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https://www.readbyqxmd.com/read/29529147/fto-genotype-impacts-food-intake-and-corticolimbic-activation
#1
Susan J Melhorn, Mary K Askren, Wendy K Chung, Mario Kratz, Tyler A Bosch, Vidhi Tyagi, Mary F Webb, Mary Rosalynn B De Leon, Thomas J Grabowski, Rudolph L Leibel, Ellen A Schur
Background: Variants in the first intron of the fat mass and obesity-associated (FTO) gene increase obesity risk. People with "high-risk" FTO genotypes exhibit preference for high-fat foods, reduced satiety responsiveness, and greater food intake consistent with impaired satiety. Objective: We sought central nervous system mechanisms that might underlie impaired satiety perception in people with a higher risk of obesity based on their FTO genotype. Design: We performed a cross-sectional study in a sample that was enriched for obesity and included 20 higher-risk participants with the AA (risk) genotype at the rs9939609 locus of FTO and 94 lower-risk participants with either the AT or TT genotype...
February 1, 2018: American Journal of Clinical Nutrition
https://www.readbyqxmd.com/read/29466054/the-role-of-rpgrip1l-a-component-of-the-primary-cilium-in-adipocyte-development-and-function
#2
Jayne F Martin Carli, Charles A LeDuc, Yiying Zhang, George Stratigopoulos, Rudolph L Leibel
Genetic variants within the FTO (α-ketoglutarate-dependent dioxygenase) gene have been strongly associated with a modest increase in adiposity as a result of increased food intake. These risk alleles are associated with decreased expression of both FTO and neighboring RPGRIP1L (retinitis pigmentosa GTPase regulator-interacting protein 1 like). RPGRIP1L encodes a protein that is critical to the function of the primary cilium, which conveys extracellular information to the cell. Rpgrip1l+/- mice exhibit increased adiposity, in part, as a result of hyperphagia...
February 21, 2018: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29444618/pathophysiology-of-drug-induced-weight-and-metabolic-effects-findings-from-an-rct-in-healthy-volunteers-treated-with-olanzapine-iloperidone-or-placebo
#3
Jacob S Ballon, Utpal B Pajvani, Laurel Es Mayer, Zachary Freyberg, Robin Freyberg, Ignacio Contreras, Michael Rosenbaum, Rudolph L Leibel, Jeffrey A Lieberman
Second generation antipsychotics are prescribed for an increasing number of psychiatric conditions, despite variable associations with weight gain, dyslipidemia, and impaired glucose tolerance. The mechanism(s) of the apparent causal relationships between these medications and metabolic effects have been inadequately defined and are potentially confounded by genetic risk of mental illness, attendant lifestyle, and concomitant medications. Therefore, we conducted a study in which 24 healthy volunteers were randomized to olanzapine (highly weight-gain liability), iloperidone (less weight-gain liability), or placebo treatment for 28 days under double-blind conditions...
February 1, 2018: Journal of Psychopharmacology
https://www.readbyqxmd.com/read/29261744/energy-homeostasis-in-leptin-deficient-lepob-ob-mice
#4
Alicja A Skowronski, Yann Ravussin, Rudolph L Leibel, Charles A LeDuc
Maintenance of reduced body weight is associated both with reduced energy expenditure per unit metabolic mass and increased hunger in mice and humans. Lowered circulating leptin concentration, due to decreased fat mass, provides a primary signal for this response. However, leptin deficient (Lepob/ob) mice (and leptin receptor deficient Zucker rats) reduce energy expenditure following weight reduction by a necessarily non-leptin dependent mechanisms. To identify these mechanisms, Lepob/ob mice were fed ad libitum (AL group; n = 21) or restricted to 3 kilocalories of chow per day (CR group, n = 21)...
2017: PloS One
https://www.readbyqxmd.com/read/28973544/loss-of-the-imprinted-non-coding-snord116-gene-cluster-in-the-interval-deleted-in-the-prader-willi-syndrome-results-in-murine-neuronal-and-endocrine-pancreatic-developmental-phenotypes
#5
Lisa Cole Burnett, Gabriela Hubner, Charles LeDuc, Michael V Morabito, Jayne F Martin Carli, Rudolph L Leibel
Global neurodevelopmental delay is a prominent characteristic of individuals with Prader-Willi syndrome (PWS). The neuromolecular bases for these delays are unknown. We identified neuroanatomical changes in the brains of mice deficient for a gene in the minimal critical deletion region for PWS (Snord116p-/m+). In Snord116p-/m+ mice, reduced primary forebrain neuron cell body size is apparent in embryonic day 15.5 fetuses, and persists until postnatal day 30 in cerebellar purkinje neurons. Snord116 is a snoRNA gene cluster of unknown function that can localize to the nucleolus...
