NJ 07018 1095, USA
Am J Physiol Regul Integr Comp Physiol 286:R143-50. 2004..Defects in leptin transport appear to be an acquired defect associated with the development of obesity and possibly age... - Abnormalities of leptin and ghrelin regulation in obesity-prone juvenile ratsBarry E Levin
Neurology Service, Department of Veterans Affairs Medical Center, 127C VA Medical Center, 385 Tremont Ave, E Orange, NJ 07018 1095, USA
Am J Physiol Endocrinol Metab 285:E949-57. 2003..These data suggest that increased ghrelin signaling is not a proximate cause of DIO, whereas reduced leptin sensitivity might play a causal role... - A new obesity-prone, glucose-intolerant rat strain (F.DIO)Barry E Levin
Neurology Service, 127C VA Medical Center, 385 Tremont Ave, E Orange, NJ 07018 1095, USA
Am J Physiol Regul Integr Comp Physiol 285:R1184-91. 2003..Preservation of the DIO and glucose intolerance traits through successive backcrosses and inbreeding cycles to produce the F.DIO strain lends further support to the idea that they inherited in a polygenic fashion... - Synergy of nature and nurture in the development of childhood obesityB E Levin
Neurology Service, VA Medical Center, 385 Tremont Avenue, East Orange, NJ 07018 1095, USA
Int J Obes (Lond) 33:S53-6. 2009.... - Interaction of perinatal and pre-pubertal factors with genetic predisposition in the development of neural pathways involved in the regulation of energy homeostasisBarry E Levin
Neurology Service 127C, Veterans Administration Medical Center, and Department of Neurology and Neurosciences, New Jersey Medical School, E Orange, Newark, NJ 07018 1095, USA
Brain Res 1350:10-7. 2010..Such studies suggest that early identification of obesity-prone humans and of the factors that can prevent them from becoming obese could provide an effective strategy for preventing the world wide epidemic of obesity... - Neuronal glucose sensing: still a physiological orphan?Barry E Levin
Neurology Service, Veterans Affairs Medical Center, East Orange, NJ 07018 1095, USA
Cell Metab 6:252-4. 2007..2007) disrupting glucose sensing in pro-opiomelanocortin neurons via differing methods have yielded disparate energy and glucose homeostasis phenotypes, suggesting that neuronal glucose sensing is not critical for these processes... - Neurotrophism and energy homeostasis: perfect togetherBarry E Levin
Neurology Service (127C, Veteran Affairs Medical Center, 385 Tremont Avenue, E. Orange, NJ 07018-1095, USA
Am J Physiol Regul Integr Comp Physiol 293:R988-91. 2007 - Differential effects of exercise on body weight gain and adiposity in obesity-prone and -resistant ratsB E Levin
Neurology Service, Veterans Affairs Medical Center, E Orange, NJ, USA
Int J Obes (Lond) 30:722-7. 2006..To determine the effect of exercise on weight gain and adiposity in obesity-prone and -resistant rats... - Why some of us get fat and what we can do about itBarry E Levin
Neurology Service, VA Medical Center, East Orange, NJ 07018 1095, USA
J Physiol 583:425-30. 2007.... - Neuronal glucosensing: what do we know after 50 years?Barry E Levin
Neurology Service 127C, Department of Veterans Affairs NJ Health Care System, 385 Tremont Ave, East Orange, NJ 07018 1095, USA
Diabetes 53:2521-8. 2004..Thus, although much is known, much remains to be learned about the physiological function of brain glucosensing neurons... - Central regulation of energy homeostasis intelligent design: how to build the perfect survivorBarry E Levin
Neurology Service, VA Medical Center, 385 Tremont Avenue, East Orange, NJ 07018 1095, USA
Obesity (Silver Spring) 14:192S-196S. 2006..Thus, effective treatment of obesity will only come with a better understanding of the physiological, metabolic, and neurochemical processes that ensure this defense of an elevated body weight... - Metabolic sensing neurons and the control of energy homeostasisBarry E Levin
Neurology Service 127C, VA Medical Center, 385 Tremont Ave, E Orange, NJ 07018 1095, USA
Physiol Behav 89:486-9. 2006..This may provide one mechanism underlying their propensity to become obese when exposed to diets high in fat and caloric density. Thus, metabolic sensing neurons may provide a potential therapeutic target for the treatment of obesity... - Exercising the obese brain: resetting the defended body weightBarry E Levin
