Database : MEDLINE
Search on : Glucose and Metabolism and Disorders [Words]
References found : 9863 [refine]
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[PMID]: 29523870
[Au] Autor:Chouinard VA; Henderson DC; Dalla Man C; Valeri L; Gray BE; Ryan KP; Cypess AM; Cobelli C; Cohen BM; Öngür D
[Ad] Address:Psychotic Disorders Division, McLean Hospital, Belmont, MA, USA. vchouinard@mclean.harvard.edu.
[Ti] Title:Impaired insulin signaling in unaffected siblings and patients with first-episode psychosis.
[So] Source:Mol Psychiatry;, 2018 Mar 09.
[Is] ISSN:1476-5578
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Patients with psychotic disorders are at high risk for type 2 diabetes mellitus, and there is increasing evidence that patients display glucose metabolism abnormalities before significant antipsychotic medication exposure. In the present study, we examined insulin action by quantifying insulin sensitivity in first-episode psychosis (FEP) patients and unaffected siblings, compared to healthy individuals, using a physiological-based model and comprehensive assessment battery. Twenty-two unaffected siblings, 18 FEP patients, and 15 healthy unrelated controls were evaluated using a 2-h oral glucose tolerance test (OGTT), with 7 samples of plasma glucose and serum insulin concentration measurements. Insulin sensitivity was quantified using the oral minimal model method. Lipid, leptin, free fatty acids, and inflammatory marker levels were also measured. Anthropometric, nutrient, and activity assessments were conducted; total body composition and fat distribution were determined using whole-body dual-energy X-ray absorptiometry. Insulin sensitivity significantly differed among groups (F = 6.01 and 0.004), with patients and siblings showing lower insulin sensitivity, compared to controls (P = 0.006 and 0.002, respectively). Body mass index, visceral adipose tissue area (cm ), lipids, leptin, free fatty acids, inflammatory markers, and activity ratings were not significantly different among groups. There was a significant difference in nutrient intake with lower total kilocalories/kilogram body weight in patients, compared to siblings and controls. Overall, the findings suggest that familial abnormal glucose metabolism or a primary insulin signaling pathway abnormality is related to risk for psychosis, independent of disease expression and treatment effects. Future studies should examine underlying biological mechanisms of insulin signaling abnormalities in psychotic disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1038/s41380-018-0045-1

  2 / 9863 MEDLINE  
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[PMID]: 29501626
[Au] Autor:Qi G; Guo R; Tian H; Li L; Liu H; Mi Y; Liu X
[Ad] Address:Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science and Engineering, Northwest A&F University, Yangling, Shaanxi 712100, China.
[Ti] Title:Nobiletin protects against insulin resistance and disorders of lipid metabolism by reprogramming of circadian clock in hepatocytes.
[So] Source:Biochim Biophys Acta;1863(6):549-562, 2018 Mar 06.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:SCOPE: Circadian clock plays a principal role in orchestrating our daily physiology and metabolism, and their perturbation can evoke metabolic diseases such as fatty liver and insulin resistance. Nobiletin (NOB) has been demonstrated to possess antitumor and neuroprotective activities. The objective of the current study is to determine potential effects of NOB on modulating the core clock gene Bmal1 regarding ameliorating glucolipid metabolic disorders. RESULTS: Our results revealed that NOB partially reverse the relatively shallow daily oscillations of circadian clock genes and reset phase-shifting circadian rhythms in primary hepatocytes under metabolic disorders conditions. Importantly, NOB was found to be effective at amplifying glucose uptake via stimulating IRS-1/AKT signaling pathway, as well as blunting palmitate-induced lipogenesis in HepG2 cells via modulating AMPK-Sirt1 signaling pathway and key enzymes of de novo lipogenesis in a Bmal1-dependent manner. NOB attenuated palmitate-stimulated excessive secretions of ROS, restored the depletions of mitochondrial membrane potential, which is similar to the recovery in expressions of mitochondrial respiration complex I-IV. CONCLUSION: This study is the first to provide compelling evidences that NOB prevent cellular glucolipid metabolic imbalance and mitochondrial function in a Bmal1-dependent manner. Overall, NOB may serve as a nutritional preventive strategy in recovering metabolic disorders relevant to circadian clock.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  3 / 9863 MEDLINE  
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[PMID]: 29476879
[Au] Autor:Ren T; Yang WS; Lin Y; Liu JF; Li Y; Yang LC; Zeng KY; Peng L; Liu YJ; Ye ZH; Luo XM; Ke YJ; Diao Y; Jin X
[Ad] Address:School of Biomedical Science, Institute of Molecular Medicine, Huaqiao University, Quanzhou 612021, China.
