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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 14 December 1989 and 17 December 1993, 43 patients undergoing kidney transplantation alone at the Children's Hospital of Pittsburgh received FK506 as the primary immunosuppressive agent. The mean recipient age was 10.2 +/- 4.8 years (range 0.7-17.4 years), with 7 (16%) children under 5 years of age and 2 (5%) under 2 years of age. Fifteen (35%) children underwent retransplantation, and 5 (12%) had a panel-reactive antibody level greater than 40%. Twenty-two (51%) transplants were with cadaveric donors and 21 (49%) were with living donors. The mean follow-up was 25 +/- 14 months; there were no deaths; 1- and 3-year actuarial graft survival was 98% and 85%. The mean serum creatinine and blood urea nitrogen were 1.2 +/- 0.6 mg/dl and 26 +/- 11 mg/dl; the calculated creatinine clearance was 75 +/- 23 ml/min per 1.73 m2. Twenty-four (62%) patients have been successfully withdrawn from steroids and 24 (62%) require no anti-hypertensive medication. Improved growth was seen, particularly in pre-adolescent children off steroids. Between 28 July 1990 and 2 December 1993, 24 children were referred for rescue therapy with FK506, 14.6 +/- 16.4 months (range 1.1-53.2 months) after transplantation. Nineteen (79%) were referred because of resistant rejection; 4 (17%) were referred because of proteinuria; 1 (4%) was switched because of steroid-related obesity. There were no deaths; 1- and 2-year graft survival was 75% and 68%; 17 (71%) patients were successfully rescued, including 1 of 2 patients who arrived on dialysis; 4 (24%) of the successfully rescued patients were weaned off steroids.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:FK506 in pediatric kidney transplantation--primary and rescue experience. 749 86

The existence of a direct relationship between body mass and arterial pressure is well recognized; however, the effect of obesity on known target organs of hypertension is not clearly understood. We undertook the present studies to assess the influence of obesity on renal function and urinary albumin excretion in 40 normotensive subjects and 80 nevertreated hypertensive patients matched for age, sex, arterial pressure level, and known duration of hypertension in whom an oral glucose tolerance test was within normal limits. Glomerular filtration rate and effective renal plasma flow (expressed as absolute values or values normalized for height) were increased in overweight compared with lean subjects whether normotensive or hypertensive. Glomerular filtration rate was positively correlated with protein intake (as assessed from urinary excretion of urea) and fasting serum insulin level. Urinary excretion of albumin but not IgG and beta 2 microglobulin was higher in hypertensive patients compared with normotensive subjects. The overweight condition clearly enhanced the influence of arterial pressure on albuminuria; in fact, a steeper regression line between albumin excretion rate and arterial pressure was found in overweight compared with lean subjects. These results indicate that the overweight condition is associated with renal hyperfiltration and hyperperfusion, irrespective of the presence of hypertension, and that obesity magnifies the effect of hypertension on albuminuria, thus raising the possibility of an increased susceptibility of obese hypertensive patients to the development of renal damage.
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PMID:Combined renal effects of overweight and hypertension. 755 20

The effect of long-term voluntary fasting on hematologic variables, biochemical profiles, and liver histologic findings was assessed in 15 obese cats (> 40% overweight). Clinical signs and laboratory results consistent with hepatic lipidosis were observed in 12 of 15 cats after 5 to 7 weeks of fasting, and were associated with 30 to 35% reduction of initial body weight. Histologic examination of successive liver biopsy specimens revealed that obesity was not associated with liver parenchymal lipid accumulation, but that fasting resulted in lipidosis in all 15 cats. The long-term fast was associated with an early (after 2 to 4 weeks of fasting) and significant (P < 0.05) reduction in serum urea, glucose, and albumin concentrations, and RBC mass. Fasting for 5 to 7 weeks was associated with a significant (P < 0.05) increase in hepatic-associated enzyme activities and in total and direct serum bilirubin concentrations. Significant (P < 0.05) changes in serum alkaline phosphatase developed as early as 3 weeks before the onset of hyperbilirubinemia. Except for development of hepatic lipidosis, cats appeared to tolerate the fast without other adverse effect. This study confirmed that long-term fasting may induce clinical hepatic lipidosis in obese cats. Fasting appears to induce a syndrome of hepatic lipidosis that is indistinguishable from feline idiopathic hepatic lipidosis and may be an appropriate model to study the pathophysiologic features and treatment of hepatic lipidosis.
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PMID:Experimental induction of hepatic lipidosis in cats. 780 98

