Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the glycine-l-14C-cholic acid (14C-GCA) test, bile salt deconjugation and excretion were studied in 26 subjects with morbid exogenous obesity before and at selected intervals after jejuno-ileal bypass. In the preoperative group there was no malabsorption or intestinal bacterial deconjugation of the bile salts. In the immediate postoperative period (with relative sterilization of the bowel) there was only a trace of 14C in the breath, but the fecal 14C was highly elevated, indicating severe malabsorption without bacterial activity. In the 8 to 10 day postoperative period both the breath and fecal 14C content were highly elevated, indicating malabsorption and normal bacterial activity. Five to 8 months postoperatively both the breath and fecal 14C content showed only moderate elevation, indicating adaptation. It is suggested that the 14C-GCA test is useful in evaluating the adequacy of small bowel bypass procedures and also in following the adaptive response after the bypass. A significant increase in the breath and fecal 14C soon after surgery followed by rapid decrease suggests an adequate bypass and unusually fast adaptation. If the increase in the breath and fecal 14C soon after the bypass is only moderate, then that suggests an inadequate bypass.
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PMID:Studies on bile salt deconjugation following small bowel bypass procedures. 113 Aug 57

Use of tobacco, moderate to heavy alcohol ingestion, infrequent consumption of raw fruits and vegetables, and low income accounted for more [figure: see text] than 98% of the SCE rates among both African American and white men and for 99% of the excess incidence among African Americans compared to whites in a case-control study in three areas of the United States [14]. Thus, it is likely that declines in the prevalence of smoking and drinking, especially among men, and increased intake of fresh fruits and vegetables may have contributed to the downward incidence and mortality rate trends reported for SCE. In addition, it seems plausible that obesity, GERD, and possibly reductions in H. pylori prevalence have contributed to the upward trends in ACE rates. Reductions in smoking, improved diet, and reductions in H. pylori prevalence probably have contributed to the consistent reductions observed for NGA. Contributing factors are less clear for the rising incidence rates of GCA during the 1970s and 1980s. These incidence rates have not continued to rise in recent years.
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PMID:Epidemiologic trends in esophageal and gastric cancer in the United States. 1242 48

Genetic variations in the leptin receptor (LEPR) gene have been conceived to affect body weight in general populations. In this study, using the tests implemented in the statistical package QTDT, we evaluated association and/or linkage of the LEPR gene with obesity phenotypes in a large sample comprising 1,873 subjects from 405 Caucasian nuclear families. Obesity phenotypes tested include body mass index (BMI), fat mass, percentage fat mass (PFM), and lean mass, with the latter three measured by dual-energy X-ray absorptiometry (DXA). Three single nucleotide polymorphisms (SNPs), namely Lys109Arg (A/G), Lys656Asn (G/C), Pro1019Pro (G/A), in the LEPR gene were analyzed. Significant linkage disequilibrium (0.394 < or = |D'| < or = 0.688, P < 0.001) was observed between pairs of the three SNPs. No significant population stratification was found for any SNP/phenotype. In single-locus analyses, evidence of association was observed for Lys656Asn with lean mass (P = 0.002) and fat mass (P = 0.015). The contribution of this polymorphism to the phenotypic variation of lean mass and fat mass was 2.63% and 1.15%, respectively. Subjects carrying allele G at the Lys656Asn site had, on average, 3.16% higher lean mass and 2.71% higher fat mass than those without it. In the analyses for haplotypes defined by the three SNPs, significant associations were detected between haplotype GCA (P = 0.005) and lean mass. In addition, marginally significant evidence of association was observed for this haplotype with fat mass (P = 0.012). No statistically significant linkage was found, largely due to the limited power of the linkage approach to detect small genetic effects in our data sets. Our results suggest that the LEPR gene polymorphisms contribute to variation in obesity phenotypes.
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PMID:Tests of linkage and/or association of the LEPR gene polymorphisms with obesity phenotypes in Caucasian nuclear families. 1497 Mar 63

