Interaction of Genetic Risk Factors Confers Increased Risk for Metabolic Syndrome: The Role of Peroxisome Proliferator-Activated Receptor γ

2014 ◽  
Vol 18 (1) ◽  
pp. 32-40 ◽  
Author(s):  
Tamara Božina ◽  
Jadranka Sertić ◽  
Jasna Lovrić ◽  
Bojan Jelaković ◽  
Iveta Šimić ◽  
...  
2008 ◽  
Vol 192 (6) ◽  
pp. 424-428 ◽  
Author(s):  
Olga O. Yevtushenko ◽  
Stephen J. Cooper ◽  
Ryan O'Neill ◽  
Jennifer K. Doherty ◽  
Jayne V. Woodside ◽  
...  

BackgroundObesity and metabolic syndrome are significant problems for patients taking antipsychotic drugs. Evidence is emerging of genetic risk factors.AimsTo investigate the influence of two candidate genes, smoking and drug treatment on obesity and metabolic syndrome in patients with schizophrenia.MethodPatients (n=134) were assessed for measures of obesity, other factors contributing to metabolic syndrome, and two genetic polymorphisms (5-HT2C receptor −759C/T and leptin −2548A/G).ResultsNeither genotype nor smoking was significantly associated with measures of obesity. However, both leptin genotype and smoking were significantly associated with metabolic syndrome. Significant interaction occurred between the genetic polymorphisms for effects on obesity, whereby a genotype combination increased risk. Drug treatment showed significant effects on measures of obesity and triglyceride concentrations; risperidone was associated with lower values than olanzapine or clozapine.ConclusionsThe findings suggest interacting genetic risk factors and smoking influence development of metabolic syndrome in patients on antipsychotic drugs.


2021 ◽  
Vol 22 (9) ◽  
pp. 4670
Author(s):  
Cinzia Buccoliero ◽  
Manuela Dicarlo ◽  
Patrizia Pignataro ◽  
Francesco Gaccione ◽  
Silvia Colucci ◽  
...  

Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) is a protein that promotes transcription of numerous genes, particularly those responsible for the regulation of mitochondrial biogenesis. Evidence for a key role of PGC1α in bone metabolism is very recent. In vivo studies showed that PGC1α deletion negatively affects cortical thickness, trabecular organization and resistance to flexion, resulting in increased risk of fracture. Furthermore, in a mouse model of bone disease, PGC1α activation stimulates osteoblastic gene expression and inhibits atrogene transcription. PGC1α overexpression positively affects the activity of Sirtuin 3, a mitochondrial nicotinammide adenina dinucleotide (NAD)-dependent deacetylase, on osteoblastic differentiation. In vitro, PGC1α overexpression prevents the reduction of mitochondrial density, membrane potential and alkaline phosphatase activity caused by Sirtuin 3 knockdown in osteoblasts. Moreover, PGC1α influences the commitment of skeletal stem cells towards an osteogenic lineage, while negatively affects marrow adipose tissue accumulation. In this review, we will focus on recent findings about PGC1α action on bone metabolism, in vivo and in vitro, and in pathologies that cause bone loss, such as osteoporosis and type 2 diabetes.


Alcohol ◽  
2020 ◽  
Vol 87 ◽  
pp. 63-72
Author(s):  
Natalia A. Osna ◽  
Rakesh Bhatia ◽  
Christopher Thompson ◽  
Surinder K. Batra ◽  
Sushil Kumar ◽  
...  

Author(s):  
H. Vielhaber ◽  
O. Debus ◽  
G. Kurlemann ◽  
R. Sträter ◽  
U. Nowak-Göttl

2020 ◽  
Vol 105 (8) ◽  
pp. 756-764 ◽  
Author(s):  
Silvia Baldacci ◽  
Michele Santoro ◽  
Alessio Coi ◽  
Lorena Mezzasalma ◽  
Fabrizio Bianchi ◽  
...  

BackgroundGastroschisis is strongly associated with young maternal age. This association suggests the need for further investigations on non-genetic risk factors. Identifying these risk factors is a public health priority in order to develop prevention strategies aimed at reducing the prevalence and health consequences in offspring.ObjectiveTo systematically assess and quantitatively synthesise the available epidemiological studies to evaluate the association between non-genetic risk factors and gastroschisis.MethodsLiterature from PubMed, EMBASE and Scopus was searched for the period 1990–2018. Epidemiological studies reporting risk estimates between lifestyle and sociodemographic risk factors and gastroschisis were included. Two pairs of reviewers independently extracted information on study characteristics following Preferred Reporting Items for Systematic Reviews and Meta-Analyses and MOOSE (Meta-analysis Of Oservational Studies in Epidemiology) guidelines. Relative risk (RR) estimates were calculated across the studies and meta-analysis was performed using random-effects model.ResultsWe identified 58 studies. Meta-analyses were conducted on 29 studies. Maternal smoking (RR 1.56, 95% CI 1.40 to 1.74), illicit drug use (RR 2.14, 95% CI 1.48 to 3.07) and alcohol consumption (RR 1.40, 95% CI 1.13 to 1.70) were associated with an increased risk of gastroschisis. A decreased risk among black mothers compared with non-Hispanic white mothers (RR 0.49, 95% CI 0.38 to 0.63) was found. For Hispanic mothers no association was observed.ConclusionsExposure to smoking, illicit drugs and alcohol during pregnancy is associated with an increased risk of gastroschisis. A significantly decreased risk for black mothers was observed. Further epidemiological studies to assess the potential role of other environmental factors are strongly recommended.PROSPERO registration numberCRD42018104284.


Hematology ◽  
2005 ◽  
Vol 2005 (1) ◽  
pp. 442-444 ◽  
Author(s):  
David Ginsburg

Abstract Arterial thrombosis is a central pathologic mechanism contributing to myocardial infarction and stroke, together the leading causes of death in developed countries. This article reviews the current state of knowledge concerning the role of inherited variation in hemostatic and inflammatory factor genes in determining the risk of arterial thrombosis/ischemic heart disease. Despite considerable progress in identifying important genetic risk factors underlying predisposition to venous thrombosis, the genetic factors contributing to the risk for arterial thrombosis remain largely unknown. However, the rapid development of powerful new genomic resources should facilitate considerably more sophisticated analyses, leading to novel insight into the molecular pathophysiology of this important set of human diseases.


Sign in / Sign up

Export Citation Format

Share Document