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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The accompanying review in this issue of Clinical Science [Chan, Barrett and Watts (2004) Clin. Sci. 107, 221-232] presented an overview of lipoprotein physiology and the methodologies for stable isotope kinetic studies. The present review focuses on our understanding of the dysregulation and therapeutic regulation of lipoprotein transport in the metabolic syndrome based on the application of stable isotope and modelling methods. Dysregulation of lipoprotein metabolism in metabolic syndrome may be due to a combination of overproduction of VLDL [very-LDL (low-density lipoprotein)]-apo (apolipoprotein) B-100, decreased catabolism of apoB-containing particles and increased catabolism of HDL (high-density lipoprotein)-apoA-I particles. These abnormalities may be consequent on a global metabolic effect of insulin resistance, partly mediated by depressed plasma adiponectin levels, that collectively increases the flux of fatty acids from adipose tissue to the liver, the accumulation of fat in the liver and skeletal muscle, the hepatic secretion of VLDL-triacylglycerols and the remodelling of both LDL (low-density lipoprotein) and HDL particles in the circulation. These lipoprotein defects are also related to perturbations in both lipolytic enzymes and lipid transfer proteins. Our knowledge of the pathophysiology of lipoprotein metabolism in the metabolic syndrome is well complemented by extensive cell biological data. Nutritional modifications may favourably alter lipoprotein transport in the metabolic syndrome by collectively decreasing the hepatic secretion of VLDL-apoB and the catabolism of HDL-apoA-I, as well as by potentially increasing the clearance of LDL-apoB. Several pharmacological treatments, such as statins, fibrates or fish oils, can also correct the dyslipidaemia by diverse kinetic mechanisms of action, including decreased secretion and increased catabolism of apoB, as well as increased secretion and decreased catabolism of apoA-I. The complementary mechanisms of action of lifestyle and drug therapies support the use of combination regimens in treating dyslipoproteinaemia in subjects with the metabolic syndrome.
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PMID:Lipoprotein transport in the metabolic syndrome: pathophysiological and interventional studies employing stable isotopy and modelling methods. 1522 21

Polycystic ovary syndrome (PCOS) is characterized by insulin resistance and consequent hyperinsulinemia. Insulin resistance also plays an important role in the metabolic syndrome (MS). We conducted a cross-sectional study to determine the prevalence of the MS in young Korean women with PCOS and whether it is associated insulin resistance. One hundred and seventeen young women with PCOS (age: 26+/-5, 16-39 years) were evaluated for the frequency of MS according to the modified Adult Treatment Panel III. Total testosterone (T), free T, androstenedione, dehydroepiandrosterone sulfate (DHEAS) and sex hormone binding globulin (SHBG) were measured, and insulin sensitivity was evaluated by euglycemic hyperinsulinemic clamp technique. The prevalence of MS in women with PCOS was 14.5%, nearly 3.5-fold higher than in age-matched women in Korean urban population (4.3%) [J.-Y. Oh, Y.-A. Sung, Y.S. Hong, E. Barrett-Conner, Prevalence and factor analysis of metabolic syndrome in an urban Korean population, Diabetes Care 27 (2004) 2027-2032]. The most frequently occurring component of MS was low HDL cholesterol (45%), and the least frequent was high fasting serum glucose level (0.9%). PCOS women with MS had significantly higher free T, and lower SHBG compared with those without MS. And women with MS showed significantly lower M-value and higher fasting/post-glucose load insulin levels. M-value was still significantly lower in women with MS even after the adjustment for BMI. MS is frequent in young Korean women with PCOS and it reflects more severe insulin resistance. These results suggest the importance of early and regular screening of metabolic disturbance in even young women with PCOS.
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PMID:The metabolic syndrome in young Korean women with polycystic ovary syndrome. 1761 Sep 84