[Ti] Title:A novel PPARα/γ agonist, propane-2-sulfonic acid octadec-9-enyl-amide, ameliorates insulin resistance and gluconeogenesis in vivo and vitro.
[So] Source:Eur J Pharmacol;826:1-8, 2018 Feb 22.
[Is] ISSN:1879-0712
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Peroxisome proliferator-activated receptor alpha/gamma (PPARα/γ) agonists have emerged as important pharmacological agents for improving insulin action. Propane-2-sulfonic acid octadec-9-enyl-amide (N15) is a novel PPARα/γ dual agonist synthesized in our laboratory. The present study investigates the efficacy and safety of N15 on insulin resistance regulation in high fat diet (HFD)-and streptozotocin (STZ)-induced diabetic mice and in palmitic acid (PA)-induced HepG2 cells. Our results showed that N15 remarkably ameliorated insulin resistance and dyslipidemia in vivo, as well as rectified the glucose consumption and gluconeogenesis in vitro. Moreover, the glucose-lowering effect of N15 was associated with PPARγ mediated up-regulation of hepatic glucose consumption and down-regulation of gluconeogenesis. Meanwhile, N15 exerted advantageous effects on glucose and lipid metabolism without triggering weight gain and hepatotoxicity in mice. In conclusion, our data demonstrated that by alleviating glucose and lipid abnormalities, N15 could be used as a potential prophylactic and therapeutic agent against type 2 diabetes and related metabolic disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  4 / 9863 MEDLINE  
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[PMID]: 29476004
[Au] Autor:Meles SK; Renken RJ; Janzen A; Vadasz D; Pagani M; Arnaldi D; Morbelli S; Nobili F; Mayer G; Leenders KL; Oertel WHO
[Ad] Address:Department of Neurology, University of Groningen, University Medical Center Groningen, Netherlands.
[Ti] Title:The metabolic pattern of idiopathic REM sleep behavior disorder reflects early-stage Parkinson's disease.
[So] Source:J Nucl Med;, 2018 Feb 23.
[Is] ISSN:1535-5667
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Idiopathic REM sleep behavior disorder (iRBD) is considered a prodromal stage of Parkinson's disease (PD) and other Lewy-body disorders. Spatial covariance analysis of [ F]-Fluorodeoxyglucose Positron Emission Tomography ( F-FDG-PET) data has disclosed a specific brain pattern of altered glucose metabolism in PD. In this study, we identify the metabolic pattern underlying iRBD and compare it to the known PD pattern. To understand the relevance of the iRBD pattern to disease progression, we study the expression of the iRBD pattern in de novo PD patients. The iRBD-related pattern was identified in F-FDG-PET scans of 21 patients with polysomnographically-confirmed iRBD and 19 controls using spatial covariance analysis. Expression of the iRBD-related pattern was subsequently computed in F-FDG-PET scans of 44 controls and 38 de novo, treatment-naïve PD patients. Of these 38 PD patients, 24 had probable RBD according to the Mayo Sleep Questionnaire. Neuropsychological evaluation showed mild cognitive impairment in 20 PD patients (PD-MCI), of whom sixteen also had concomitant RBD and roughly half (11/20) had bilateral motor symptoms. The iRBD-related pattern was characterized by relative hypermetabolism in cerebellum, brainstem, thalamus, sensorimotor cortex, and hippocampus, and by relative hypometabolism in middle cingulate, temporal, occipital and parietal cortices. This topography partially overlapped with the PD-related pattern (PDRP). The iRBD-related pattern was significantly expressed in PD patients compared to controls (P<0.0001). iRBD-related pattern expression was not significantly different between PD patients with and without probable RBD, or between PD patients with unilateral or bilateral parkinsonism. iRBD-related pattern expression was higher in PD-MCI patients, compared to PD patients with preserved cognition ( = 0.001). Subject scores on the iRBD-related pattern were highly correlated to subject scores on the PDRP (r=0.94, P<0.0001). In conclusion, our results show that the iRBDRP is an early manifestation of the PDRP. Expression of both PDRP and iRBDRP was higher in patients with a more severe form of PD (PD-MCI), which indicates that expression of the two patterns increases with disease severity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 9863 MEDLINE  
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[PMID]: 29425111
[Au] Autor:MacDonald A; Webster R; Whitlock M; Gerrard A; Daly A; Preece MA; Evans S; Ashmore C; Chakrapani A; Vijay S; Santra S
[Ad] Address:Consultant Dietitian in Inherited Metabolic Disorders, Dietetic Department, Birmingham Women's and Children's Hospital NHS Foundation Trust, Steelhouse Lane, Birmingham, B4 6NH, UK.
