Patricia Glazebrook
MetroHealth
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Publication
Featured researches published by Patricia Glazebrook.
The Journal of Neuroscience | 2005
David D. Kline; Maria C F Buniel; Patricia Glazebrook; Ying Jie Peng; Angelina Ramirez-Navarro; Nanduri R. Prabhakar; Diana L. Kunze
Mutations in the potassium channel gene Kv1.1 are associated with human episodic ataxia type 1 (EA-1) syndrome characterized by movement disorders and epilepsy. Ataxic episodes in EA-1 patients are often associated with exercise or emotional stress, which suggests a prominent role for the autonomic nervous system. Many of these alterations are reproduced in the Kv1.1-null mouse. Kv1.1 also regulates excitability of sensory neurons essential in cardiovascular and respiratory reflexes. We examined the neural control of the respiratory system of littermate wild-type (control) and Kv1.1-null mice during low O2 (hypoxia). Immunohistochemical studies demonstrated Kv1.1 in the afferent limb of the carotid body chemoreflex (the major regulator in the response to hypoxia), consisting of the carotid body, petrosal ganglion, and nucleus of the solitary tract (NTS). Respiration was examined by plethysmography. Null mice exhibited a greater increase in respiration during hypoxia compared with controls. In vitro carotid body sensory discharge during hypoxia was greater in null than control mice. In the caudal NTS, evoked EPSCs in brainstem slices were similar between control and null mice. However, the frequency of spontaneous and miniature EPSCs was greater in null mice. Null mice also exhibited more asynchronous release after a stimulus train. These results demonstrate the important role of Kv1.1 in afferent chemosensory activity and suggest that mutations in the human Kv1.1 gene have functional consequences during stress responses that involve respiratory reflexes.
Endocrinology | 2017
Virtu Calabuig-Navarro; Maricela Haghiac; Judi Minium; Patricia Glazebrook; Geraldine Cheyana Ranasinghe; Charles L. Hoppel; Sylvie Hauguel deMouzon; Patrick M. Catalano; Perrie O'Tierney-Ginn
Obese women, on average, give birth to babies with high fat mass. Placental lipid metabolism alters fetal lipid delivery, potentially moderating neonatal adiposity, yet how it is affected by maternal obesity is poorly understood. We hypothesized that fatty acid (FA) accumulation (esterification) is higher and FA β-oxidation (FAO) is lower in placentas from obese, compared with lean women. We assessed acylcarnitine profiles (lipid oxidation intermediates) in mother-baby-placenta triads, in addition to lipid content, and messenger RNA (mRNA)/protein expression of key regulators of FA metabolism pathways in placentas of lean and obese women with normal glucose tolerance recruited at scheduled term Cesarean delivery. In isolated trophoblasts, we measured [3H]-palmitate metabolism. Placentas of obese women had 17.5% (95% confidence interval: 6.1, 28.7%) more lipid than placentas of lean women, and higher mRNA and protein expression of FA esterification regulators (e.g., peroxisome proliferator-activated receptor γ, acetyl-CoA carboxylase, steroyl-CoA desaturase 1, and diacylglycerol O-acyltransferase-1). [3H]-palmitate esterification rates were increased in trophoblasts from obese compared with lean women. Placentas of obese women had fewer mitochondria and a lower concentration of acylcarnitines, suggesting a decrease in mitochondrial FAO capacity. Conversely, peroxisomal FAO was greater in placentas of obese women. Altogether, these changes in placental lipid metabolism may serve to limit the amount of maternal lipid transferred to the fetus, restraining excess fetal adiposity in this population of glucose-tolerant women.