Esophageal adenocarcinoma and its precursor Barrett's esophagus are increasing in incidence in western populations. Gastroesophageal reflux and high body mass index (BMI) are known risk factors. Studies about Barrett's esophagus in obese patients have emphasised the role of central adiposity as a stronger risk factor than BMI in the development of specialized intestinal metaplasia and subsequently esophagus adenocarcinoma. The proinflammatory impact of adipocytokines of the abdominal fat associated with the metabolic syndrome is also relevant. Except cardiovascular diseases, type 2 diabetes and non alcoholic steatohepatitis, abdominal obesity and metabolic syndrome are responsible of an increase of prevalence of esophageal adenocarcinoma, but also other cancer sites. In this review, we study the up to date main epidemiologic and physiopathologic data concerning this association that could be important in future for a preventive action in obese patients, especially when metabolic syndrome is present.
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PMID:[Review of the association between obesity and gastroesophageal reflux and its complications]. 1925 Jul 82

Obesity is an established risk factor for esophageal adenocarcinoma, although the mechanism is unclear. A pathway from reflux to inflammation through metaplasia is the dominant hypothesis, and an added role relating to visceral adiposity and the metabolic syndrome has been mooted in Barrett's esophagus (BE) patients. Whether BE differs from gastroesophageal reflux disease (GERD) in obesity and metabolic syndrome profiles is unclear, and this was the focus of this study. Patients with proven BE or GERD were randomly selected from the unit data registry and invited to attend for metabolic syndrome screening, anthropometry studies including segmental body composition analysis, and laboratory tests including fasting lipids, insulin, and C-reactive protein. Metabolic syndrome was defined using the National Cholesterol Education Program (NCEP) and the International Diabetes Federation (IDF) criteria. One hundred and eighteen BE patients and 113 age- and sex-matched GERD controls were studied. The incidence of obesity (body mass index >30 kg/m(2)) was 36% and 38%, respectively, with the pattern of fat deposition predominantly central and an estimated trunk fat mass of 13 and 14 kg, respectively. Using the NCEP criteria, metabolic syndrome was significantly more common in the BE cohort (30% vs 20%, P < 0.05), but there was no significant difference using IDF criteria (42% vs 37%, P= 0.340). Central obesity and the metabolic syndrome are common in both Barrett's and GERD cohorts, but not significantly different, suggesting that central obesity and the metabolic syndrome does not per se impact on the development of BE in a reflux population. In BE, the importance of obesity and the metabolic syndrome in disease progression merits further study.
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PMID:Lack of differential pattern in central adiposity and metabolic syndrome in Barrett's esophagus and gastroesophageal reflux disease. 2035 43

Gastroesophageal reflux disease (GERD), previously uncommon in Asia, has now become an important disease in the region. Although much variability exists between studies, most endoscopy-based studies show a prevalence of erosive esophagitis of more than 10%. Symptom-based studies also show a prevalence of 6-10%. Two longitudinal follow-up studies on GERD symptoms have shown an increase with time, and several endoscopy-based time trend studies have also shown a significant increase in erosive reflux esophagitis. Studies on Barrett's esophagus have been confounded by the description of short (SSBE) and long segment (LSBE) Barrett's esophagus. Great variation in prevalence rates has been reported. SSBE vary from 0.1% to more than 20% while LSBE vary from 1-2%. Of the putative causative factors, obesity has been the most important. Many studies have linked GERD-esophagitis as well as occurrence of reflux symptoms with an increase in body mass index (BMI), obesity, especially visceral or central obesity, and metabolic syndrome. A decline in Helicobacter pylori infection with growing affluence in Asia has been broadly thought to result in healthier stomachs and a higher gastric acid output resulting in reflux disease. However, variable results have been obtained from association and H. pylori eradication studies.
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PMID:Gastroesophageal reflux disease in Asia: A historical perspective and present challenges. 2119 9