[Ti] Title:The safety of Lipistart, a medium-chain triglyceride based formula, in the dietary treatment of long-chain fatty acid disorders: a phase I study.
[So] Source:J Pediatr Endocrinol Metab;31(3):297-304, 2018 Mar 28.
[Is] ISSN:2191-0251
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:BACKGROUND: Children with long-chain fatty acid ß-oxidation disorders (LCFAOD) presenting with clinical symptoms are treated with a specialist infant formula, with medium chain triglyceride (MCT) mainly replacing long chain triglyceride (LCT). It is essential that the safety and efficacy of any new specialist formula designed for LCFAOD be tested in infants and children. METHODS: In an open-label, 21-day, phase I trial, we studied the safety of a new MCT-based formula (feed 1) in six well-controlled children (three male), aged 7-13 years (median 9 years) with LCFAOD (very long chain acyl CoA dehydrogenase deficiency [VLCADD], n=2; long chain 3-hydroxyacyl CoA dehydrogenase deficiency [LCHADD], n=2; carnitine acyl carnitine translocase deficiency [CACTD], n=2). Feed 1 (Lipistart; Vitaflo) contained 30% energy from MCT, 7.5% LCT and 3% linoleic acid and it was compared with a conventional MCT feed (Monogen; Nutricia) (feed 2) containing 17% energy from MCT, 3% LCT and 1.1% linoleic acid. Subjects consumed feed 2 for 7 days then feed 1 for 7 days and finally resumed feed 2 for 7 days. Vital signs, blood biochemistry, ECG, weight, height, food/feed intake and symptoms were monitored. RESULTS: Five subjects completed the study. Their median daily volume of both feeds was 720 mL (range 500-1900 mL/day). Feed 1 was associated with minimal changes in tolerance, free fatty acids (FFA), acylcarnitines, 3-hydroxybutyrate (3-HB), creatine kinase (CK), blood glucose, liver enzymes and no change in an electrocardiogram (ECG). No child complained of muscle pain or symptoms associated with LCFAOD on either feed. CONCLUSIONS: This is the first safety trial reported of an MCT formula specifically designed for infants and children with LCFAOD. In this short-term study, it appeared safe and well tolerated in this challenging group.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process

  6 / 9863 MEDLINE  
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[PMID]: 29519318
[Au] Autor:Ding T; Wang S; Zhang X; Zai W; Fan J; Chen W; Bian Q; Luan J; Shen Y; Zhang Y; Ju D; Mei X
[Ad] Address:Department of Nephrology, Changhai Hospital, Second Military Medical University, Shanghai 200433, PR China.
[Ti] Title:Kidney protection effects of dihydroquercetin on diabetic nephropathy through suppressing ROS and NLRP3 inflammasome.
[So] Source:Phytomedicine;41:45-53, 2018 Mar 01.
[Is] ISSN:1618-095X
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:BACKGROUND: Diabetic nephropathy (DN), the leading cause of end-stage renal disease, is acknowledged as an independent risk factor for cardiovascular disease, which underlines the urgent need for new medications to DN. Dihydroquercetin (DHQ), an important natural dihydroflavone, exerts significant antioxidant, anti-inflammatory, and antifibrotic properties, but its effects on DN have not been investigated yet. PURPOSE: We aimed to explore the kidney protection effects of DHQ on DN rats induced by high-fat diet/streptozotocin in vivo and the underlying mechanisms of DHQ on renal cells including HBZY-1 and HK2 exposed to high glucose in vitro. METHODS: Major biochemical indexes were measured including urine microalbumin, fasting serum glucose, serum levels of creatinine, total cholesterol and low density lipoprotein cholesterol. Renal histologic sections were stained with hematoxylin-eosin, periodic acid-Schiff and Masson. The cell proliferation was assessed by MTT assay. Reactive oxygen species (ROS) generation was detected by DCFH-DA assay and laser scanning confocal microscope. Expression of all proteins was examined by western-blot. RESULTS: In high-fat diet/streptozotocin-induced DN rats, DHQ at the dose of 100 mg/kg/day significantly attenuated the increasing urine microalbumin excretion, hyperglycemia and lipid metabolism disorders, and mitigated renal histopathological lesions. In in vitro studies, DHQ significantly suppressed cell proliferation and the excessive ROS generation, and alleviated the activation of nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome and the expression of renal fibrosis-associated proteins in renal cells exposed to high glucose. CONCLUSION: The results revealed that DHQ possesses kidney protection effects including attenuating urine microalbumin excretion, hyperglycemia and lipid metabolism disorders, and mitigating renal histopathological lesions on DN, and one of the possible renal-protective mechanisms is suppressing ROS and NLRP3 inflammasome.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process

  7 / 9863 MEDLINE  
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[PMID]: 29518757
[Au] Autor:Lazaridou S; Dinas K; Tziomalos K
[Ad] Address:First Propedeutic Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, AHEPA Hospital, Thessaloniki, Greece.
