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)

Serum levels of protein 1 (P1), a Clara cell secretory protein, in 746 healthy subjects were measured and their correlations with different types of serum lipids and lipoproteins-that is, triglyceride (TG), total cholesterol (TCh), free cholesterol (FCh), high-density lipoprotein (HDL), low-density lipoprotein (LDL), and apoproteins (apo) A-I, A-II, and B-were examined. P1 serum levels were examined for their correlation with body mass index (BMI), and were compared for 47 obese, 70 normal, and 17 lean males. P1 serum levels in 69 patients with diabetes mellitus and 24 patients with atherosclerotic stenosis of the carotid artery or coronary artery were also compared to those in healthy control subjects. P1 showed a significant positive correlation with TG, TCh, FCh, apo A-I, apo A-II, apo B, and BMI (r = 0.93, 0.26, 0.42, 0.11, 0.35, 0.58, and 0.20, respectively; p < 0.0001 to 0.05), and an inverse correlation with HDL (r = -0.32; p < 0.01). P1 values in obese men (mean +/- SD: 139.2 +/- 98.2 micrograms/L) were significantly higher than those in normal (90.3 +/- 57.1) and lean ones (65.6 +/- 40.8) (p < 0.01). In both diabetic and atherosclerotic patients, P1 serum levels did not significantly differ from those in healthy subjects. From these results, we conclude the following: (1) the serum levels of P1 correlate significantly with those of lipids and lipoproteins; (2) P1 serum levels increase in the case of obesity.
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PMID:Clara cell protein correlation with hyperlipidemia. 879 90

The objective of this study was to determine whether phenolic constituents present in red wine and grape juice modulate plasma lipid and lipoprotein concentrations in healthy human subjects. All subjects consumed in random order 375 ml of red or white wine per day or 500 ml of two different grape juices (high and low phenols) per day for periods of 4 weeks separated by 2-week periods of abstention while continuing normal activity and food intake, and their normal lives in a community setting. The subjects were 24 healthy males aged 26-45 years screened by clinical examination and laboratory tests to exclude hypertension, diabetes mellitus, hyperlipidemia and obesity, among others. Fasting blood was collected at the beginning and end of each beverage schedule for analysis of lipids and lipoproteins. Changes in plasma lipids and lipoproteins in response to each beverage were measured to determine whether these were altered by red wine and grape juice phenolics independently of the effects of ethanol. Both grape juices had virtually no effect. Red and white wines raised plasma HDL-cholesterol and apo A-I and apo A-II concentrations as well as the apo A-I:apo B ratio to a similar extent. Red wine also raised plasma triglyceride and total cholesterol concentrations. Neither wine affected plasma apo B or apo (a) concentrations. The favourable effects of wines in modulating plasma lipid and lipoprotein concentrations are probably due to their alcohol content and cannot be reproduced by grape juices.
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PMID:Wine: does the colour count? 881 66

