Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
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The amino acid composition of the diet ingested by reference and cafeteria diet-fed lean and obese Zucker rats has been analyzed from day 30 to 60 after birth. Their body protein amino acid composition was measured, as well as the urinary and faecal losses incurred during the period studied. The protein actually selected by the rats fed the cafeteria diet had essentially the same amino acid composition as the reference diet. The mean protein amino acid composition of the rat showed only small changes with breed, age or diet. Cafeteria-fed rats had a higher dietary protein digestion/absorption efficiency than reference diet-fed rats. Obese rats wasted a high proportion of dietary amino acids when given the reference diet, but not on the cafeteria diet. In all cases, the amino acids lost as such in the urine were a minimal portion of available amino acids. In addition to breed, the rates of protein accretion are deeply influenced by diet, but even more by the age-or size-of the animals: cafeteria-fed rats grew faster, to higher body protein settings, but later protein accrual decreased considerably; this is probably due to a limitation in the 'blueprint for growth' which restricts net protein deposition when a certain body size is attained. Obese rats, however, kept accruing protein with high rates throughout. Diet composition--and not protein availability or quality--induced deep changes in amino acid metabolism. Since the differences in the absolute levels of dietary protein or carbohydrate energy ingested by rats fed the reference or cafeteria diets were small, it can be assumed that high (lipid) energy elicits the changes observed in amino acid metabolism by the cafeteria diet. The effects induced in the fate of the nitrogen ingested were more related to the fractional protein energy proportion than to its absolute values. Cafeteria-fed rats tended to absorb more amino acids and preserve them more efficiently; these effects were shown even under conditions of genetic obesity. There were deep differences in handling of dietary amino acids by dietary or genetically obese rats. The former manage to extract and accrue larger proportions of their dietary amino acids than the latter. The effects of both 'models' of amino acid management were largely additive, suggesting that the mechanisms underlying the development of obesity did not run in parallel to those affecting the control of amino acid utilization. Obesity may be developed in both cases despite a completely different strategy of amino acid assimilation, accrual and utilization.
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PMID:Individual amino acid balances in young lean and obese Zucker rats fed a cafeteria diet. 851 Jun 73

Protein catabolic rate (PCR) and PCR normalized to standard weight (PCRN) are important indices of nutrition in patients on continuous peritoneal dialysis. The purpose of this study was to test whether urea clearance is among the predictors of PCR and PCRN in a multivariate analysis. Stepwise logistic regression was used to develop separate models for low PCR and low PCRN on a set of 143 urea kinetic studies in 92 patients on continuous peritoneal dialysis. The regression models were tested on an independent sample of 189 urea kinetic studies in 102 patients on continuous peritoneal dialysis by deriving the area under a receiver operating characteristic curve. In the derivation set, low serum urea, high serum creatinine, low urine and dialysate drain volumes, and low body surface area were identified as predictors of PCR < or = 50 g daily. The area under the receiver operating characteristic curve in the validation set was 0.930 (95% confidence interval: 0.915-0.945). Low serum urea, male gender, high body mass index and low urea fractional clearance (KT/V) were predictors of PCRN < or = 0.80 g/kg daily. The receiver operating characteristic area for this model was 0.948 (95% confidence interval: 0.926-0.970). Logistic regression analysis was repeated twice after adding urea nitrogen excretion normalized to standard weight (UNEN) as a candidate variable. This process identified low UNEN, male gender, and obesity as the predictors of low PCRN, and low UNEN, male gender, low urine volume, low drain volume normalized by body water, and high serum albumin as predictors of low KT/V urea. The authors conclude that PCR and PCRN can be predicted by models that incorporate serum azotemic indices, body size and composition, and direct or indirect measurements of urea clearance. Small body size and lean body composition predict low PCR but high PCRN values. Both PCRN and KT/V urea are predicted by UNEN. Multivariate analysis cannot, therefore, rule out the hypothesis that PCRN and KT/V are linked mathematically.
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PMID:Protein catabolic rate in patients on continuous peritoneal dialysis. A multivariate predictive model. 880 58

Recent reports describe poor growth in treated children with phenylketonuria (PKU). That poor growth is not a concomitant of the disorder and need not result from therapy is demonstrated by data from the U.S.A. PKU Collaborative Study and from recent data from the U.S.A. In these studies, sufficient protein equivalent was supplied by medical food containing either a low phenylalanine (Phe) casein hydrolysate or Phe-free L-amino acids. Protein and energy intakes of infants and children with PKU who grew well are compared to intakes of normal North American children. Factors that influence nitrogen (N) requirements include: state of health, energy intake, the form in which N is administered and the size of the dose. Failure to prevent poor growth in childhood may lead to a stunted adult [13] who is at risk for obesity. The use of actual body weight as a basis for calculating protein and energy requirements is appropriate only when the child is growing normally. Based on experience with PKU in the U.S.A., the following are recommended: (1) a protocol that prescribes a range for Phe, protein, and energy for infants and children should be developed; (2) adequate protein equivalent to cover N losses due to poor utilization of amino acids and protein hydrolysates should be prescribed; (3) medical food should be administered in several doses throughout the day; (4) a source of Phe should be fed with the medical food; (5) adequate energy should be prescribed to prevent excess use of amino acid for energy purposes; (6) nutrition support during illness should be appropriate to help prevent muscle protein catabolism with attendant elevated plasma Phe.
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PMID:Recommendations for protein and energy intakes by patients with phenylketonuria. 882 26