Neurology Service (127C, Veterans Affairs Medical Center, 385 Tremont Avenue, East Orange, New Jersey 07018-1095, USA
Endocrinology 146:1674-5. 2005 - F-DIO obesity-prone rat is insulin resistant before obesity onsetBarry E Levin
Neurology Service 127C, VA Medical Center, 385 Tremont Avenue, E Orange, NJ 07018 1095, USA
Am J Physiol Regul Integr Comp Physiol 289:R704-11. 2005..Thus F-DIO rats represent a novel and potentially useful model for the study of DIO, insulin resistance, and perinatal factors that influence the development and persistence of obesity... - Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasisBarry E Levin
Neurology Service 127C, Veterans Administration Medical Center, East Orange, NJ 07018 1095, USA
Philos Trans R Soc Lond B Biol Sci 361:1107-21. 2006..Such prevention should begin in the perinatal period with the identification and avoidance of factors which produce permanent, adverse alterations in neural pathways which control energy homeostasis... - Glucosensing neurons: the metabolic sensors of the brain?B E Levin
Neurology Service, VA Medical Center, E Orange, New Jersey 07018 1095, USA
Diabetes Nutr Metab 15:274-80; discussion 281. 2002 - Developmental gene x environment interactions affecting systems regulating energy homeostasis and obesityBarry E Levin
Neurology Service, VA Medical Center, E Orange, NJ 07018 1095, USA
Front Neuroendocrinol 31:270-83. 2010..These studies suggest that early identification of obesity-prone humans and of the factors that can prevent them from becoming obese could provide an effective strategy for preventing the world-wide epidemic of obesity... - Maternal obesity alters adiposity and monoamine function in genetically predisposed offspringBarry E Levin
Neurology Service, Veterans Affairs Medical Center, East Orange, NJ 07018 1095, USA
Am J Physiol Regul Integr Comp Physiol 283:R1087-93. 2002..Thus maternal obesity was associated with alterations in offspring brain monoamine metabolism, which varied as a function of genotype and the development of offspring obesity... - Ventromedial hypothalamic glucokinase is an important mediator of the counterregulatory response to insulin-induced hypoglycemiaBarry E Levin
Neurology Service, Department of Veterans Affairs New Jersey Health Care System, East Orange, New Jersey 07018 1095, USA
Diabetes 57:1371-9. 2008.... - The obesity epidemic: metabolic imprinting on genetically susceptible neural circuitsB E Levin
Department of Neurosciences, NJ Medical School, Newark 07103, USA
Obes Res 8:342-7. 2000.... - Brain glucose sensing and body energy homeostasis: role in obesity and diabetesB E Levin
Neurology Service, Veterans Affairs Medical Center, East Orange 07018, USA
Am J Physiol 276:R1223-31. 1999..Thus the challenge for the future is to define the role of brain glucose sensing in the physiological regulation of energy balance and in the pathophysiology of obesity and diabetes... - Reduced glucose-induced neuronal activation in the hypothalamus of diet-induced obese ratsB E Levin
Neurology Service 127C, VA Medical Center, 385 Tremont Avenue, East Orange, NJ 07018 1095, USA
Brain Res 808:317-9. 1998..This suggests that enhanced glucose-induced sympathetic activation in DIO rats is related to a failure of glucose to produce neuronal activation in these areas... - In vivo and in vitro regulation of [3H]glyburide binding to brain sulfonylurea receptors in obesity-prone and resistant rats by glucoseB E Levin
Neurology Service 127C, VA Medical Center, E Orange, NJ 07018, USA
Brain Res 776:146-53. 1997..Again, there was little effect on high-affinity binding. Thus, glucose may affect the firing of glucose-responsive neurons by indirectly altering KATP channel function via its effects on low-affinity cell body SUR... - Differential effects of diet and obesity on high and low affinity sulfonylurea binding sites in the rat brainB E Levin
Neurology Service 127C, DVA Medical Center, NJ 07018, USA