American Journal of Physiology-endocrinology and Metabolism | 2015
Michael O. Boylan; Patricia Glazebrook; Milos Tatalovic; M. Michael Wolfe
Previous reports have suggested that the abrogation of gastric inhibitory polypeptide (GIP) signaling could be exploited to prevent and treat obesity and obesity-related disorders in humans. This study was designed to determine whether immunoneutralization of GIP, using a newly developed specific monoclonal antibody (mAb), would prevent the development of obesity. Specific mAb directed against the carboxy terminus of mouse GIP was identified, and its effects on the insulin response to oral and to intraperitoneal (ip) glucose and on weight gain were evaluated. Administration of mAb (30 mg/kg body wt, BW) to mice attenuated the insulin response to oral glucose by 70% and completely eliminated the response to ip glucose coadministered with human GIP. Nine-week-old C57BL/6 mice injected with GIP mAbs (60 mg·kg BW(-1)·wk(-1)) for 17 wk gained 46.5% less weight than control mice fed an identical high-fat diet (P < 0.001). No significant differences in the quantity of food consumed were detected between the two treatment groups. Furthermore, magnetic resonance imaging demonstrated that subcutaneous, omental, and hepatic fat were 1.97-, 3.46-, and 2.15-fold, respectively, lower in mAb-treated animals than in controls. Moreover, serum insulin, leptin, total cholesterol (TC), low-density lipoprotein (LDL), and triglycerides were significantly reduced, whereas the high-density lipoprotein (HDL)/TC ratio was 1.25-fold higher in treated animals than in controls. These studies support the hypothesis that a reduction in GIP signaling using a GIP-neutralizing mAb might provide a useful method for the treatment and prevention of obesity and related disorders.
Journal of Maternal-fetal & Neonatal Medicine | 2017
Xiaohua Yang; Patricia Glazebrook; Geraldine Cheyana Ranasinghe; Maricela Haghiac; Virtu Calabuig-Navarro; Judi Minium; Perrie O’Tierney-Ginn
Abstract Objective: Fetal fatty acid (FA) delivery is ultimately controlled by placental transport. Focus has been the maternal-placental interface, but regulation at the feto-placental interface is unknown. Methods: Placental macrovascular endothelial cells (EC) (nu2009=u20094/group) and trophoblasts (TB) (nu2009=u20095/group) were isolated from lean (pregravid BMI <25u2009kg/m2) and obese (body mass index (BMI)u2009>u200930) women. Fatty acid transporters FAT/CD36, FABPpm, FATP4, FABP 3, 4 and 5, PLIN2 and PPARα, δ, γ expression, was measured in EC and TB. Transporter response to 24u2009h palmitate (PA) was assessed. Results: mRNA expression of FABP3, 4, 5 and PPARγ was 2- to 3-fold reduced in EC of obese versus lean women (pu2009<u2009.03), but not in TB. Protein level of FABPpm was 20% lower in obese (pu2009<u2009.05). Palmitate (PA) up-regulated CD36, FABP3, FABP4, and PLIN2 gene expression by 3- to 4-fold in lean but not obese EC (pu2009<u2009.05), while PA increased FABP4 and PLIN2 in lean and obese TB, and FABP5 in lean (pu2009<u2009.05) EC. PA exposure up-regulated peroxisome proliferator activated receptors (PPARs) 2-fold in lean and obese EC (pu2009<u2009.05), but not in TB. Conclusions: In obese women, FA transporter expression is lower in placental EC, but not TB, and less sensitive to saturated FA, compared to lean women. FA transport may be regulated at the feto-placental interface.
The American Journal of Clinical Nutrition | 2016
Virtu Calabuig-Navarro; Michelle A. Puchowicz; Patricia Glazebrook; Maricela Haghiac; Judi Minium; Patrick M. Catalano; Sylvie Hauguel deMouzon; Perrie F. O’Tierney-Ginn
Gastroenterology | 2016
Michael O. Boylan; Raghav Sood; Patricia Glazebrook; M. Michael Wolfe
Gastroenterology | 2015
Michael O. Boylan; Patricia Glazebrook; Milos Tatalovic; M. Michael Wolfe
Gastroenterology | 2015
M. Michael Wolfe; Patricia Glazebrook; Milos Tatalovic; Michael O. Boylan
PMC | 2014
Grace Santa Cruz Chavez; Bai-Yan Li; Patricia Glazebrook; Diana L. Kunze; John H. Schild
Archive | 2013
Scott M. Smith; Lakshmi Putcha; Clarence P. Sams; Suzanne M. Schneider; Linda Shackelford; Deborah L. Harm; Richard T. Jennings; Janice V. Meck; Natalia M. Arzeno; Michael B. Stenger; Stuart M. C. Lee; Robert Ploutz-Snyder; H Steven; Donald E. Watenpaugh; Alan R. Hargens; Alan H. Feiveson; Brandon R. Macias; Grace C. Santa; Cruz Chavez; Patricia Glazebrook; Diana L. Kunze