The study purpose was to determine the following in a large sample of hospitalized patients: (1) the prevalence of hyperuricemia, (2) the association of hyperuricemia with other metabolic disorders, and (3) the factors independently predicting hyperuricemia. Five hundred adult patients (250 men and 250 women) were randomly selected from those admitted as inpatients over a period of 5 months. In all patients, body mass index (BMI), blood pressure, and serum glucose, lipid, creatinine, urea nitrogen, and urate concentrations were measured. The presence of diseases or use of medications known to affect serum urate levels were recorded. The mean level of serum urate was 5.6 mg/dL in the whole sample, 6.0 mg/dL in men and 5.3 mg/dL in women (P = .003, men v women). The prevalence of hyperuricemia was 27.6% (28.8% and 26.4% in men v women, P = nonsignificant). A definite or probable secondary hyperuricemia was found in 87.7% of the subjects. Hyperuricemia was rarely isolated (21%), whereas it was frequently associated with hypertension (60.1%), hyperlipidemia (31.2%), diabetes (28.3%), and obesity (21.7%). In 26.8% of the subjects, hyperuricemia was associated with two metabolic disorders, in 13.8% with three, and in 2.9% with four. Multiple metabolic disorders (three to four) were found in 16.7% of subjects with hyperuricemia. Serum urate levels progressively increased across a range of subjects from those without diabetes, hyperlipidemia, hypertension, or obesity to those with one, two, or a greater number of associated metabolic abnormalities. Multiple stepwise regression analysis showed that 43% of serum urate variability was explained by urea nitrogen levels, triglyceride levels, diuretic therapy, the inverse of creatinine (as an index linearly related to creatinine clearance), and BMI. These results indicate that in hospitalized subjects, hyperuricemia is (1) frequent, (2) a secondary phenomenon in most cases, and (3) frequently associated with other metabolic disorders. The major predictors of high serum urate levels are BMI, triglycerides, parameters of renal function, and use of diuretics. These variables explain a large proportion of serum urate variability.
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PMID:Serum uric acid and related factors in 500 hospitalized subjects. 896 92

The purpose of the study was to examine the distribution of macronutrient density patterns in relation to obesity. This was done in a sample of 323 Danish men and women aged 35-65 years, selected randomly from a larger population sample of adult Danes. Dietary reporting bias of energy and protein intake, in relation to body fat percentage, was assessed by comparing intake data from a diet history interview with data estimated from PABA-validated 24-hour nitrogen excretion and estimated 24-hour energy expenditure. The results of the study showed that degree of obesity was positively associated with protein underreporting of total energy and protein, whereas compared with total energy reported, protein was overreported by the obese subjects. These associations were evident despite control for gender, age and smoking (p = 0.0003). In conclusion, errors in dietary reporting of protein seem to occur disproportionately with respect to total energy, suggesting a differential reporting pattern of different foodstuffs. Although, on average, all subjects over-reported energy percent from protein, over-reporting was most common in obese. It may therefore be speculated that snack type foods are preferentially forgotten when dietary omission occurs in obese individuals. The results of the present study seem in agreement with the general assumption that obese subjects tend to specifically under-report fat and sugar-rich foods, rather than generally under-report their total intake. These results may have wide implications for the interpretation of studies of diet and comorbidities to obesity.
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PMID:[Obese individuals underestimate their food intake--which food groups are under-reported?]. 898 52

We examined 23 pairs of black and white premenopausal women to determine whether there were ethnic differences in body composition. The pairs were matched on weight and height. Each woman had measurements of total body water taken by a tritiated water dilution technique, total body nitrogen, and total body carbon by neutron-activation, mineral ash by dual x-ray absorptiometry, and body potassium by whole body counting. Differences between blacks and whites were compared with the use of both the two-compartment and four-compartment models. The two-compartment model showed that in premenopausal black and white women of similar age, heights, and weights, blacks had significantly more lean mass. The four-compartment model resulted in similar conclusions. The black women had larger protein, mineral, and water compartments and less fat than whites. It may be that body weight measurements as an indicator of obesity should be adjusted for black versus white women.
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PMID:Comparison of body composition in black and white premenopausal women. 904 10