The aim of the present study was to examine the effect of variation at the apolipoprotein (apo) A-II gene locus on lipoprotein levels in visceral obesity. A total of 145 sedentary men, free from metabolic disorders requiring pharmacotherapy, were classified into two groups on the basis of their apo A-II-MspI genotype determined by the polymerase chain reaction: 1) 43 M1 carriers or M1M2, including two M1M1 homozygotes and 41 M1M2 heterozygotes, and 2) 102 M2M2 homozygotes for the presence of a MspI restriction site. The two genotypic groups did not differ for body mass index (BMI, expressed in kg/m2), body fat mass, visceral adipose tissue (AT) accumulation, as well as for insulin, glucose and free fatty acids levels measured in the fasting state and in response to an oral glucose tolerance test. In addition, 65 and 63% of M1 carriers had plasma HDL2 cholesterol levels and a HDL2/HDL3 cholesterol ratio below the 50th percentile of their distributions compared with 45%(P < 0.05) and 46%(P = 0.06), respectively, in M2M2 homozygotes. When subjects were further divided on the basis of visceral AT accumulation (below and above a value of 130 cm2), M1 carriers with low levels of visceral AT were characterized by high plasma HDL cholesterol and HDL2 cholesterol concentrations as well as by a higher HDL2/HDL3 ratio, compared with M1 carriers with high levels of visceral AT (> 130 cm2), or with M2M2 homozygotes with either a high or a low accumulation of visceral AT. Furthermore, M1 carriers with high levels of visceral AT showed a trend for lower plasma HDL2 cholesterol levels and were characterized by a significantly lower HDL2/HDL3 cholesterol ratio compared with the other three groups. No difference in HDL and HDL2 cholesterol levels and in the HDL2/HDL3 cholesterol ratio was noted when M2 homozygotes with lower versus higher levels of visceral AT were compared. The contribution of hyperinsulinemia was also examined by dividing subjects on the basis of the 50th percentile of the integrated insulin response to an oral glucose challenge. Significantly lower plasma HDL2 cholesterol levels and a reduced HDL2/HDL3 cholesterol ratio were noted among M1 carriers with high plasma insulin responses compared with M1 carriers with low insulin responses. Among M2M2 homozygotes, no difference was noted in plasma HDL cholesterol and in HDL2 cholesterol concentrations between men with low versus high insulin responses to the oral glucose load. These results suggest that the apo A-II-MspI polymorphism could modulate plasma HDL cholesterol levels among visceral obese, insulin-resistant men.
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PMID:The MspI polymorphism of the apolipoprotein A-II gene as a modulator of the dyslipidemic state found in visceral obesity. 905 Jul 75

Fatty liver has prevailed by 14% in the healthy population of this country. The factors contributing genesis of fatty liver were gender (male), obesity, high alcohol consumption, glucose intolerance and hypertriglyceridemia. And hypertriglyceridemia seems to be the common underlying factor to all other causes. The mechanism for accumulation of triglycerides in the liver can be explained at least by increased HTGL activities and elevated apo A-II levels, a postulated co-factor of HTGL. An hypertriglyceridemic patients with fatty liver had the insulin resistance.
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PMID:Hypertriglyceridemia and fatty liver: clinical diagnosis of fatty liver and lipoprotein profiles in hypertriglyceridemic patients with fatty liver. 922 32

Native Americans are predisposed to insulin resistance and associated cardiovascular risk. Therefore, we studied whether BMI (body mass index) in a population of Cherokee children and adolescents is associated with HDL-C (HDL cholesterol), and the HDL particles Lp (lipoprotein) A-I and LpA-I:A-II. Subjects were grouped by BMI Z score quartiles within three gender-specific age brackets (5-9, 10-14, and 15-19 y) to examine for trends in lipoprotein and HOMA-IR (homeostasis index insulin resistance) values associated with adiposity and age. HDL-C decreased by BMI Z score quartiles in all three age groups for both genders. HDL-C, LpA-I, and LpA-I:A-II decreased with age in boys but not girls. Log HOMA-IR increased by BMI Z score quartiles in all three age groups for both genders. Linear regression modeling showed BMI Z score, triglyceride, and age to be associated with HDL-C, whereas HOMA-IR was associated with LpA-I:A-II but not with HDL-C or LpA-I. When waist circumference was substituted for BMI Z score in the same models, it was associated with HDL-C and both lipoprotein particles. In conclusion, adiposity is more associated with HDL-C lowering than with declines in the lipoprotein particles. HOMA-IR is less associated with HDL-C but may selectively influence LpA-I:A-II. Greater decreases in HDL-C, LpA-I, and LpA-I:A-II with age in boys is attributed to gender-specific hormonal changes. The early onset of HDL lowering in these Native American children and adolescents, particularly boys, warrants intervention strategies to prevent obesity and associated cardiovascular risk.
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PMID:Body mass index and high-density lipoproteins in Cherokee Indian children and adolescents. 1614 59

