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Genetics of Metabolic Syndrome

Maryam Zarkesh, Golaleh Asghari, Parisa Amiri, Nima Hosseinzadeh, Mehdi Hedayati, Arash Ghanbarian, Fereidoun Azizi
BACKGROUND: Since genetic and most environmental factors shape the context of families, some studies have been initiated to investigate the role of familial relationships in metabolic syndrome (MetS). OBJECTIVES: To estimate the familial aggregation of MetS and its components by identifying both case and control probands among Tehranian adults with different socio-behavioral and reproductive characteristics. PATIENTS AND METHODS: This case-controlled/family-based study was conducted on 1,777 families (635 case probands) who participated in the Tehran Lipid and Glucose Study (TLGS)...
August 2016: Iranian Red Crescent Medical Journal
Christina M Jacobsen
Sclerostin, a known inhibitor of the low density lipoprotein related protein 5 and 6 (LRP5 and LRP6) cell surface signaling receptors, is integral in the maintenance of normal bone mass and strength. Patients with loss of function mutations in SOST or missense mutations in LRP5 that prevent Sclerostin from binding and inhibiting the receptor, have significantly increased bone mass. This observation leads to the development of Sclerostin neutralizing therapies to increase bone mass and strength. Anti-Sclerostin therapy has been shown to be effective at increasing bone density and strength in animal models and patients with osteoporosis...
October 22, 2016: Bone
Juan M González-Morena, María I Montañez, Giancarlo Aldini, Francisco J Sánchez-Gómez, Dolores Pérez-Sala
Drug hypersensitivity reactions result from the activation of the immune system by drugs or their metabolites. The clinical presentations of drug hypersensitivity can range from relatively mild local manifestations to severe systemic syndromes that can be life-threatening. As in other allergic reactions, the causes are multifactorial as genetic, metabolic and concomitant factors may influence the occurrence of drug hypersensitivity. Formation of drug protein adducts is considered a key step in drug adverse reactions, and in particular in the immunological recognition in drug hypersensitivity reactions...
September 27, 2016: Current Pharmaceutical Design
Chong Kun Cheon
The Prader-Willi syndrome (PWS) is a human imprinting disorder resulting from genomic alterations that inactivate imprinted, paternally expressed genes in human chromosome region 15q11-q13. This genetic condition appears to be a contiguous gene syndrome caused by the loss of at least 2 of a number of genes expressed exclusively from the paternal allele, including SNRPN, MKRN3, MAGEL2, NDN and several snoRNAs, but it is not yet well known which specific genes in this region are associated with this syndrome...
September 2016: Annals of Pediatric Endocrinology & Metabolism
Tarek K Motawi, Olfat G Shaker, Nancy N Shahin, Nancy M Ahmed
BACKGROUND: According to the WHO report in 2015, obesity is the fifth leading cause of death worldwide, and the prevalence of Egyptian female obesity is 37.5 %. Since obesity is highly influenced by genetics, and adipose tissue renin-angiotensin system is over-activated in obesity, the effect of angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism on obesity and related disorders was studied in several populations, because of its effect on ACE activity. Our objective was to study the association of ACE I/D polymorphism with obesity and certain related disorders, namely hypertension, insulin resistance and metabolic syndrome, in Egyptian females...
2016: Nutrition & Metabolism
Shiho Fujisaka, Siegfried Ussar, Clary Clish, Suzanne Devkota, Jonathan M Dreyfuss, Masaji Sakaguchi, Marion Soto, Masahiro Konishi, Samir Softic, Emrah Altindis, Ning Li, Georg Gerber, Lynn Bry, C Ronald Kahn
Interactions of diet, gut microbiota, and host genetics play important roles in the development of obesity and insulin resistance. Here, we have investigated the molecular links between gut microbiota, insulin resistance, and glucose metabolism in 3 inbred mouse strains with differing susceptibilities to metabolic syndrome using diet and antibiotic treatment. Antibiotic treatment altered intestinal microbiota, decreased tissue inflammation, improved insulin signaling in basal and stimulated states, and improved glucose metabolism in obesity- and diabetes-prone C57BL/6J mice on a high-fat diet (HFD)...
October 24, 2016: Journal of Clinical Investigation
Sohee Oh, Iksoo Huh, Seung Yeoun Lee, Taesung Park
Most genome-wide association studies (GWAS) have been conducted by focusing on one phenotype of interest for identifying genetic variants associated with common complex phenotypes. However, despite many successful results from GWAS, only a small number of genetic variants tend to be identified and replicated given a very stringent genome-wide significance criterion, and explain only a small fraction of phenotype heritability. In order to improve power by using more information from data, we propose an alternative multivariate approach, which considers multiple related phenotypes simultaneously...
