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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To identify the factors responsible for increases in serum uric acid (SUA), a cohort of 1,312 hyperuricemia-free (SUA < 7.5 mg/dL and no medication for hyperuricemia or hypertension) male office workers aged 30 to 52 years were examined annually for 8 successive years. Subjects who were found to have become hyperuricemic (SUA > or = 7.5 mg/dL) or who started medication for hyperuricemia during repeat surveys were defined as incidence cases. The SUA trend was also examined in 1,062 subjects for whom 9 consecutive SUA values were available and who did not start medication for hyperuricemia or hypertension during the observation period. Multivariate analyses, excluding the baseline SUA level as a factor in the Cox proportional-hazards model, indicated that age (negative), body mass index (BMI), log triglyceride level, hemoglobin A(1c) (HbA(1c)) level (negative), white blood cell count, and alcohol intake at study entry were significantly associated with the incidence of hyperuricemia. In the model including the baseline SUA level, baseline SUA level was the strongest factor for the incidence of hyperuricemia, and BMI, white blood cell count, and alcohol intake at study entry remained as independent factors. From stepwise linear regression analyses for SUA slope, excluding the baseline SUA level as a factor, significant correlates with SUA slope were, in order of their relative importance, slopes of BMI, HbA(1c) (negative), blood urea nitrogen, log triglyceride level, total protein, and baseline levels of hematocrit (negative), white blood cells, and HbA(1c) (negative). In stepwise linear regression analyses, including the baseline SUA level as a factor, SUA level (negative) and alcohol intake at study entry emerged as significant factors for SUA slope. The cumulative percentage of variation for SUA slope was 25.6%. In conclusion, obesity, alcohol intake, and multimetabolic disorders were determined to be independent predictors for the development of hyperuricemia. In addition, the white blood cell level may be a contributory factor.
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PMID:Predictors for development of hyperuricemia: an 8-year longitudinal study in middle-aged Japanese men. 1139 34

Vegetarians have lower blood pressure and lower cardiovascular mortality. Vegetarian diets may have lower cardiovascular risks through positive influence on endothelium-dependent relaxation and related functions. The objectives of this study were to assess the differences of vascular dilatory functions between middle-aged vegetarians and sex and age-matched omnivores before they develop any clinical manifestations of atherosclerosis. Twenty healthy vegetarians over the age of 50 and 20 healthy omnivores over the age of 50 were recruited for this study. Subjects with known risk factors for atherosclerosis such as hypertension, diabetes, obesity, hypercholesteremia, cigarette smoking, family history of vascular diseases, or taking any regular medication were excluded. Medical history, body weight, height, and duration of vegetarian diet were recorded. Baseline CBC, urinalysis and biochemical data such as fasting blood glucose, thyroid function, blood urea nitrogen, creatinine, serum electrolytes (sodium, potassium, chloride, calcium and magnesium), lipid profiles [total cholesterol, triglycerides, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol] were obtained after a 14 h fast. Blood pressures and heart rate were recorded in supine position. Vascular dilatory functions, both flow-mediated (endothelium-dependent) and nitroglycerin-induced (endothelium-independent), were evaluated by using a non-invasive ultrasonographic method. The results show that there were no significant differences in the baseline characteristic between the vegetarians and the omnivores. There were also no significant differences in serum glucose, lipid profiles and thyroid function between these two groups. However, vasodilatation responses (both flow-mediated and nitroglycerin-induced) were significantly better in the vegetarian group and the degree of vasodilatation appeared to be correlated with years on vegetarian diets. Our findings suggest that vegetarian diets, by themselves, have a direct beneficial effect on vascular endothelial and smooth muscle function and may help to account for the lower incidence of atherosclerosis and cardiovascular mortality.
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PMID:Vascular dilatory functions of ovo-lactovegetarians compared with omnivores. 1150 Jan 98