The main objective of the Stanislas cohort is to study the role and the contribution of genetic and environmental factors to cardiovascular status. We plan: a) to describe the degree of association of a large number of cardiovascular risk indicators with cardiovascular endpoints, b) to evaluate the contribution of genetic and that of environmental factors to this association, c) to follow the evolution of these risk indicators during a period of at least ten years, d) to search for the determinants influencing this evolution. The principal variables studied are: a) blood pressure, cardiac mass, and wall thickness of carotid and femoral arteries, b) obesity and fat mass, c) indicators of lipid metabolism, d) genetic polymorphisms of several cardiovascular risk candidate genes, e) food, tobacco and alcohol consumption, f) consumption of drugs and anti-oxidant vitamins. Between September 1993 and August 1995, 1006 families consisting of the two biological parents with at least two children were recruited totalling 4295 individuals. This cohort will be followed up until 2004. There will be two health examinations five and ten years after the initial examination. A bank of blood samples (serum and plasma) in liquid nitrogen and DNA (-80 degrees C) has been established.
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PMID:Objectives, design and recruitment of a familial and longitudinal cohort for studying gene-environment interactions in the field of cardiovascular risk: the Stanislas cohort. 959 84

Fructan is a general term used for any carbohydrate in which one or more fructosyl-fructose link constitutes the majority of osidic bonds. This review focuses on the fate of inulin-type fructans (namely native chicory inulin, oligofructose produced by the partial enzymatic hydrolysis of chicory inulin, and synthetic fructans produced by enzymatic synthesis from sucrose) in the gastrointestinal tract, as well as on their systemic physiological effects on mineral absorption, carbohydrate and lipid metabolism, hormone balance, and nitrogen homeostasis. The scientific evidence for the functional claims of inulin-type fructans is discussed, as well as their potential application in risk reduction of disease, namely constipation, infectious diarrhea, cancer, osteoporosis, atherosclerotic cardiovascular disease, obesity, and non-insulin dependent diabetes.
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PMID:Dietary fructans. 970 21

Dietary treatment of pediatric obesity is a challenge given the need for adequate nutrients to support the maintenance of lean tissue and growth. The primary purpose of this investigation was to assess the effects of reduced energy intake on protein turnover in obese children aged 8 to 10 years. Following a 2-week baseline period, 16 subjects reduced energy intake during a 6-week intervention period. At baseline and following the intervention, 15N-glycine methodology was used to measure nitrogen flux (Q), protein synthesis (PS), protein breakdown (PB), and net turnover ([NET] PS - PB). Other criterion measures included resting metabolic rate (RMR), fat mass (FM), fat-free mass (FFM), urinary creatinine to height ratio (Cr:Ht), and nitrogen balance (NB). On average, subjects lost 2.2 +/- 0.3 kg, of which greater than 85% was FM. Decreased Q (P = .03) indicated downregulation of protein turnover in response to diet-induced weight loss. While PB did not change, NET declined slightly (P = .06) as a consequence of reduced PS (P = .03). Reductions in FFM (P = .09), Cr:Ht (P = .02), and NB (P = .03) accompanied alterations in protein turnover, but there was no change in the RMR. In conclusion, while short-term therapy promoted the loss of FM and did not compromise RMR, practitioners must be cautious when prescribing diets, given the observed changes in protein utilization and somatic protein status. Longitudinal studies are needed to further characterize the metabolic responses of obese children to long-term diet therapy.
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PMID:Effects of reduced energy intake on protein utilization in obese children. 986 70

Growth hormone (GH) can induce an accelerated lipolysis. Impaired secretion of GH in obesity results in the consequent loss of the lipolytic effect of GH. Dietary restriction as a basic treatment for obesity is complicated by poor compliance, protein catabolism, and slow rates or weight loss. GH has an anabolic effect by increasing insulin-like growth factor (IGF)-I. We investigated the effects of GH treatment and dietary restriction on lipolytic and anabolic actions, as well as the consequent changes in insulin and GH secretion in obesity. 24 obese subjects (22 women and 2 men; 22-46 years old) were fed a diet of 25 kcal/kg ideal body weight (IBW) with 1.2 g protein/kg IBW daily and were treated with recombinant human GH (n = 12, 0.18 U/kg IBW/week) or placebo (n = 12, vehicle injection) in a 12-week randomized, double-blind and placebo-controlled trial. GH treatment caused a 1.6-fold increase in the fraction of body weight lost as fat and a greater loss of visceral fat area than placebo treatment (35.3 vs. 28.5%, p < 0.05). In the placebo group, there was a loss in lean body mass (-2.62 +/- 1.51 kg) and a negative nitrogen balance (-4.52 +/- 3.51 g/day). By contrast, the GH group increased in lean body mass (1.13 +/- 1.04 kg) and had a positive nitrogen balance (1.81 +/- 2.06 g/day). GH injections caused a 1.6-fold increase in IGF-I, despite caloric restriction. GH response to L-dopa stimulation was blunted in all subjects and it was increased after treatment in both groups. GH treatment did not induce a further increase in insulin levels during an oral glucose tolerance test (OGTT) but significantly decreased free fatty acid (FFA) levels during OGTT. The decrease in FFA area under the curve during OGTT was positively correlated with visceral fat loss. This study demonstrates that in obese subjects given a hypocaloric diet, GH accelerates body fat loss, exerts anabolic effects and improves GH secretion. These findings suggest a possible therapeutic role of low-dose GH with caloric restriction for obesity.
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PMID:Low-dose growth hormone treatment with diet restriction accelerates body fat loss, exerts anabolic effect and improves growth hormone secretory dysfunction in obese adults. 1035 97


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