The study of intestinal and hepatic uptake of amino acids by obese rats has been the main objective of this work. The obese animals used were either from genetic or from nutritional basis. In fed state, the intestinal release of amino acids was higher in obese animals than in lean ones (around the double values), but nutritionally and genetically obese rat showed a related pattern, specially for the case of alanine (increased release in relation to controls by a factor of 10). The higher alanine release by intestine is not reversed by 12-h food deprivation. The hepatic availability was also higher in obesity models than in lean animals (increases over 30%). However, the hepatic uptake was increased in genetically obese animals (more than 35%) and decreased in nutritionally obese animals (more than 40%), especially due to alanine uptake (2419, 1100 and 3794 nmols/min/g protein in lean, Diet-ob and fa/fa animals respectively). In obese animals the food deprivation tended to normalize the hepatic uptake of alanine. The differences in alanine uptake between both types of obesity may reflect the differences of urea synthesis.
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PMID:Splanchnic amino acid pattern in genetic and dietary obesity in the rat. 785 38

Glutamate-induced obesity of Wistar-rats is known to develop under normophagic and normoinsulinemic conditions, although hyperphagia and hyperinsulinemia are common to obese individuals. Rats of this obesity model show retarded growth, reduced mass of some organs, carcass and whole body as well as an extraordinary high fat content, whereas protein content is reduced. In this study, nitrogen (N) balance, urinary excretion of urea-N, ammonia-N, creatine-N and alpha-amino acid-N and plasma free fatty acid concentration of growing, glutamate-induced obese rats were determined. The main results were independent of frame of reference (mmol N/kg body mass; mmol N/kg0.75 metabolic body mass; N in % of nitrogen intake): Nitrogen intake, urinary excretion of alpha-amino acids and nitrogen excretion in faeces were equal between lean and obese rats. Nitrogen excretion in urine was elevated in obese rats, mainly resulting from increased amounts of urea and ammonia. Nitrogen balance was positive in both groups, but reduced in obese rats. These data point to normal digestion of food proteins, but an unusual high oxidative desamination rate of the absorbed amino acids in obese rats. Taking into account the various hormonal and nerval alterations in glutamate-induced obese rats, resulting e.g. in increased hepatic insulin concentration, the retained amino acid carbon should be channelled into hepatic fatty acid synthesis. Really, unfasted and overnight fasted obese rats showed elevated plasma free fatty acid concentrations. Channeling of amino acids into lipogenesis may explain the low muscle mass and striking fat accumulation--despite normophagia and peripheral normoinsulinemia--of growing, glutamate-induced obese Wistar-rats.
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PMID:Reduced, positive nitrogen balance and elevated plasma free fatty acid concentration in growing, glutamate-induced obese rats. 790 47

A purified moderately high fat diet has been developed to examine diet-induced obesity in rats. Male Sprague-Dawley rats were fed this or an AIN-76A diet for 15 wk and energy metabolism indices were monitored. Food intake, body weight and water balance indices were recorded on a weekly or daily basis. Over the 15-wk period, rats fed the experimental diet diverged into two groups differing in the rate of body weight gain. Animals were labeled as "gainers" or "resisters" depending on their susceptibility to obesity. Following the dietary period, rats were decapitated and trunk blood was collected for glucose and insulin measurements. Gainers consumed slightly more energy than resisters over the experimental period (P < 0.05), but due to greater fecal energy loss, absorbed energy did not differ. Hence gainers became obese without significantly altered energy retention. Urinary creatinine, urea nitrogen and water balance were not different between the groups and consequently could not explain body weight differences. Further, gainers had significantly greater plasma glucose concentration than controls, indicating a potential for these animals to become diabetic. Results suggest metabolic differences must account for the divergence in weight gain observed in the two groups. The dietary model characterized in this study should provide a useful tool to study diet-induced obesity and to determine its underlying mechanism.
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PMID:Development and characterization of a purified diet to identify obesity-susceptible and resistant rat populations. 796 1