[Ti] Title:Prevalence, pathogenesis and management of prediabetes and type 2 diabetes mellitus in patients with polycystic ovary syndrome.
[So] Source:Hormones (Athens);16(4):373-380, 2017 Oct.
[Is] ISSN:1109-3099
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women of reproductive age. PCOS is not only the leading cause of anovulatory infertility but is also associated with an array of metabolic disorders, among which impaired glucose metabolism has been a topic of intense research. The aim of the present narrative review is to summarize the findings of the studies that have evaluated the prevalence and incidence of prediabetes and type 2 diabetes mellitus (T2DM) in patients with PCOS, to analyze the factors underpinning the association between T2DM and PCOS and to discuss the current strategies for screening and management of impaired glucose metabolism in this population. Both prediabetes and T2DM are highly prevalent in patients with PCOS. Accordingly, regular screening is recommended in this population for the early identification of impaired glucose metabolism, particularly in overweight or obese patients and in those with a family history of T2DM. Prevention of T2DM in patients with prediabetes is primarily based on lifestyle changes, while metformin might be considered in selected cases. The treatment of T2DM is similar in patients with and without PCOS but appropriate contraceptive measures should be implemented in patients receiving treatments other than insulin, metformin or glyburide.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process
[do] DOI:10.14310/horm.2002.1757

  8 / 9863 MEDLINE  
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[PMID]: 29518061
[Au] Autor:Sato F; Kohsaka A; Bhawal UK; Muragaki Y
[Ad] Address:Department of Pathology, Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama 641-8509, Japan. fsatoDEC1DEC2@yahoo.co.jp.
[Ti] Title:Potential Roles of Dec and Bmal1 Genes in Interconnecting Circadian Clock and Energy Metabolism.
[So] Source:Int J Mol Sci;19(3), 2018 Mar 08.
[Is] ISSN:1422-0067
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:The daily rhythm of mammalian energy metabolism is subject to the circadian clock system, which is made up of the molecular clock machinery residing in nearly all cells throughout the body. The clock genes have been revealed not only to form the molecular clock but also to function as a mediator that regulates both circadian and metabolic functions. While the circadian signals generated by clock genes produce metabolic rhythms, clock gene function is tightly coupled to fundamental metabolic processes such as glucose and lipid metabolism. Therefore, defects in the clock genes not only result in the dysregulation of physiological rhythms but also induce metabolic disorders including diabetes and obesity. Among the clock genes, ( / / ), ( / ), and ( / ) have been shown to be particularly relevant to the regulation of energy metabolism at the cellular, tissue, and organismal levels. This paper reviews our current knowledge of the roles of , , and in coordinating the circadian and metabolic pathways.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process

  9 / 9863 MEDLINE  
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[PMID]: 29451141
[Au] Autor:Zhang R; Dong SY; Wang F; Ma C; Zhao XL; Zeng Q; Fei A
[Ad] Address:International Medical Center, Health Management Institute, Chinese PLA General Hospital, Beijing 100853; Department of Cardiology, Chinese Navy General Hospital, Beijing 100048, China.
[Ti] Title:Associations between Body Composition Indices and Metabolic Disorders in Chinese Adults: A Cross-Sectional Observational Study.
[So] Source:Chin Med J (Engl);131(4):379-388, 2018 Feb 20.
