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

Obesity is a major nutritional disorder that produces many abnormal metabolic responses. The effect of injury-induced stresses acting synergistically with the state of excessive body fat is not well known. Plasma levels of circulating free amino acids reflect the net status of protein breakdown and utilization. Hypoaminoacidemia is a common finding in severe injury and its significance in obese subjects was investigated. We measured in 10 obese (body mass index [BMI] greater than 30) and 10 non-obese (BMI less than 30) traumatized (Injury Severity Score [ISS] 17 to 50) patients, the plasma levels of free amino acids in the early "flow" phase of injury when subjects were receiving maintenance fluids without calories or nitrogen. Postabsorptive control samples were obtained from 10 obese and 10 non-obese volunteers. Obese controls showed an increase in valine, leucine, isoleucine, and glutamic acid levels, and a decrease in glycine, tryptophan, threonine, histidine, taurine, citrulline, and cystine levels compared with lean controls. Hypoaminoacidemia was equally seen in traumatized obese and non-obese patients, and it was mainly due to a 24% decrease in nonessential amino acids. Remarkably, essential amino acid levels were the same in all groups. Arginine and ornithine levels were significantly different in traumatized obese compared with non-obese patients. The hypoglycinemia seen in non-obese trauma patients was absent in obese patients. The changes in levels of sulphur-containing amino acids also suggest that monitoring of these levels should be included in the nutritional management of obese trauma patients.
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PMID:Altered plasma free amino acid levels in obese traumatized man. 201 Oct 79

Twenty obese and 20 lean LA/N-cp male rats and 20 male Sprague-Dawley rats were fed a diet containing either 54 percent sucrose or starch for six weeks. After a 14-16 hour fast, rats were killed. Liver and kidney enzyme activities were determined in the LA/N-cp rats while plasma urea and selected amino acids were determined in all rats. Liver glucose-6-phosphatase (G6PASE), fructose-1,6-bisphosphatase (FBPASE), phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), malic enzyme (ME), glucokinase (GK), pyruvate kinase (PK), phosphofructokinase (PFK), glutamic-oxaloacetic-transaminase (GOT), glutamic-pyruvic transaminase (GPT), arginase (ARGASE), arginine-synthase (ARG-SYN) and ornithine transcarbamylase (OTC) levels were significantly affected by phenotype (obese greater than lean). All the above changes in enzyme levels were exaggerated by sucrose-feeding with the exception of PK, PFK, GOT, GPT, ARGASE and ARG-SYN. Kidney cortex G6PASE, PEPCK and ARGASE activities were higher in the obese rats as compared to the lean littermates. Sucrose feeding resulted in higher cortex G6PASE, FBPASE and PEPCK as compared to starch-fed rats. A phenotype effect was noted with plasma glutamate, urea, leucine, isoleucine and valine (obese greater than lean) and a diet effect was seen with aspartate, phenylalanine, leucine and valine (sucrose greater than starch) concentration. Sprague-Dawley rats had higher plasma urea and lower alanine than lean LA/N-cp males. Metabolic obesity in the LA/N-cp rat appears to involve an elevated capacity for pathways of glycolysis, gluconeogensis, lipogenesis and amino acid catabolism in the liver.
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PMID:Effect of dietary carbohydrate on liver and kidney enzyme activities and plasma amino acids in the LA/N-cp rat. 204 12

Poorly-controlled type I diabetic patients have elevated rates of leucine appearance (indicating increased proteolysis), which are reduced with insulin therapy. It also has been suggested that obesity increases leucine appearance rate by reducing sensitivity to insulin. In the present study, we examined whether non-diabetic obese women or poorly-controlled obese type II diabetic patients have elevated leucine appearance rates, and whether diabetic patients have a reduction in leucine appearance with treatment of their hyperglycemia. Among non-diabetic women, postabsorptive leucine appearance rate was positively correlated with the percentage of body weight as fat (r = 0.92, P less than 0.01). Obese women with untreated type II diabetes did not have a higher mean (+/- s.e.m.) leucine appearance rate (2.13 +/- 0.18 mumols/min/kg fat-free mass, determined by infusion of 1-[1-13C] leucine as a tracer) than obese non-diabetic women with a similar fat-free mass (2.49 +/- 0.09 mumols/min/kg fat-free mass). After two weeks of glyburide therapy mean glucose concentrations decreased 24 percent and glucose production decreased 18 percent, but leucine appearance rate was not altered (2.08 +/- 0.18 mumols/min/kg fat-free mass). After 2 weeks of insulin therapy, mean fasting glucose concentration and glucose production rate were normal (55 per cent and 46 per cent below pre-treatment levels), but leucine appearance rates remained unchanged (2.17 +/- 0.18 mumols/min/kg fat-free mass). We conclude that type II diabetes in obese patients is not associated with elevated proteolysis, that treatments that significantly improve or normalize postabsorptive glucose metabolism in obese type II diabetic patients do not affect postabsorptive proteolysis, and that obesity per se (without diabetes) increases proteolysis.
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PMID:Failure of glyburide and insulin treatment to decrease leucine flux in obese type II diabetic patients. 212 56