Acetyl-CoA carboxylase catalyzes the first committed step in the synthesis of long chain fatty acids. In this study, we observed that treatment of 3T3-L1 cells with biotin chloroacetylated at the 1' nitrogen reduced the enzymatic activity of cytosolic acetyl-CoA carboxylase and concomitantly inhibited the differentiation of 3T3-L1 cells in a dose-dependent manner. Treatment with chloroacetylated biotin blocked the induction of PPARgamma, STAT1, and STAT5A expression that normally occurs with adipogenesis. Moreover, addition of chloroacetylated biotin inhibited lipid accumulation, as judged by Oil Red O staining. Our results support recent studies that indicate that acetyl-CoA carboxylase may be a suitable target for an anti-obesity therapeutic.
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PMID:A biotin analog inhibits acetyl-CoA carboxylase activity and adipogenesis. 1190 24

Increased release and action of proinflammatory cytokines are thought to be responsible for the occurrence of insulin resistance in inflammatory and metabolic diseases including obesity-linked diabetes. Recent work has identified several signal transduction pathways activated by cytokines which can impede on insulin receptor signaling in skeletal muscle, liver, and adipose cells. A majority of these complex and interrelated pathways appear to converge at the level of insulin receptor substrate-1 by promoting its serine phosphorylation in order to mediate heterologous inhibition of insulin receptor substrate-1 signaling which, in turn, counterregulates the insulin response. Other possible mechanisms of insulin resistance in cytokine-treated cells include nitration of insulin receptor substrate-1 tyrosine residues by nitric oxide-derived reactive nitrogen species as well as direct interference with insulin signaling molecules further downstream such as protein kinase B/Akt. A detailed knowledge of the complex network of intracellular signaling pathways triggered by cytokines may be instrumental in the development of new approaches to prevent insulin resistance in acute and chronic inflammatory settings.
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PMID:Mediators of cytokine-induced insulin resistance in obesity and other inflammatory settings. 1210 72

Oxidant formation in the vasculature contributes to vascular disease and dysfunction associated with obesity. In contrast, exercise-dependent production of oxidants may stimulate adaptive responses that protect against the development of such diseases. In this review, we discuss current concepts in the biology of reactive oxygen and nitrogen species and how their function is modulated in the context of vascular disease, obesity, and aerobic exercise.
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PMID:Obesity, aerobic exercise, and vascular disease: the role of oxidant stress. 1222 46

Large prospective epidemiologic studies have shown that long-term use of oral contraceptives containing estrogen induce an increase in blood pressure and sharply increase the risk of hypertension. Susceptibility to the hypertensive effects of oral contraceptives is heightened where risk factors such as age, family history of hypertension, preexisting or occult renal disease, parity and obesity exist. Hypertension among pill users usually develops within the first 6 months of usage and occasionally is delayed for as long as 6 years. Anitihypertensive therapy is seldom needed as the hypertension that developes is generally mild and uncomplicated, and rapidly reverses when the pills are discontinued. However, a small percentage of patients develop severe, even life-threatening hypertension and the hypertensive effects are felt long after the pills are discontinued. Cases of malignant hypertension and irreversible renal failure requiring maintenance hemodialysis, bilateral nephrectomy, and renal transplantation have occurred following administration of oral contraceptive pills. The mechanism by which oral pills induce hypertension in susceptible women is not known and needs further research. Before oral contraceptives are prescribed, physicians should take a careful history and perform a detailed physicial examination with special attention to the cardiovascular system. Multiple blood pressure measurements should be made and routine laboratory studies including urinalysis, blood urea and nitrogen and serum creatinine should be performed. It is preferable to start with a relatively low (50 mcg) estrogenic content preparation. Patients who develop hypertension (diastolic pressure, 90 mm Hg) on oral contraceptives should stop taking the pills immediately, and should be considered to have estrogen-induced hypertension. They should never again receive estrogen-containing oral pills, although they can try pills containing only progestogen. There is no contraindication to pregnancy in these patients, as most women who become hypertensive on oral pills go on to have normotensive pregnancies. Pregnancy in women who are susceptible to essential hypertension however should be treated as high risk.
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PMID:Hypertension and oral contraceptives. 1226 83