[Is] ISSN:0366-6999
[Cp] Country of publication:China
[La] Language:eng
[Ab] Abstract:Background: Obesity induces dyslipidemia, hypertension, glucose intolerance, and inflammatory state, which results in atherogenic processes, diabetes, and cardiovascular disease. We usually use body composition indices, such as body mass index (BMI), body fat percentage (BFP), waist circumference-height ratio (WHtR), and waist-hip ratio (WHR) to reflect the obesity. The aim of this large population-based cross-sectional study was to investigate the associations between body composition indices and metabolic parameters in Chinese adults. Methods: A total of 12,018 Chinese adults were included. Body composition indices, such as BMI, BFP, WHtR, and WHR, and metabolic parameters, such as systolic blood pressure (SBP), diastolic blood pressure (DBP), total cholesterol (TC), triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), fasting blood glucose (FBG), 2 h postprandial blood glucose (2h PBG), glycosylated hemoglobin (HbA1c), fasting insulin (FINS), insulin resistance index (HOMA-IR), high-sensitivity C-reactive protein (hs-CRP), and white blood cell count (WBC), were measured and analyzed. All analyses were stratified by gender. Results: All body composition indices and metabolic parameters except 2h PBG differed significantly between males and females (all P < 0.001). BMI was positively associated with SBP, DBP, LDL-C, TC, TG, FBG, 2h PBG, HbA1c, FINS, HOMA-IR, hs-CRP, and WBC, and inversely associated with HDL-C; similar relationships were identified between the metabolic parameters and BFP, WHtR, and WHR. In the multivariate analysis, the odds of impaired glucose regulation, dyslipidemia, insulin resistance, and increased hs-CRP were 1.36, 1.92, 3.44, and 1.27 times greater in the overweight group than those in the normal weight group, respectively, and 1.66, 3.26, 7.53, and 1.70 times greater in the obese group than those in the normal weight group, respectively. The odds of dyslipidemia and hs-CRP were 1.29 and 1.38 times greater in the BFP ≥28.0% group than in the BFP <28.0% group, respectively. The odds of dyslipidemia, HOMA-IR, and hs-CRP were 1.55, 1.26, and 1.48 times greater in the WHtR ≥0.96 group than in the WHtR <0.96 group, respectively. Among males, the odds of HOMA-IR were 1.46 times greater in the WHR ≥0.54 group than in the WHR <0.54 group. Similar results were observed in females. Conclusions: This study identified positive associations between all evaluated body composition indices and metabolic parameters in Chinese adults. Among the body composition indices, BMI predicted four of the five evaluated metabolic disorders in both gender groups.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.4103/0366-6999.225059

  10 / 9863 MEDLINE  
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[PMID]: 29377004
[Au] Autor:Guo B; Huang X; Lee MR; Lee SA; Broxmeyer HE
[Ad] Address:Department of Microbiology and Immunology, Indiana University School of Medicine (IUSM), Indianapolis, Indiana, USA.
[Ti] Title:Antagonism of PPAR-γ signaling expands human hematopoietic stem and progenitor cells by enhancing glycolysis.
[So] Source:Nat Med;24(3):360-367, 2018 Mar.
[Is] ISSN:1546-170X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hematopoietic stem cells (HSCs) quiescently reside in bone marrow niches and have the capacity to self-renew or differentiate to form all of the blood cells throughout the lifespan of an animal. Allogeneic HSC transplantation is a life-saving treatment for malignant and nonmalignant disorders. HSCs isolated from umbilical cord blood (CB) are used for hematopoietic cell transplantation (HCT), but due to the limited numbers of HSCs in single units of umbilical CB, a number of methods have been proposed for ex vivo expansion of human HSCs. We show here that antagonism of peroxisome proliferator-activated receptor (PPAR)-γ promotes ex vivo expansion of phenotypically and functionally defined subsets of human CB HSCs and hematopoietic progenitor cells (HSPCs). PPAR-γ antagonism in CB HSPCs strongly downregulated expression of several differentiation-associated genes, as well as fructose-bisphosphatase 1 (FBP1; which encodes a negative regulator of glycolysis), and enhanced glycolysis without compromising mitochondrial metabolism. The expansion of CB HSPCs by PPAR-γ antagonism was completely suppressed by removal of glucose or inhibition of glycolysis. Moreover, knockdown of FBP1 expression promoted glycolysis and ex vivo expansion of long-term repopulating CB HSPCs, whereas overexpression of FBP1 suppressed the expansion of CB HSPCs that was induced by PPAR-γ antagonism. Our study suggests the possibility for a new and simple means for metabolic reprogramming of CB HSPCs to improve the efficacy of HCT.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1038/nm.4477


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