Barry Levin

Summary

Affiliation: New Jersey
Country: USA

Publications

  1. request reprint
    Levin B, Brown K, Dunn Meynell A. Differential effects of diet and obesity on high and low affinity sulfonylurea binding sites in the rat brain. Brain Res. 1996;739:293-300 pubmed
    ..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...
  2. request reprint
    Levin B, Dunn Meynell A. In vivo and in vitro regulation of [3H]glyburide binding to brain sulfonylurea receptors in obesity-prone and resistant rats by glucose. Brain Res. 1997;776:146-53 pubmed
    ..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...
  3. request reprint
    Levin B, Richard D, Michel C, Servatius R. Differential stress responsivity in diet-induced obese and resistant rats. Am J Physiol Regul Integr Comp Physiol. 2000;279:R1357-64 pubmed
    ..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...
  4. request reprint
    Levin B, Dunn Meynell A. Sibutramine alters the central mechanisms regulating the defended body weight in diet-induced obese rats. Am J Physiol Regul Integr Comp Physiol. 2000;279:R2222-8 pubmed
    ..Thus sibutramine lowered the defended body weight in association with compensatory changes in those central pathways involved in energy homeostasis...
  5. request reprint
    Levin B, Dunn Meynell A, Ricci M, Cummings D. Abnormalities of leptin and ghrelin regulation in obesity-prone juvenile rats. Am J Physiol Endocrinol Metab. 2003;285:E949-57 pubmed
    ..These data suggest that increased ghrelin signaling is not a proximate cause of DIO, whereas reduced leptin sensitivity might play a causal role. ..
  6. request reprint
    Levin B, Dunn Meynell A, Banks W. Obesity-prone rats have normal blood-brain barrier transport but defective central leptin signaling before obesity onset. Am J Physiol Regul Integr Comp Physiol. 2004;286:R143-50 pubmed
    ..Defects in leptin transport appear to be an acquired defect associated with the development of obesity and possibly age. ..
  7. request reprint
    Levin B, Govek E, Dunn Meynell A. Reduced glucose-induced neuronal activation in the hypothalamus of diet-induced obese rats. Brain Res. 1998;808:317-9 pubmed
    ..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. ..
  8. request reprint
    Levin B, Dunn Meynell A. Defense of body weight depends on dietary composition and palatability in rats with diet-induced obesity. Am J Physiol Regul Integr Comp Physiol. 2002;282:R46-54 pubmed
    ..Thus genetic background, diet composition, and palatability interact to produce disparate levels of defended body weight and central neuropeptide expression...
  9. request reprint
    Levin B. Metabolic sensors: viewing glucosensing neurons from a broader perspective. Physiol Behav. 2002;76:397-401 pubmed
    ..Thus, the role of glucosensing is postulated to be a relative one that is dependent upon the supply of peripheral glucose...
  10. Levin B, Becker T, Eiki J, Zhang B, Dunn Meynell A. Ventromedial hypothalamic glucokinase is an important mediator of the counterregulatory response to insulin-induced hypoglycemia. Diabetes. 2008;57:1371-9 pubmed publisher
    ....

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Detail Information

Publications10

  1. request reprint
    Levin B, Brown K, Dunn Meynell A. Differential effects of diet and obesity on high and low affinity sulfonylurea binding sites in the rat brain. Brain Res. 1996;739:293-300 pubmed
    ..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...
  2. request reprint
    Levin B, Dunn Meynell A. In vivo and in vitro regulation of [3H]glyburide binding to brain sulfonylurea receptors in obesity-prone and resistant rats by glucose. Brain Res. 1997;776:146-53 pubmed
    ..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...
  3. request reprint
    Levin B, Richard D, Michel C, Servatius R. Differential stress responsivity in diet-induced obese and resistant rats. Am J Physiol Regul Integr Comp Physiol. 2000;279:R1357-64 pubmed
    ..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...
  4. request reprint
    Levin B, Dunn Meynell A. Sibutramine alters the central mechanisms regulating the defended body weight in diet-induced obese rats. Am J Physiol Regul Integr Comp Physiol. 2000;279:R2222-8 pubmed
    ..Thus sibutramine lowered the defended body weight in association with compensatory changes in those central pathways involved in energy homeostasis...
  5. request reprint
    Levin B, Dunn Meynell A, Ricci M, Cummings D. Abnormalities of leptin and ghrelin regulation in obesity-prone juvenile rats. Am J Physiol Endocrinol Metab. 2003;285:E949-57 pubmed
    ..These data suggest that increased ghrelin signaling is not a proximate cause of DIO, whereas reduced leptin sensitivity might play a causal role. ..
  6. request reprint
    Levin B, Dunn Meynell A, Banks W. Obesity-prone rats have normal blood-brain barrier transport but defective central leptin signaling before obesity onset. Am J Physiol Regul Integr Comp Physiol. 2004;286:R143-50 pubmed
    ..Defects in leptin transport appear to be an acquired defect associated with the development of obesity and possibly age. ..
  7. request reprint
    Levin B, Govek E, Dunn Meynell A. Reduced glucose-induced neuronal activation in the hypothalamus of diet-induced obese rats. Brain Res. 1998;808:317-9 pubmed
    ..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. ..
  8. request reprint
    Levin B, Dunn Meynell A. Defense of body weight depends on dietary composition and palatability in rats with diet-induced obesity. Am J Physiol Regul Integr Comp Physiol. 2002;282:R46-54 pubmed
    ..Thus genetic background, diet composition, and palatability interact to produce disparate levels of defended body weight and central neuropeptide expression...
  9. request reprint
    Levin B. Metabolic sensors: viewing glucosensing neurons from a broader perspective. Physiol Behav. 2002;76:397-401 pubmed
    ..Thus, the role of glucosensing is postulated to be a relative one that is dependent upon the supply of peripheral glucose...
  10. Levin B, Becker T, Eiki J, Zhang B, Dunn Meynell A. Ventromedial hypothalamic glucokinase is an important mediator of the counterregulatory response to insulin-induced hypoglycemia. Diabetes. 2008;57:1371-9 pubmed publisher
    ....