September 6, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28931519/%C3%AE-cell-replacement-in-mice-using-human-type-1-diabetes-nuclear-transfer-embryonic-stem-cells
#6
Lina Sui, Nichole Danzl, Sean R Campbell, Ryan Viola, Damian Williams, Yuan Xing, Yong Wang, Neil Phillips, Greg Poffenberger, Bjarki Johannesson, Jose Oberholzer, Alvin C Powers, Rudolph L Leibel, Xiaojuan Chen, Megan Sykes, Dieter Egli
β-Cells derived from stem cells hold great promise for cell replacement therapy for diabetes. Here we examine the ability of nuclear transfer embryonic stem cells (NT-ESs) derived from a patient with type 1 diabetes to differentiate into β-cells and provide a source of autologous islets for cell replacement. NT-ESs differentiate in vitro with an average efficiency of 55% into C-peptide-positive cells, expressing markers of mature β-cells, including MAFA and NKX6.1. Upon transplantation in immunodeficient mice, grafted cells form vascularized islet-like structures containing MAFA/C-peptide-positive cells...
January 2018: Diabetes
https://www.readbyqxmd.com/read/28898979/obesity-pathogenesis-an-endocrine-society-scientific-statement
#7
Michael W Schwartz, Randy J Seeley, Lori M Zeltser, Adam Drewnowski, Eric Ravussin, Leanne M Redman, Rudolph L Leibel
Obesity is among the most common and costly chronic disorders worldwide. Estimates suggest that in the United States obesity affects one-third of adults, accounts for up to one-third of total mortality, is concentrated among lower income groups, and increasingly affects children as well as adults. A lack of effective options for long-term weight reduction magnifies the enormity of this problem; individuals who successfully complete behavioral and dietary weight-loss programs eventually regain most of the lost weight...
August 1, 2017: Endocrine Reviews
https://www.readbyqxmd.com/read/28617454/corrigendum-mc4r-dependent-suppression-of-appetite-by-bone-derived-lipocalin-2
#8
Ioanna Mosialou, Steven Shikhel, Jian-Min Liu, Antonio Maurizi, Na Luo, Zhenyan He, Yiru Huang, Haihong Zong, Richard A Friedman, Jonathan Barasch, Patricia Lanzano, Liyong Deng, Rudolph L Leibel, Mishaela Rubin, Thomas Nickolas, Wendy Chung, Lori M Zeltser, Kevin W Williams, Jeffrey E Pessin, Stavroula Kousteni
This corrects the article DOI: 10.1038/nature21697.
June 14, 2017: Nature
https://www.readbyqxmd.com/read/28273060/mc4r-dependent-suppression-of-appetite-by-bone-derived-lipocalin-2
#9
Ioanna Mosialou, Steven Shikhel, Jian-Min Liu, Antonio Maurizi, Na Luo, Zhenyan He, Yiru Huang, Haihong Zong, Richard A Friedman, Jonathan Barasch, Patricia Lanzano, Liyong Deng, Rudolph L Leibel, Mishaela Rubin, Thomas Nickolas, Wendy Chung, Lori M Zeltser, Kevin W Williams, Jeffrey E Pessin, Stavroula Kousteni
Bone has recently emerged as a pleiotropic endocrine organ that secretes at least two hormones, FGF23 and osteocalcin, which regulate kidney function and glucose homeostasis, respectively. These findings have raised the question of whether other bone-derived hormones exist and what their potential functions are. Here we identify, through molecular and genetic analyses in mice, lipocalin 2 (LCN2) as an osteoblast-enriched, secreted protein. Loss- and gain-of-function experiments in mice demonstrate that osteoblast-derived LCN2 maintains glucose homeostasis by inducing insulin secretion and improves glucose tolerance and insulin sensitivity...
March 16, 2017: Nature
https://www.readbyqxmd.com/read/28132887/pc1-3-deficiency-impacts-pro-opiomelanocortin-processing-in-human-embryonic-stem-cell-derived-hypothalamic-neurons
#10
Liheng Wang, Lina Sui, Sunil K Panigrahi, Kana Meece, Yurong Xin, Jinrang Kim, Jesper Gromada, Claudia A Doege, Sharon L Wardlaw, Dieter Egli, Rudolph L Leibel
We recently developed a technique for generating hypothalamic neurons from human pluripotent stem cells. Here, as proof of principle, we examine the use of these cells in modeling of a monogenic form of severe obesity: PCSK1 deficiency. The cognate enzyme, PC1/3, processes many prohormones in neuroendocrine and other tissues. We generated PCSK1 (PC1/3)-deficient human embryonic stem cell (hESC) lines using both short hairpin RNA and CRISPR-Cas9, and investigated pro-opiomelanocortin (POMC) processing using hESC-differentiated hypothalamic neurons...