Excess body weight (EBW) is an independent risk factor for many human malignancies, including cancers throughout the gastrointestinal and hepatobiliary tract from the esophagus to the colorectum. The relative risk of gastrointestinal cancer in obese individuals is approximately 1.5-2.0 times that for normal weight individuals, with organ-specific and gender-specific differences for specific cancers. The association between EBW and risk of premalignant stages of gastrointestinal carcinogenesis, such as colorectal adenoma and Barrett esophagus, is similar, implying a role for EBW during the early stages of carcinogenesis that could be relevant to preventative strategies. EBW also impacts negatively on gastrointestinal cancer outcomes. The mechanistic basis of the association between EBW and carcinogenesis remains incompletely understood. Postulated mechanisms include increased insulin and insulin-like growth factor signaling and chronic inflammation (both linked to the metabolic syndrome), as well as signaling via adipokines, such as leptin. The role of obesity-related changes in the intestinal microbiome in gastrointestinal carcinogenesis deserves further attention. Whether weight loss leads to reduced future gastrointestinal and liver cancer risk has yet to be fully explored. There is some support for the idea that weight loss negatively regulates colorectal carcinogenesis. In addition, data suggest a reduction in risk of several cancers in the first 10 years after bariatric surgery.
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PMID:Excess body weight and obesity--the link with gastrointestinal and hepatobiliary cancer. 2138 10

Ethnic differences in the prevalence of gastro-oesophageal reflux disease (GORD) and its complications, including Barrett's oesophagus (BO), are well described in multiracial Asian patient populations. These findings together with familial aggregation of GORD symptoms and twin studies suggest the possibility of a genetic component to GORD. Nevertheless, environmental factors, e.g. Helicobacter pylori infection, abdominal adiposity and metabolic syndrome, could equally account for these differences. Indian (South Asian) race is a risk factor for Barrett' oesophagus. This may be related to the Caucasian genetic make-up of Indians as opposed to an Oriental one as is the case of most other Asians. The HLA-B07 gene commonly found in South Asian and Caucasian populations, but not Orientals, may confer an increased risk for BO. Nevertheless, the high prevalence of H. pylori in South Asians and the consequent atrophic gastritis and hypochlorhydria may partially ameliorate this genetic predisposition to BO. The higher prevalence of obesity and the metabolic syndrome amongst certain Asiatic races may also contribute to the observed increased risk for BO. Future research should target the search for GORD/BO genes, ethnic differences in parietal cell mass and hiatal hernia, H. pylori colonization factors (e.g. MUC1 and MUC2) and adhesion molecules (BabA). Racial differences in lifestyle factors, i.e. abdominal adiposity, consumption of fruit and vegetables as well as smoking, should all be investigated as potential causes for this interethnic variation in GORD and BO. Nature or nurture, the clues are teasing and tantalizing and illustrate the complex relationship between the genetic make-up of man and the environment.
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PMID:Barrett's oesophagus in Asians--are ethnic differences due to genes or the environment? 2181 67

Metagenomics which combines the power of genomics, bioinformatics, and systems biology, provide new access to the microbial world. Metagenomics permit the genetic analysis of complex microbial populations without requiring prior cultivation. Through the conceptual innovations in metagenomics and the improvements in DNA high-throughput sequencing and bioinformatics analysis technology, gastrointestinal microbiology has entered the metagenomics era and become a hot topic worldwide. Human microbiome research is underway, however, most studies in this area have focused on the composition and function of the intestinal microbiota and the relationship between intestinal microbiota and metabolic diseases (obesity, diabetes, metabolic syndrome, etc.) and intestinal disorders [inflammatory bowel disease, colorectal cancer, irritable bowel syndrome (IBS), etc.]. Few investigations on microbiota have been conducted within the upper gastrointestinal tract (esophagus, stomach and duodenum). The upper gastrointestinal microbiota is essential for several gastrointestinal illnesses, including esophagitis, Barrett's esophagus, and esophageal carcinoma, gastritis and gastric cancer, small intestinal bacterial overgrowth, IBS and celiac disease. However, the constitution and diversity of the microbiota in different sections of the upper gastrointestinal tract under health and various disease states, as well as the function of microbiota in the pathogenesis of various digestive diseases are still undefined. The current article provides an overview of the recent findings regarding the relationship between upper gastrointestinal microbiota and gastrointestinal diseases; and discusses the study limitations and future directions of upper gastrointestinal microbiota research.
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PMID:Upper gastrointestinal microbiota and digestive diseases. 2353 78