Brain Res 739:293-300. 1996..These studies demonstrate a significant population of low affinity sulfonylurea binding sites throughout the forebrain which, along with high affinity sites, are regulated as a function of both weight gain phenotype and diet composition... - Glucose-regulated dopamine release from substantia nigra neuronsB E Levin
Neurology Service 127C, VA Medical Center, 385 Tremont Ave, E Orange, NJ 17018, USA
Brain Res 874:158-64. 2000..These interactions could provide a mechanism whereby glucose modulates motor activity involved in food intake... - Differential stress responsivity in diet-induced obese and resistant ratsB E Levin
Neurology Service, Department of Veterans Affairs Medical Center, East Orange 07018, USA
Am J Physiol Regul Integr Comp Physiol 279:R1357-64. 2000..Thus DIO rats are hyporesponsive to chronic stress compared with DR rats. This is in keeping with several other known differences in hypothalamopituitary and autonomic function in this model... - Metabolic imprinting on genetically predisposed neural circuits perpetuates obesityB E Levin
Department of Neurosciences, New Jersey Medical School, Newark, New Jersey, USA
Nutrition 16:909-15. 2000..Thus, early intervention in mothers, infants, children, and adults may be the only way to prevent the formation of permanent neural connections that promote and perpetuate obesity in genetically predisposed individuals... - Reduced central leptin sensitivity in rats with diet-induced obesityBarry E Levin
Neurology Service 127C, Department of Veterans Affairs Medical Center, East Orange, NJ 07018 1095, USA
Am J Physiol Regul Integr Comp Physiol 283:R941-8. 2002..Thus NPY expression and food intake are less sensitive to the leptin's suppressive effects in DIO rats. While this may predispose them to develop DIO, it does not fully explain their defense of a higher body weight on HE diet... - Metabolic sensors: viewing glucosensing neurons from a broader perspectiveBarry E Levin
Neurology Service 127C, VA Medical Center, 385 Tremont Avenue, East Orange, NJ 07018 1095, USA
Physiol Behav 76:397-401. 2002..Thus, the role of glucosensing is postulated to be a relative one that is dependent upon the supply of peripheral glucose... - Metabolic sensing and the brain: who, what, where, and how?Barry E Levin
Neurology Service 127C, Veterans Affairs Medical Center, 385 Tremont Avenue, East Orange, New Jersey 07018, USA
Endocrinology 152:2552-7. 2011..Thus, these specialized neurons are capable of monitoring and integrating multiple signals from the periphery as a means of regulating peripheral energy homeostasis... - Peripheral glucose homeostasis: does brain insulin matter?Barry E Levin
Neurology Service 127C, VA Medical Center, East Orange, New Jersey 07018, USA
J Clin Invest 121:3392-5. 2011.... - Glucosensing neurons do more than just sense glucoseB E Levin
Neurology Service, VA Medical Center, E Orange, New Jersey 07018 1095, USA
Int J Obes Relat Metab Disord 25:S68-72. 2001..The outputs of these neurons are integral components of effector systems which regulate energy homeostasis. Thus, arcuate NPY and POMC neurons are probably prototypes of this important class of sensor-integrator-effector neurons... - Defense of body weight depends on dietary composition and palatability in rats with diet-induced obesityBarry E Levin
Neurology Service 127C, Veterans Affairs Medical Center, East Orange, NJ 07018 1095, USA
Am J Physiol Regul Integr Comp Physiol 282:R46-54. 2002..Thus genetic background, diet composition, and palatability interact to produce disparate levels of defended body weight and central neuropeptide expression... - Sibutramine alters the central mechanisms regulating the defended body weight in diet-induced obese ratsB E Levin
Neurology Service, Department of Veterans Affairs New Jersey Health Care System, East Orange 07018, USA
Am J Physiol Regul Integr Comp Physiol 279:R2222-8. 2000..Thus sibutramine lowered the defended body weight in association with compensatory changes in those central pathways involved in energy homeostasis... - Convergence of pre- and postsynaptic influences on glucosensing neurons in the ventromedial hypothalamic nucleusZ Song
Department of Pharmacology and Physiology, New Jersey Medical School (UMDNJ, Newark, New Jersey 07103, USA