Patients with different forms of systemic vasculitis experience long-term morbidity and mortality caused by cardiovascular disease due to premature atherosclerosis. Epidemiologic reports of patients with GCA suggest that long-term mortality in this disease is not increased compared with the general population of the same age. The risk of a stroke, however, in particular in the vertebrobasilar territory, is increased. In addition, the occurrence of aortic aneurysmal disease and aortic dissection is also clearly increased in GCA. Mortality due to ischaemic heart disease, however, is not increased. In Takayasu arteritis accelerated atherosclerosis has been clearly documented both clinically and in autopsy reports. Atherosclerotic plaques in the carotid artery may be present in the carotid arteries especially in patients with a documented history of arteritis involving the carotid artery. It is controversial whether Kawasaki disease is associated with accelerated atherosclerosis. Young adults with a history of Kawasaki disease may have abnormal brachial artery reactivity, increased carotid IMT values and increased arterial stiffness. At autopsy examinations of KD patients, however, no significant atherosclerotic lesions are detected and carotid IMT measurements were found to be clearly different from those in young adults with familiar hypercholesterolaemia, suggesting that the remodeling process in KD is different from atherosclerosis. In ANCA-associated vasculitis (AAV), an increased mortality as a consequence of cardiovascular disease is well-documented. In these patients the relative risk for coronary heart disease is two- to fourfold that in control subjects. In addition, a similar relative risk has been found for stroke. Diabetes, hypertension, dyslipidemia, abdominal obesity (metabolic syndrome), impaired renal function, persistent proteinuria and increased production of C-reactive protein are common risk factors for premature atherosclerosis in patients with systemic vasculitis. Furthermore, cholesterol and its modifications play a pivotal role in the pathogenesis of accelerated atherosclerosis in vasculitis. The (preventive) therapy for accelerated atherosclerosis in systemic vasculitis is based on an aggressive approach against inflammation and against risk factors of premature atherosclerosis such as smoking, inactivity, obesity and unhealthy diet. In addition, patients should be treated with angiotensin-converting enzyme inhibitors and/or angiotensin receptor-1 blockers for hypertension and statins for dyslipidemia. Finally, low dose acetylsalicylic acid should be prescribed in patients with large vessel vasculitis, i.e., both in GCA and TA, who do not have contraindications for ASA.
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PMID:Cardiovascular disease due to accelerated atherosclerosis in systemic vasculitides. 2350 55

The developmental origins of health and disease hypothesis states that adverse early life exposures can have lasting, detrimental effects on lifelong health. Exposure to maternal cigarette smoking during pregnancy is associated with morbidity and mortality in offspring, including increased risks for miscarriage, stillbirth, low birth weight, preterm birth, asthma, obesity, altered neurobehavior, and other conditions. Maternal cigarette smoking during pregnancy interferes with placental growth and functioning, and it has been proposed that this may occur through the disruption of normal and necessary placental epigenetic patterns. Epigenome-wide association studies have identified a number of differentially methylated placental genes that are associated with maternal smoking during pregnancy, including RUNX3, PURA, GTF2H2, GCA, GPR135, and HKR1. The placental methylation status of RUNX3 and NR3C1 has also been linked to adverse infant outcomes, including preterm birth and low birth weight, respectively. Candidate gene analyses have also found maternal smoking-associated placental methylation differences in the NR3C1, CYP1A1, HTR2A, and HSD11B2 genes, as well as in the repetitive elements LINE-1 and AluYb8. The differential methylation patterns of several genes have been confirmed to also exhibit altered gene expression patterns, including CYP1A1, CYP19A1, NR3C1, and HTR2A. Placental methylation patterns associated with maternal smoking during pregnancy may be largely gene-specific and tissue-specific and, to a lesser degree, involve global changes. It is important for future research to investigate the mechanistic roles that these differentially methylated genes may play in mediating the association between maternal smoking during pregnancy and disease in later life, as well as to elucidate the potential influence of emerging tobacco product use during pregnancy, including the use of electronic cigarettes, on placental epigenetics.
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PMID:Altered placental DNA methylation patterns associated with maternal smoking: current perspectives. 2620 95