The water balance in Wistar, Zucker obese and Zucker lean rats, aged 60 days, was measured by determining the amount of water they drank, that contained in the solid food eaten, the water lost through urine and droppings, the net water accrued (estimated from the composition of the body and the daily increase in body weight), the measurement of the water vapour lost and the calculation of metabolic water production by means of the measurement of oxygen consumption, carbon dioxide production and protein oxidation in a 24 hr period. 1. Despite widely different body weights, all three groups of animals accrued a similar proportion of their daily water budget (4.3-4.9%, i.e. 1.2-1.4% of the total rat water mass). 2. Wistar and Zucker obese rats had a similar daily water budget despite very different body weights, lean Zucker rats had lower water budgets. 3. Obese and lean Zucker rats produced a more concentrated, and excreted much less urine (the highest urea concentration was found in obese rats) than Wistar rats. 4. The water lost in the droppings was in the same range as that in urine for obese rats, slightly less for lean Zucker rats and much less in Wistar rats. Obese rats produced a higher amount of stool with respect to the amount of food eaten than the lean animals studied. 5. The contribution of metabolic water to the daily water budget was a 23.6% for Zucker obese, 22.5% for Zucker lean and 15.9% for Wistar rats.
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PMID:Water balance in Zucker obese rats. 809 86

Total blood and plasma free amino acids and plasma urea levels were studied in fed and 24 h fasted Zucker rats. In fed animals there were no differences between obese and lean rats in the overall essential and non essential blood free amino acids. However, starvation reduced blood amino acid levels in the obese animals compared to the lean group, mainly due to changes in the plasma compartment. The reduction of available amino acids from plasma in the obese rats during starvation affected most of the amino acids, including the branched chain amino acids, which showed higher levels in the fed situation than in lean rats. Of particular interest is the opposite response to starvation in lean and obese Zucker rats concerning the plasma ratio of tryptophan (Trp) to the large neutral amino acids (LNAA) which could be implicated in the alteration of food intake and energy expenditure characteristic of obesity.
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PMID:Opposite response to starvation of Trp/LNAA ratio in lean and obese Zucker rats. 848 65

The role of insulin in the pathogenesis of hypertension was explored in normal men and male patients with impaired glucose-tolerance. They were classified as normal (n = 94), borderline (n = 164), impaired tolerance (IGT, n = 104), or diabetes mellitus (n = 100) according to their response to an oral 75g glucose challenge. Besides routine laboratory examinations, fasting immunoreactive insulin and post-glucose insulin levels at 30 minutes were measured. Patients with impaired glucose tolerance were older and more obese than the normal subjects. Serum cholesterol and triglyceride concentrations increased with severity of the glucose tolerance impairment. However, renal function, as estimated by blood urea nitrogen levels did not differ among these four groups. Multiple regression analysis revealed that blood pressure correlates significantly with the obesity index, blood glucose, serum cholesterol and serum insulin in all four groups. Among these groups, the partial F ratios for the obesity index were the greatest in both normal and diabetic groups, but in both borderline and IGT groups those for insulin were the greatest. These results indicate that in patients with impaired glucose tolerance is hypertension associated more closely with hyperinsulinemia than it is in normal subjects or diabetic patients.
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PMID:Role of insulin in the pathogenesis of hypertension associated with glucose intolerance. 849 May 97

The aim of this work was to ascertain if diabetes and obesity can affect gastric colonization by Helicobacter pylori. 59 hospitalized subjects with dyspepsia and endoscopic antral gastritis were selected. They were divided into three groups: I) 13 patients with normal body weight and without disease other than gastritis (control group); II) 15 patients with essential obesity of whom 10 had impaired glucose tolerance (IGT); III) 31 patients with type II diabetes mellitus, of whom 14 were obese. Three gastric biopsies were obtained from each patient for histologic examination and H. pylori detection by means of rapid urea test, culture and histological evidence of Helicobacter-Like Organisms (HLO). Age, sex, blood glucose, cholesterol, triglycerides, HDL-cholesterol, basal gastrine, duration of illness, body weight were statistically analysed. Differences between the three groups were not statistically significant. There was a higher prevalence of H. pylori infection both in obese and in diabetic patients with respect to control subjects. Prevalence became still higher in obese patients with impaired glucose tolerance. Among the three tests used for the detection of H. pylori, culture and rapid urea were reliable and specific, while the histologic test was highly sensitive but barely specific. Our data suggest that both obesity and type II diabetes may be associated with an increased incidence of H. pylori-colonization. This could be related to the reduced gastric motility observed in both pathologies and chemical changes in gastric mucosa following non-enzymatic glycosylation processes.
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PMID:Gastric infection by Helicobacter pylori and antral gastritis in hyperglycemic obese and in diabetic subjects. 872 11


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