Diabetes 50:2673-81. 2001..Finally, all types of glucosensing neurons were both fewer in number and showed abnormal responses to glucose in a rodent model of diet-induced obesity and type 2 diabetes... - Phosphorylation modulates the activity of the ATP-sensitive K+ channel in the ventromedial hypothalamic nucleusV H Routh
Department of Pharmacology, University of Medicine and Dentistry of New Jersey, Newark 07104, USA
Brain Res 778:107-19. 1997..These data suggest that while the inhibitory effect of ATP is not phosphorylation dependent, phosphorylation state is an important regulator of the VMN K-ATP channel... - The regulation of glucose-excited neurons in the hypothalamic arcuate nucleus by glucose and feeding-relevant peptidesR Wang
Department of Pharmacology and Physiology, New Jersey Medical School (UMDNJ, Newark, New Jersey 07101-1709, USA
Diabetes 53:1959-65. 2004..ARC glucose-excited neurons did not show pro-opiomelanocortin immunoreactivity. These data suggest that ARC glucose-excited neurons may serve an integrative role in the regulation of energy balance... - The role of norepinephrine in adult rat somatosensory (SmI) cortical metabolism and plasticityB E Levin
Neurology Service, Veterans Administration Medical Center, E Orange, NJ 07019
Brain Res 443:261-71. 1988..NE inhibits the spread of metabolic activity beyond the activated barrel and column in the intact cortex, but independently modulates plastic enlargement in the partially deafferented SmI cortex... - Glucokinase is a critical regulator of ventromedial hypothalamic neuronal glucosensingLing Kang
Department of Neurology and Neuroscience, New Jersey Medical School, Newark, USA
Diabetes 55:412-20. 2006..98 mmol/l) and a decrease in glucose-inhibited neurons (IC(50) = 0.025 micromol/l) held at 0.5 mmol/l glucose. Together, these data support a critical role for glucokinase in neuronal glucosensing... - Prior hypoglycemia enhances glucose responsiveness in some ventromedial hypothalamic glucosensing neuronsLing Kang
Department of Neurology and Neurosciences, New Jersey Medical School, University of Medicine and Dentistry, Newark, New Jersey, USA
Am J Physiol Regul Integr Comp Physiol 294:R784-92. 2008..5 mmol/l glucose. These data suggest that the increased VMH glucokinase after IIH may contribute to the increased responsiveness of VMH glucosensing neurons to glucose and the associated blunting of the AMR... - Hypothalamic neural projections are permanently disrupted in diet-induced obese ratsSebastien G Bouret
Neuroscience Program, The Saban Research Institute, Childrens Hospital Los Angeles, University of Southern California, Los Angeles, CA 90027, USA
Cell Metab 7:179-85. 2008.... - Obesity-prone rats have preexisting defects in their counterregulatory response to insulin-induced hypoglycemiaNancy C Tkacs
University of Pennsylvania School of Nursing, Philadelphia 19104-6096, USA
Am J Physiol Regul Integr Comp Physiol 287:R1110-5. 2004..These data suggest that DIO rats have a preexisting defect in their CRR to IIH but that IIH does not affect the expression of their hypothalamic neuropeptides or weight gain as it does in DR rats... - Effects of leptin on rat ventromedial hypothalamic neuronsBoman G Irani
Department of Neurology and Neurosciences, New Jersey Medical School, Newark, NJ 07103, USA
Endocrinology 149:5146-54. 2008..ARC neurons, and acts on both glucosensing and non-glucosensing VMN neurons in a glucose-independent fashion with inhibition primarily dependent upon activation of the ATP-sensitive K+ channel... - Physiological and molecular characteristics of rat hypothalamic ventromedial nucleus glucosensing neuronsLing Kang
Department of Neurology and Neurosciences, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey, USA
Diabetes 53:549-59. 2004..Thus, although GK may mediate glucosensing in up to 60% of VMN neurons, other regulatory mechanisms are likely to control glucosensing in the remaining ones... - Stress facilitates body weight gain in genetically predisposed rats on medium-fat dietChantal Michel
Neurology Service, Veterans Affairs Medical Center, Orange, NJ 07018-1095, USA