The incidence of oesophageal adenocarcinoma has increased dramatically in the developed world in the last half century. Over approximately the same period there has been an increase in the prevalence of obesity. Multiple epidemiological studies and meta-analyses have confirmed that obesity, especially abdominal, visceral obesity, is a risk factor for gastro-oesophageal reflux, Barrett's oesophagus and oesophageal adenocarcinoma. Although visceral obesity enhances gastro-oesophageal reflux, the available data also show that visceral obesity increases the risk of Barrett's oesophagus and adenocarcinoma via reflux-independent mechanisms. Several possible mechanisms could link obesity with the risk of oesophageal adenocarcinoma in addition to mechanical effects increasing reflux. These include reduced gastric Helicobacter pylori infection, altered intestinal microbiome, factors related to lifestyle, the metabolic syndrome and associated low-grade inflammation induced by obesity and the secretion of mediators by adipocytes which may directly influence the oesophageal epithelium. Of these adipocyte-derived mediators, increased leptin levels have been independently associated with progression to oesophageal adenocarcinoma and in laboratory studies leptin enhances malignant behaviours in cell lines. Adiponectin is also secreted by adipocytes and levels decline with obesity: decreased serum adiponectin levels are associated with malignant progression in Barrett's oesophagus and experimentally adiponectin exerts anticancer effects in Barrett's cell lines and inhibits growth factor signalling. At present there are no proven chemopreventative interventions that may reduce the incidence of obesity-associated oesophageal cancer: observational studies suggest that the combined use of a statin and aspirin or another cyclo-oxygenase inhibitor is associated with a significantly reduced cancer incidence in patients with Barrett's oesophagus.
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PMID:The role of obesity in oesophageal cancer development. 2536 84

In recent decades there has been a dramatic rise in the incidence of esophageal adenocarcinoma (EAC) in the developed world. Over approximately the same period there has also been an increase in the prevalence of obesity. Obesity, especially visceral obesity, is an important independent risk factor for the development of gastro-esophageal reflux disease, Barrett's esophagus and EAC. Although the simplest explanation is that this mediated by the mechanical effects of abdominal obesity promoting gastro-esophageal reflux, the epidemiological data suggest that the EAC-promoting effects are independent of reflux. Several, not mutually exclusive, mechanisms have been implicated, which may have different effects at various points along the reflux-Barrett's-cancer pathway. These mechanisms include a reduction in the prevalence of Helicobacter pylori infection enhancing gastric acidity and possibly appetite by increasing gastric ghrelin secretion, induction of both low-grade systemic inflammation by factors secreted by adipose tissue and the metabolic syndrome with insulin-resistance. Obesity is associated with enhanced secretion of leptin and decreased secretion of adiponectin from adipose tissue and both increased leptin and decreased adiponectin have been shown to be independent risk factors for progression to EAC. Leptin and adiponectin have a set of mutually antagonistic actions on Barrett's cells which appear to influence the progression of malignant behaviour. At present no drugs are of proven benefit to prevent obesity associated EAC. Roux-en-Y reconstruction is the preferred bariatric surgical option for weight loss in patients with reflux. Statins and aspirin may have chemopreventative effects and are indicated for their circulatory benefits.
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PMID:Pathophysiological mechanisms linking obesity and esophageal adenocarcinoma. 2540 Sep 97


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