February 14, 2017: Stem Cell Reports
https://www.readbyqxmd.com/read/28107353/weight-perturbation-alters-leptin-signal-transduction-in-a-region-specific-manner-throughout-the-brain
#11
Michael V Morabito, Yann Ravussin, Bridget R Mueller, Alicja A Skowronski, Kazuhisa Watanabe, Kylie S Foo, Samuel X Lee, Anders Lehmann, Stephan Hjorth, Lori M Zeltser, Charles A LeDuc, Rudolph L Leibel
Diet-induced obesity (DIO) resulting from consumption of a high fat diet (HFD) attenuates normal neuronal responses to leptin and may contribute to the metabolic defense of an acquired higher body weight in humans; the molecular bases for the persistence of this defense are unknown. We measured the responses of 23 brain regions to exogenous leptin in 4 different groups of weight- and/or diet-perturbed mice. Responses to leptin were assessed by quantifying pSTAT3 levels in brain nuclei 30 minutes following 3 mg/kg intraperitoneal leptin...
2017: PloS One
https://www.readbyqxmd.com/read/28094769/ipsc-derived-%C3%AE-cells-model-diabetes-due-to-glucokinase-deficiency
#12
Haiqing Hua, Linshan Shang, Hector Martinez, Matthew Freeby, Mary Pat Gallagher, Thomas Ludwig, Liyong Deng, Ellen Greenberg, Charles LeDuc, Wendy K Chung, Robin Goland, Rudolph L Leibel, Dieter Egli
No abstract text is available yet for this article.
March 1, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27978598/the-subgingival-microbiome-systemic-inflammation-and-insulin-resistance-the-oral-infections-glucose-intolerance-and-insulin-resistance-study
#13
Ryan T Demmer, Alexander Breskin, Michael Rosenbaum, Aleksandra Zuk, Charles LeDuc, Rudolph Leibel, Bruce Paster, Moïse Desvarieux, David R Jacobs, Panos N Papapanou
BACKGROUND: Inflammation might link microbial exposures to insulin resistance. We investigated the cross-sectional association between periodontal microbiota, inflammation and insulin resistance. METHODS: The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGINS) enrolled 152 diabetes-free adults (77% female) aged 20-55 years (mean = 34 ± 10). Three hundred and four subgingival plaque samples were analysed using the Human Oral Microbe Identification Microarray to measure the relative abundances of 379 taxa...
March 2017: Journal of Clinical Periodontology
https://www.readbyqxmd.com/read/27941249/deficiency-in-prohormone-convertase-pc1-impairs-prohormone-processing-in-prader-willi-syndrome
#14
Lisa C Burnett, Charles A LeDuc, Carlos R Sulsona, Daniel Paull, Richard Rausch, Sanaa Eddiry, Jayne F Martin Carli, Michael V Morabito, Alicja A Skowronski, Gabriela Hubner, Matthew Zimmer, Liheng Wang, Robert Day, Brynn Levy, Ilene Fennoy, Beatrice Dubern, Christine Poitou, Karine Clement, Merlin G Butler, Michael Rosenbaum, Jean Pierre Salles, Maithe Tauber, Daniel J Driscoll, Dieter Egli, Rudolph L Leibel
Prader-Willi syndrome (PWS) is caused by a loss of paternally expressed genes in an imprinted region of chromosome 15q. Among the canonical PWS phenotypes are hyperphagic obesity, central hypogonadism, and low growth hormone (GH). Rare microdeletions in PWS patients define a 91-kb minimum critical deletion region encompassing 3 genes, including the noncoding RNA gene SNORD116. Here, we found that protein and transcript levels of nescient helix loop helix 2 (NHLH2) and the prohormone convertase PC1 (encoded by PCSK1) were reduced in PWS patient induced pluripotent stem cell-derived (iPSC-derived) neurons...
January 3, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27789403/induced-pluripotent-stem-cells-ipsc-created-from-skin-fibroblasts-of-patients-with-prader-willi-syndrome-pws-retain-the-molecular-signature-of-pws
#15
Lisa C Burnett, Charles A LeDuc, Carlos R Sulsona, Daniel Paull, Sanaa Eddiry, Brynn Levy, Jean Pierre Salles, Maithe Tauber, Daniel J Driscoll, Dieter Egli, Rudolph L Leibel
Prader-Willi syndrome (PWS) is a syndromic obesity caused by loss of paternal gene expression in an imprinted interval on 15q11.2-q13. Induced pluripotent stem cells were generated from skin cells of three large deletion PWS patients and one unique microdeletion PWS patient. We found that genes within the PWS region, including SNRPN and NDN, showed persistence of DNA methylation after iPSC reprogramming and differentiation to neurons. Genes within the PWS minimum critical deletion region remain silenced in both PWS large deletion and microdeletion iPSC following reprogramming...