September 9, 2016: Journal of Bioinformatics and Computational Biology
Jerrold J Heindel, Bruce Blumberg, Mathew Cave, Ronit Machtinger, Alberto Mantovani, Michelle A Mendez, Angel Nadal, Paola Palanza, Giancarlo Panzica, Robert Sargis, Laura N Vandenberg, Frederick Vom Saal
The recent epidemics of metabolic diseases, obesity, type 2 diabetes(T2D), liver lipid disorders and metabolic syndrome have largely been attributed to genetic background and changes in diet, exercise and aging. However, there is now considerable evidence that other environmental factors may contribute to the rapid increase in the incidence of these metabolic diseases. This review will examine changes to the incidence of obesity, T2D and non-alcoholic fatty liver disease (NAFLD), the contribution of genetics to these disorders and describe the role of the endocrine system in these metabolic disorders...
October 16, 2016: Reproductive Toxicology
Chaudhari Archana Somabhai, Ruma Raghuvanshi, G Nareshkumar
AIMS: To assess protective efficacy of genetically modified Escherichia coli Nissle 1917 (EcN) on metabolic effects induced by chronic consumption of dietary fructose. MATERIALS AND METHODS: EcN was genetically modified with fructose dehydrogenase (fdh) gene for conversion of fructose to 5-keto-D-fructose and mannitol-2-dehydrogenase (mtlK) gene for conversion to mannitol, a prebiotic. Charles foster rats weighing 150-200 g were fed with 20% fructose in drinking water for two months...
2016: PloS One
Elena V Galitsyna, Andrey V Zhelankin, Igor A Sobenin, Alexander N Orekhov
In addition to external factors, such as exercise, food and the environment, genetic predisposition makes great contribution to the development of metabolic disorders and cardiovascular disease. This review is aimed to examine the genetic basis of complex metabolic disorders conventionally described as "metabolic syndrome" (MetS), with the special focus on currently known mutations in the nuclear and mitochondrial genomes, which are associated both with the individual components of MetS and combinations thereof, and also on the studies of the relationship of MetS phenotype as a binary trait...
October 18, 2016: Current Pharmaceutical Design
Petra Rust, Cem Ekmekcioglu
Excessive dietary salt (sodium chloride) intake is associated with an increased risk for hypertension, which in turn is especially a major risk factor for stroke and other cardiovascular pathologies, but also kidney diseases. Besides, high salt intake or preference for salty food is discussed to be positive associated with stomach cancer, and according to recent studies probably also obesity risk. On the other hand a reduction of dietary salt intake leads to a considerable reduction in blood pressure, especially in hypertensive patients but to a lesser extent also in normotensives as several meta-analyses of interventional studies have shown...
October 19, 2016: Advances in Experimental Medicine and Biology
Daoyan Liu
OBJECTIVE: Increased transient receptor potential canonical type 3 (TRPC3) channels have been observed in essential hypertensive patients and spontaneously hypertensive rats (SHR). Our previous study shows that mitochondrial respiratory dysfunctions of blood mononuclear cells link with cardiac disturbance in patients with early-stage heart failure. Telmisartan has beneficial effect on both hypertension and metabolic syndrome. In the present study we tested the hypothesis that telmisartan administration inhibited mitochondrial respiratory function was associated with decreased TRPC3 function in monocytes from genetic hypertensive rats (SHR)...
September 2016: Journal of Hypertension
GwangPyo Ko
Recently, there were dramatically increased interests on human microbiome research worldwide. Human microbiome has been considered as the second genome in addition to our own genome and played very crucial roles in maintaining human health. Human microbiota typically reside on the surface of epithelial cells and play various biological roles ranging from metabolism, immune development, mental health, and to organ development. Since 2008, we have determined the diversity of Korean microbiome and determined the genes and pathways of gut microbiome using Korean Twin Cohort...
September 2016: Journal of Hypertension
Asadur Rahman, Yui Takeshige, Yoshihide Fujisawa, Hirofumi Hitomi, Daisuke Nakano, Akira Nishiyama
OBJECTIVE: Disrupted circadian rhythm of blood pressure is associated with cardiovascular events in metabolic syndrome and obesity. Experiments were conducted to examine the effects of sodium-glucose co-transporter 2 (SGLT2) inhibitors on circadian rhythm of blood pressure in a genetic model of obese metabolic syndrome (SHR/NDmcr-cp (+/+) (SHRcp)) and salt-treated obese Otsuka Long Evans Tokushima Fatty (OLETF) rats. DESIGN AND METHOD: Luseogliflozin (10 mg/kg/day, p...