To investigate the relationship between obesity, small-solute clearances, and nutrition in continuous peritoneal dialysis (CPD), we compared clearances and nutrition indices between 270 obese and 502 normal-weight CPD patients. Degree of obesity was classified by the ratio of body weight (W) to desired weight (DW) at the first clearance study. The DWs were obtained from the tables of the Metropolitan Life Insurance Company, assuming a medium skeletal frame. The obese patients (group I) had W/DW > 1.2 (1.38 +/- 0.17), and the normal-weight patients (group II) had 0.9 < or = W/DW < or = 1.2 (1.05 +/- 0.08). Nutrition indices derived from urea nitrogen and creatinine excretion were normalized by both W and DW. The following variables differed between group I (first value) and group II: sex (women: 48.2% vs. 33.9%), W (87.6 +/- 14.4 kg vs. 68.2 +/- 8.7 kg), body surface area (1.95 +/- 0.22 m2 vs. 1.77 +/- 0.16 m2), body water by method of Watson (41.2 +/- 7.7 L vs. 36.3 +/- 5.5 L), body mass index (31.8 +/- 3.9 vs 24.3 +/- 2.0), protein nitrogen appearance (PNA: 62.9 +/- 17.6 kg in 24 h vs. 57.7 +/- 15.7 kg in 24 h), PNA normalized to DW (1.08 +/- 0.29 g/kg in 24 h vs. 0.96 +/- 0.26 g/kg in 24 h), creatinine excretion (CrEx: 1111 +/- 396 mg in 24 h vs. 991 +/- 348 mg in 24 h), CrEx/W (12.6 +/- 3.7 g/kg in 24 h vs. 15.4 +/- 4.5 g/kg in 24 h), CrEx/DW (17.3 +/- 5.3 g/kg in 24 h vs. 15.1 +/- 4.8 g/kg in 24 h), lean body mass (LBM: 49.3 +/- 13.8 kg vs. 43.6 +/- 11.9 kg), LBM/W (0.56 +/- 0.12 vs. 0.64 +/- 0.15), and LBM/DW (0.77 +/- 0.18 vs 0.67 +/- 0.16), all at p < or = 0.034. Marginal differences (0.10 > p > 0.05) were found in the diabetes prevalence (53.0% vs. 40.8%), height (165.9 +/- 11.7 cm vs. 167.4 +/- 9.8 cm), and serum albumin (3.64 +/- 0.55 g/dL vs. 3.53 +/- 0.62 g/dL). No differences were found in age, duration of CPD until the first clearance study, percent of subjects with anuria, Kt/V urea, creatinine clearance, blood urea nitrogen, serum creatinine, and PNA normalized to W. Obese CPD patients tend to have better nutrition indices than do normal-weight CPD patients with similar small-solute clearances. In obese subjects, normalization by W creates inappropriately low values for nutrition indices derived from urea nitrogen and creatinine excretion. Normalization of those indices by DW appears preferable.
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PMID:Small solute clearances and nutrition indices in obese patients on continuous peritoneal dialysis. 1240 84

A total of 28 patients with stage II hypertensive disease (HD) were examined, their age ranging between 32 to 64 years. Of these, 17 subjects were diagnosed as having had alimentary obesity. The control group comprised 11 subjects with normal level of arterial pressure and body mass. Studied in the above patients were blood serum content of nitrogen oxide by determining levels of its stable metabolites NO2- and NO3- anions. HD patients presenting with normal body weight and those with obesity demonstrated significantly lower blood serum levels of anions NO2- and NO3- as compared to healthy subjects. In HD patients, obesity is accompanied by a more significant reduction in blood serum levels of NO2- and NO3-, which fact might be caused by inhibition of nitratereductase.
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PMID:[Endothelial dysfunction in obese hypertensive patients]. 1271 5