The renin angiotensin system (RAS; most well-known for its critical roles in the regulation of cardiovascular function and hydromineral balance) has regained the spotlight for its potential roles in various aspects of the metabolic syndrome. It may serve as a causal link among obesity and several co-morbidities. Drugs that reduce the synthesis or action of angiotensin-II (A-II; the primary effector peptide of the RAS) have been used to treat hypertension for decades and, more recently, clinical trials have determined the utility of these pharmacological agents to prevent insulin resistance. Moreover, there is evidence that the RAS contributes to body weight regulation by acting in various tissues. This review summarizes what is known of the actions of the RAS in the brain and throughout the body to influence various metabolic disorders. Special emphasis is given to the role of the RAS in body weight regulation. The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009.
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PMID:The renin angiotensin system and the metabolic syndrome. 2038 10

Dysfunction of high-density lipoprotein (HDL) particles that even become proinflammatory or lose atheroprotective properties is known through analyses of HDL isolated from diabetic subjects. Recently, high concentrations of HDL or apolipoprotein (apo) A-I in individuals with diabetes or coronary heart disease were found to reveal dysfunction in some population-based studies. Such dysfunction of HDL and its apos A-I, A-II, and C-III has been observed in a general population for the first time among Turkish adults. Functional defectiveness manifested itself by unexpected correlations with inflammatory biomarkers and, in long-term follow-up, by lack of protection against diabetes and coronary heart disease, accounting for the excess incidences in Turks. Female sex was more pronouncedly affected by this process that presumably exists in other ethnicities in South Asia, East Europe, and the Middle East. In contradistinction, in Western and East Asian population, only individuals with glucose intolerance or those at risk for cardiometabolic disease are considered to be or were documented in a review of clinical trials to have been affected by impaired function of HDL. High-density lipoprotein dysfunctionality is closely linked to obesity and low-grade inflammation yet seems to act partly independently of them. Cigarette smoking in overweight women with low-grade inflammation appears to offer limited protection against cardiometabolic risk. The great impact in public health of the dysfunction of protective serum proteins requires individual clinical recognition, appropriate preventive measures, and delineation of management, including with anti-inflammatory drugs.
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PMID:Low-grade inflammation, and dysfunction of high-density lipoprotein and its apolipoproteins as a major driver of cardiometabolic risk. 2058 Jul 81

Obesity is an established risk factor for pancreatic ductal adenocarcinoma (PDA). Despite recent identification of metabolic alterations in this lethal malignancy, the metabolic dependencies of obesity-associated PDA remain unknown. Here we show that obesity-driven PDA exhibits accelerated growth and a striking transcriptional enrichment for pathways regulating nitrogen metabolism. We find that the mitochondrial form of arginase (ARG2), which hydrolyzes arginine into ornithine and urea, is induced upon obesity, and silencing or loss of ARG2 markedly suppresses PDA. In vivo infusion of 15N-glutamine in obese mouse models of PDA demonstrates enhanced nitrogen flux into the urea cycle and infusion of 15N-arginine shows that Arg2 loss causes significant ammonia accumulation that results from the shunting of arginine catabolism into alternative nitrogen repositories. Furthermore, analysis of PDA patient tumors indicates that ARG2 levels correlate with body mass index (BMI). The specific dependency of PDA on ARG2 rather than the principal hepatic enzyme ARG1 opens a therapeutic window for obesity-associated pancreatic cancer.Obesity is an established risk factor for pancreatic ductal adenocarcinoma (PDA). Here the authors show that obesity induces the expression of the mitochondrial form of arginase ARG2 in PDA and that ARG2 silencing or loss results in ammonia accumulation and suppression of obesity-driven PDA tumor growth.
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PMID:Critical role for arginase 2 in obesity-associated pancreatic cancer. 2880 55


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