September 2016: Journal of Hypertension
Jing-Ran Ma, Dan-Hua Wang
Breastfeeding is well-known for its benefits of preventing communicable and non-communicable diseases. Human breastmilk consists not only of nutrients, but also of bioactive substances. What's more, the epigenetic effects of human breast milk may also play an important role. Alterations in the epigenetic regulation of genes may lead to profound changes in phenotype. Clarifying the role of human breast milk on genetic expression can potentially benefit the infant's health and his later life. This review article makes a brief summary of the epigenetic mechanism of breast milk, and its epigenetic effects on neonatal necrotizing enterocolitis, infectious diseases, metabolism syndrome, cognitive function and anaphylactic diseases...
October 2016: Zhongguo Dang Dai Er Ke za Zhi, Chinese Journal of Contemporary Pediatrics
Geir Bjørklund, Salvatore Chirumbolo
Diet may be defined as a complex process that should involve a deeper comprehension of metabolism, energy balance, and the molecular pathways involved in cellular stress response and survival, gut microflora genetics, enzymatic polymorphism within the human population, and the role of plant-derived polyphenols in this context. Metabolic syndrome, encompassing pathologies with a relatively high morbidity, such as type 2 diabetes, obesity, and cardiovascular disease, is a bullet point of the big concern about how daily dietary habits should promote health and prevent metabolic impairments to prevent hospitalization and the need for health care...
August 8, 2016: Nutrition
Adrienne Wang, Jacob Mouser, Jason Pitt, Daniel Promislow, Matt Kaeberlein
Pediatric mitochondrial disorders are a devastating category of diseases caused by deficiencies in mitochondrial function. Leigh Syndrome (LS) is the most common of these diseases with symptoms typically appearing within the first year of birth and progressing rapidly until death, usually by 6-7 years of age. Our lab has recently shown that genetic inhibition of the mechanistic target of rapamycin (TOR) rescues the short lifespan of yeast mutants with defective mitochondrial function, and that pharmacological inhibition of TOR by administration of rapamycin significantly rescues the shortened lifespan, neurological symptoms, and neurodegeneration in a mouse model of LS...
October 11, 2016: Oncotarget
E D Rosen
Insulin resistance is one of the defining features of type 2 diabetes and the metabolic syndrome and accompanies many other clinical conditions, ranging from obesity to lipodystrophy to glucocorticoid excess. Extraordinary efforts have gone into defining the mechanisms that underlie insulin resistance, with most attention focused on altered signalling as well as mitochondrial and endoplasmic reticulum stress. Here, nuclear mechanisms of insulin resistance, including transcriptional and epigenomic effects, will be discussed...
October 14, 2016: Journal of Internal Medicine
Sylva Skalova, Stepan Kutilek
Transient hyperphosphatasemia of infancy and early childhood (THI) is characterized by transiently increased activity of serum alkaline phosphatase (S-ALP), predominantly its bone or liver isoform, in children under five years of age. There are no signs of metabolic bone disease or hepatopathy corresponding with the increased S-ALP. THI is benign disorder, rather laboratory than clinical disorder, which is usually accidentally detected in both healthy and sick children. When encountered in a child with either chronic bone, liver or kidney disease, it might concern the physician...
July 2016: Jornal Brasileiro de Nefrologia: ʹorgão Oficial de Sociedades Brasileira e Latino-Americana de Nefrologia
Verena Zoller, Jan-Bernd Funcke, Michaela Keuper, Muad Abd El Hay, Klaus-Michael Debatin, Martin Wabitsch, Pamela Fischer-Posovszky
Tumor necrosis factor-α (TNFα) and other ligands of the TNF superfamily are potent regulators of adipose tissue metabolism and play a crucial role in the obesity-induced inflammation of adipose tissue. Adipose tissue expression levels of TRAIL (TNF-related apoptosis-inducing ligand) and its receptor were shown to be upregulated by overfeeding and decreased by fasting in mice. In the present study we aimed to elucidate the impact of TRAIL on adipogenesis. To this end, human Simpson-Golabi-Behmel syndrome (SGBS) preadipocytes as well as stromal-vascular cells isolated from human white adipose tissue were used as model systems...
October 13, 2016: Cell Death & Disease
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