November 2016: Stem Cell Research
https://www.readbyqxmd.com/read/27460711/models-of-energy-homeostasis-in-response-to-maintenance-of-reduced-body-weight
#16
Michael Rosenbaum, Rudolph L Leibel
OBJECTIVE: To test three proposed models for adaptive thermogenesis in compartments of energy expenditure following different degrees of weight loss. Specifically, (1) there is no adaptive thermogenesis [constant relationship of energy expenditure (EE) to metabolic mass]. (2) There is a fixed degree of adaptive thermogenesis once fat stores are below a "threshold." (3) The degree of adaptive thermogenesis is proportional to weight loss. METHODS: The relationship between weight loss and EE was examined in 17 inpatient subjects with stable weight and obesity studied at usual weight and again following a 10% and a 20% weight loss...
August 2016: Obesity
https://www.readbyqxmd.com/read/27385608/energy-expenditure-and-body-composition-changes-after-an-isocaloric-ketogenic-diet-in-overweight-and-obese-men
#17
Kevin D Hall, Kong Y Chen, Juen Guo, Yan Y Lam, Rudolph L Leibel, Laurel Es Mayer, Marc L Reitman, Michael Rosenbaum, Steven R Smith, B Timothy Walsh, Eric Ravussin
BACKGROUND: The carbohydrate-insulin model of obesity posits that habitual consumption of a high-carbohydrate diet sequesters fat within adipose tissue because of hyperinsulinemia and results in adaptive suppression of energy expenditure (EE). Therefore, isocaloric exchange of dietary carbohydrate for fat is predicted to result in increased EE, increased fat oxidation, and loss of body fat. In contrast, a more conventional view that "a calorie is a calorie" predicts that isocaloric variations in dietary carbohydrate and fat will have no physiologically important effects on EE or body fat...
August 2016: American Journal of Clinical Nutrition
https://www.readbyqxmd.com/read/27367166/efficient-generation-of-hypothalamic-neurons-from-human-pluripotent-stem-cells
#18
Liheng Wang, Dieter Egli, Rudolph L Leibel
The hypothalamus comprises neuronal clusters that are essential for body weight regulation and other physiological functions. Insights into the complex cellular physiology of this region of the brain are critical to understanding the pathogenesis of obesity, but human hypothalamic cells are largely inaccessible for direct study. Here we describe a technique for generation of arcuate-like hypothalamic neurons from human pluripotent stem (hPS) cells. Early activation of SHH signaling and inhibition of BMP and TGFβ signaling, followed by timed inhibition of NOTCH, can efficiently differentiate hPS cells into NKX2...
July 1, 2016: Current Protocols in Human Genetics
https://www.readbyqxmd.com/read/27353377/znf70-a-novel-ildr2-interacting-protein-contributes-to-the-regulation-of-hes1-gene-expression
#19
Kazuhisa Watanabe, Kazuhiro Nakayama, Satoshi Ohta, Kenji Tago, Supichaya Boonvisut, Elizabeth J Millings, Stuart G Fischer, Charles A LeDuc, Rudolph L Leibel, Sadahiko Iwamoto
A diabetes susceptibility gene, immunoglobulin-like domain containing receptor 2 (Ildr2), encodes a transmembrane protein localized to the endoplasmic reticulum membrane that is closely related to hepatic lipid metabolism. The livers of ob/ob mice in which Ildr2 is transiently overexpressed are relieved of hepatic steatosis. However, the molecular mechanisms through which ILDR2 affects these changes in hepatic lipid metabolism remain unknown. This study aimed to identify ILDR2-interacting proteins to further elucidate the molecular mechanisms underlying the role of ILDR2 in lipid homeostasis...
September 2, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27064284/hypomorphism-of-fto-and-rpgrip1l-causes-obesity-in-mice
#20
George Stratigopoulos, Lisa Cole Burnett, Richard Rausch, Richard Gill, David Barth Penn, Alicja A Skowronski, Charles A LeDuc, Anthony J Lanzano, Pumin Zhang, Daniel R Storm, Dieter Egli, Rudolph L Leibel
Noncoding polymorphisms in the fat mass and obesity-associated (FTO) gene represent common alleles that are strongly associated with effects on food intake and adiposity in humans. Previous studies have suggested that the obesity-risk allele rs8050136 in the first intron of FTO alters a regulatory element recognized by the transcription factor CUX1, thereby leading to decreased expression of FTO and retinitis pigmentosa GTPase regulator-interacting protein-1 like (RPGRIP1L). Here, we evaluated the effects of rs8050136 and another potential CUX1 element in rs1421085 on expression of nearby genes in human induced pluripotent stem cell-derived (iPSC-derived) neurons...
May 2, 2016: Journal of Clinical Investigation
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