Am J Physiol Regul Integr Comp Physiol 285:R791-9. 2003..Thus a single stress triggers a complex interaction among weight gain phenotype, diet, and stress responsivity, which determines the body weight and adiposity of a given individual... - Ontogeny of diet-induced obesity in selectively bred Sprague-Dawley ratsMatthew R Ricci
Research Diets, Inc, New Brunswick, NJ, USA
Am J Physiol Regul Integr Comp Physiol 285:R610-8. 2003..Their failure to reduce caloric intake, despite high levels of leptin, suggests that selectively bred DIO rats might have reduced leptin sensitivity similar to that seen in the outbred DIO parent strain... - CNS sensing and regulation of peripheral glucose levelsBarry E Levin
Neurology Service, VA Medical Center, East Orange, New Jersey 07018, USA
Int Rev Neurobiol 51:219-58. 2002..It is our challenge to identify the mechanisms by which these neurons sense and respond to these metabolic cues... - Glucokinase is the likely mediator of glucosensing in both glucose-excited and glucose-inhibited central neuronsAmbrose A Dunn-Meynell
Neurology Service, Department of Veterans Affairs Medical Center, 385 Tremont Avenue, East Orange, NJ 07018 1095, USA
Diabetes 51:2056-65. 2002..These data suggest a critical role for GK as a regulator of glucosensing in both GE and GI neurons in the brain... - Dysregulation of hypothalamic serotonin turnover in diet-induced obese ratsMohammed Hassanain
Department of Neurosciences, New Jersey Medical School (UMDNJ, Newark, NJ 07103, USA
Brain Res 929:175-80. 2002..Once obesity develops, these abnormalities, like those of several other hypothalamic transmitters and peptides, are normalized. This may contribute to the persistence of obesity once it develops... - Three weeks of early-onset exercise prolongs obesity resistance in DIO rats after exercise cessationChrista M Patterson
Department of Neurosciences, New Jersey Medical School, Newark, NJ, USA
Am J Physiol Regul Integr Comp Physiol 294:R290-301. 2008..Thus, early-onset exercise may favorably alter, while early caloric restriction may unfavorably influence, the development of the hypothalamic pathways controlling energy homeostasis during brain development... - A single episode of central glucoprivation reduces the adrenomedullary response to subsequent hypoglycemia in ratsAlejandro Marin-Spiotta
University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Neurosci Lett 360:81-4. 2004..These data support the hypothesis that the brain contributes to the loss of responsiveness to repeated hypoglycemia that may ultimately result in HAAF... - Third ventricular alloxan reversibly impairs glucose counterregulatory responsesNicole M Sanders
Department of Neurology and Neurosciences, New Jersey Medical School, Newark, NJ, USA
Diabetes 53:1230-6. 2004..At this time there were significant decreases in GK, NPY, and proopiomelanocortin mRNA. Thus, neural substrates near and around the 3v affected by alloxan may be critically involved in the expression of these glucoprivic responses... - Feeding and neuroendocrine responses after recurrent insulin-induced hypoglycemiaNicole M Sanders
Division of Endocrinology Metabolism, Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA
Physiol Behav 87:700-6. 2006..Thus, neuroendocrine and behavioral (stimulation of food intake) CRR are differentially regulated by recurrent hypoglycemia experience... - Postnatal environment overrides genetic and prenatal factors influencing offspring obesity and insulin resistanceJudith N Gorski
Department of Neurology and Neurosciences, New Jersey Medical School, University of Medicine and Dentistry New Jersey, USA
Am J Physiol Regul Integr Comp Physiol 291:R768-78. 2006..These results demonstrate that postnatal factors can overcome both genetic predisposition and prenatal factors in determining the development of adiposity, insulin sensitivity, and the brain pathways that mediate these functions... - Orexins: neuropeptides for all seasons and functionsBarry E Levin
Am J Physiol Regul Integr Comp Physiol 291:R885-8. 2006 - Cortical Fluoro-Jade staining and blunted adrenomedullary response to hypoglycemia after noncoma hypoglycemia in ratsNancy C Tkacs
School of Nursing, University of Pennsylvania, Philadelphia, PA 19104 6096, USA