The study population in this report by Lin et al. was ob/ob mice that have an inherited genetic deficiency of the appetite-suppressing hormone leptin. These mice develop hyperinsulinemia, insulin resistance, and fatty livers. Compared with their lean littermates and wild-type C57BL-6 mice, ob/ob mice have hepatomegaly. In this study, the authors compared three different groups of adult mice (aged 8-10 wk), including male ob/ob C57BL-6 mice, their lean littermates, and wild-type C57BL-6 mice of the same age and sex. The primary purpose of this study was to test the efficacy of metformin for treatment of fatty liver disease in obese, ob/ob mice that develop hyperinsulinemia or insulin resistance and fatty livers. Metformin therapy was found to eliminate fatty liver disease in this model. The potential mechanisms of the action of metformin were the inhibition of hepatic tumor necrosis factor (TNF)alpha and several TNF-inducible responses, which are likely to promote hepatic steatosis and necrosis. In these experiments, ob/ob mice were divided into three treatment groups. Group 1 consisted of eight mice that were treated with metformin and permitted to consume a nutritiously replete liquid mouse diet ad libitum. Mice in group 2 (n = 8) did not receive metformin but were pair-fed the same volume of liquid diet that the mice in the metformin-treated group had consumed on the previous day. Obese ob/ob mice in group 3 (n = 4) and lean mice received no metformin, as with the mice in group 2, but were permitted to consume the liquid diet ad libitum. Liquid diet was given to facilitate accurate daily comparison of food intake among the various treatment groups. All mice were weighed at the beginning of the study and weekly thereafter until killed and then sera, fat, and liver tissues were collected. Tissues were either fixed in buffered formalin and processed from the deceased mice for histology or snap frozen in liquid nitrogen and stored until RNA and proteins were isolated. The feeding protocol was repeated with a second group of 18 ob/ob mice. After 4 wk, hepatocytes were obtained by in situ liver perfusion with collagenase and assayed for cellular adenosine triphosphate (ATP) content. In each experiment, hepatocytes isolated from 3 mice from each treatment group were suspended in a medium and pooled for subsequent analysis to evaluate cell viability, determine the number of obtained cells, and to assay cellular ATP content. These experiments were repeated using another 3 mice from each treatment group, so that analysis of hepatocytes took place from six ob/ob mice in each feeding group.Hepatic steatosis was decreased significantly only in the metformin-treated group. The authors found that metformin's beneficial effect on the fatty liver disease of mice was not due to its ability to constrain hyperphagia, nor due to decreased caloric ingestion, because the daily caloric intakes of the metformin-treated mice and the pair-fed control mice were virtually identical. These caloric intakes were consistently approximately 20% less than that of another obese control group that was permitted to consume diet ad libitum. The authors also observed no significant effect of metformin on serum glucose concentration from fed, ob/ob mice. Metformin is known to reduce hyperinsulinemia by about 40% in both of these obese hyperinsulinemic and insulin-resistant rodent strains. In conclusion, Lin et al. documented that metformin improves fatty liver disease and reverses hepatomegaly, steatosis, and aminotransferase abnormalities in mice. In addition, the authors suggest that metformin might inhibit dieting-induced redistribution of lipid from the liver to adipose tissue depots. In summary, this study identifies a potential treatment for fatty liver disease in humans.
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PMID:Current biochemical studies of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis suggest a new therapeutic approach. 1449 93

Most reports of outcome following obesity surgery report weight and co-morbidity changes only. We studied body composition changes in 17 adult patients (15 F, 2 M, age 43+/-2 years, range 28-58 years), with morbid obesity (initial BMI 40.4+/-4.9 kg/m(2), range 34.7-48.8) who were managed surgically by laparoscopically inserting an adjustable gastric band. Body composition was studied before and after surgery (mean interval of 909+/-51 days, range 441-1155 days) using anthropometry (abdominal circumference, AC, sum of four skinfold thicknesses, SFSUM), whole-body potassium counting (TBK), in vivo neutron activation analysis total body nitrogen (TBProtein) and whole-body dual-energy ray absorptiometry (total body percent fat TBF%, and total body bone mineral density TBBMD). Weight loss over the study period was 23.4+/-2.5 kg. ( p<0.0003) with an AC reduction of 20.0+/-4.5 cm ( p<0.008). Both SFSUM and TBF% were significantly reduced ( p<0.02 and p<0.0005 respectively). Both TBK and TBProtein after normalization for sex and height, were significantly ( p<0.0054 and p<0.001 respectively) reduced, but the ratio of loss of fat mass to fat-free mass, at 4.4:1 was usual for weight loss, and there was no significant changes in the ratio of potassium to protein. TBBMD, after normalization relative to a young same sex adult, was not significantly changed. In this group of patients, most of the substantial weight loss over a 2- to 3-year period was due to loss of fat mass, with relatively less reduction in the components of fat-free mass. Adjustable laparoscopic gastric banding induces fat loss without significant other deleterious effects on body composition.
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PMID:Body composition changes following laparoscopic gastric banding for morbid obesity. 1461 90


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