J Cereb Blood Flow Metab 25:1645-55. 2005.... - Reduced anorexic effects of insulin in obesity-prone rats fed a moderate-fat dietDeborah J Clegg
University of Cincinnati, Department of Psychiatry, Cincinnati, Ohio, USA
Am J Physiol Regul Integr Comp Physiol 288:R981-6. 2005.... - Altered hypothalamic leptin, insulin, and melanocortin binding associated with moderate-fat diet and predisposition to obesityBoman G Irani
Department of Neurology, New Jersey Medical School, Newark, USA
Endocrinology 148:310-6. 2007..These results corroborate our previous findings demonstrating a preexisting decrease in DIO hypothalamic leptin and insulin signaling and demonstrate that HE diet intake reduces hypothalamic melanocortin and hippocampal insulin binding... - Role of exercise in the central regulation of energy homeostasis and in the prevention of obesityChrista M Patterson
Department of Neurology and Neurosciences, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA
Neuroendocrinology 87:65-70. 2008.... - Reduced brain CRH and GR mRNA expression precedes obesity in juvenile rats bred for diet-induced obesityChantal Michel
Neurology Service (127C, VA Medical Center, 385 Tremont Avenue, E. Orange, NJ 07018, USA
Behav Brain Res 154:511-7. 2004..The reduced expression of brain GR and CRH expression at the end of this period might contribute to the propensity of DIO rats to become obese selectively on HE diet after 5 weeks of age... - Maternal obesity increases hypothalamic leptin receptor expression and sensitivity in juvenile obesity-prone ratsJudith N Gorski
Department of Neurology and Neurosciences, New Jersey Medical School, University of Medicine and Dentistry, Newark, NJ, USA
Am J Physiol Regul Integr Comp Physiol 292:R1782-91. 2007..Because they later go onto become more obese, it is possible that interventions during this time period might prevent the subsequent development of obesity... - The drive to regain is mainly in the brainBarry E Levin
Am J Physiol Regul Integr Comp Physiol 287:R1297-300. 2004 - Neurobiology of exerciseRod K Dishman
Department of Exercise Science, The University of Georgia, Ramsey Center, 330 River Road, Athens, GA 30602 6554, USA
Obesity (Silver Spring) 14:345-56. 2006....
Research Grants
- Obesity: neural control of body weight and metabolismBarry E Levin; Fiscal Year: 2010..The ultimate goal is to identify factors that might provide therapeutic targets for the prevention and treatment of childhood and adult obesity. ..
- BRAIN GLUCOSENSING NEURONS IN HEALTH AND DIABETESBarry Levin; Fiscal Year: 2009..diet-resistant rats fed low and HE diets to identify potential sites responsible for their abnormalities of GS and potential defects in fatty acid sensing to explain their propensity to become obese and insulin resistant on HE diet. ..
- OBESITY: NEURAL CONTROL OF METABOLISM AND WEIGHT GAINBarry Levin; Fiscal Year: 2009..The overall goal of this proposal is to identify sites within the leptin signaling pathway at which pharmacological or other interventions might be developed to prevent or treat obesity in humans. ..
- BRAIN GLUCOSENSING NEURONS IN HEALTH AND DIABETESBarry Levin; Fiscal Year: 2007..diet-resistant rats fed low and HE diets to identify potential sites responsible for their abnormalities of GS and potential defects in fatty acid sensing to explain their propensity to become obese and insulin resistant on HE diet. ..
- BRAIN GLUCOSENSING NEURONS IN HEALTH AND DIABETESBarry Levin; Fiscal Year: 2004..Specific Aim V: Demonstrate that brain glucosensing neurons are the target of toxins known to destroy pancreatic beta-cells (alloxan) and ARC neurons (gold thioglucose) using molecular and functional tests. ..
- BRAIN GLUCOSENSING NEURONS IN HEALTH AND DIABETESBarry Levin; Fiscal Year: 2000..These studies are expected to provide important insights into the ways in which the brain regulates glucose metabolism in health and disease. ..
- BRAIN GLUCOSENSING NEURONS IN HEALTH AND DIABETESBarry E Levin; Fiscal Year: 2010..The ultimate goal is to identify potential therapeutic target molecules to prevent the adverse effects of recurrent hypoglycemia in diabetics and obesity. ..