The immediate metabolic response to eating has been compared in a group of grossly obese subjects (W/H2 = 45) with that in lean controls (W/H2 = 22). Dietary intake of energy for obese subjects was based on their estimated basal energy expenditure for ideal body weight (given at an hourly rate of 3 X BMR over a 4-h period). Lean subjects were measured twice: control 1 with the same intake of energy as the obese in terms of ideal body weight and control 2 with the same energy intake in relation to each subject's measured resting energy expenditure (2.2 X REE). The changes in energy expenditure and nutrient disposal with the onset of eating have been assessed by a method of combined respiratory gas analysis and intravenous infusion of 13C-labelled leucine. Leucine kinetics were used to quantitate rapid changes in protein oxidation and to assess protein synthesis and degradation. 1) Total energy expenditure was 20-30 per cent greater in obese subjects than lean subjects in fasting and feeding. Energy expenditure expressed per kg fat-free mass, from D2O dilution, was similar in obese and lean subjects in both fasting (5.8 v. 5.5 kJ/kg FFM/h) and feeding [6.7 v. 6.3 (Control 2) kJ/kg FFM/h]. 2) The onset of eating was associated with increased carbohydrate and protein oxidation with decreased fat oxidation in both lean and obese individuals. In obese subjects, however, both the decrease in fat oxidation and the increase in protein oxidation were significantly smaller (P less than 0.05) than the corresponding increments in lean subjects (Control 2). 3) The rate of protein synthesis was significantly (P less than 0.05) higher in obese subjects both in the fasting state (99 v. 84 mumols leucine/kg FFM/h) and in the fed state [94 v. 67 (Control 2) mumols leucine/kg FFM/h]. The rate of protein degradation was also higher in obese individuals in fasting (117 +/- 6 v. 106 +/- 4 mumol leucine/kg FFM/h) and feeding [65 +/- 4 v. 54 +/- 6 (Control 2) mumol leucine/kg FFM/h] though these differences are not statistically significant (P greater than 0.05). 4) The observed differences between obese and lean individuals in protein and energy metabolism in the fasted state and in the immediate response to eating do not support a hypothesis of greater metabolic efficiency in obesity.
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PMID:Nutrient oxidation patterns and protein metabolism in lean and obese subjects. 222 98

We have recently shown that in addition to beta-endorphin the opioid peptides Met- and Leu-enkephalin and their apparent precursors are localized in islet endocrine cells of the rat pancreas. To begin evaluating a possible role for these pancreatic opiates in the pathophysiology of genetic diabetes in rodents, immunoreactive beta-endorphin and Met- and Leu-enkephalins were measured in acetic acid extracts of pancreas and pituitary of C57BL/KsJ db/db mice and their lean littermates. Groups of animals were studied during three phases of development of the diabetic syndrome in the mutant mice: at 4 (hyperinsulinemic and prediabetic); 6, 9, and 12 (frankly obese and diabetic); and 30 (hypoinsulinemic) wk of age. Elevations or decreases (P less than .05) were found in db/db mice (vs. lean littermates) as follows: pituitary content of Met-enkephalin was twofold higher at all ages studied; pituitary free Leu-enkephalin was lower at 4 wk and reversed to higher at 6-30 wk; pancreatic beta-endorphin was 30% lower at 4 wk and reversed to threefold higher at 6-12 wk; Met- and Leu-enkephalin-containing larger peptides were elevated at one or more points between 6 and 12 wk in both the pancreas and the pituitary. Thus, the onset of overt obesity between 4 and 6 wk of age was accompanied by a marked rise in both pancreatic beta-endorphin and pituitary Leu-enkephalin; similar elevations in these parameters have been reported previously in C57BL/6J ob/ob mice at approximately 12 wk of age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered beta-endorphin, Met- and Leu-enkephalins, and enkephalin-containing peptides in pancreas and pituitary of genetically obese diabetic (db/db) mice during development of diabetic syndrome. 294 83

One mechanism through which the brain obtains information about the composition of the diet involves food-induced changes in the plasma amino acid pattern (principally the "plasma tryptophan ratio"), which then cause increases or decreases in brain tryptophan levels, and in the synthesis of a neurotransmitter, serotonin, which is formed from the tryptophan. A carbohydrate-rich, protein-poor meal stimulates insulin secretion; this diminishes plasma levels of the amino acids which compete with tryptophan for transport into the brain (e.g., leucine, isoleucine and valine), thus increasing tryptophan's flux across the blood-brain barrier and its brain levels. In contrast, a high-protein meal contributes so much more of these latter amino acids to the blood stream than of the relatively-scarce tryptophan that it diminishes tryptophan's entry into the brain. This article reviews evidence that the brain actually utilizes the food-induced changes in brain serotonin in order to make choices about what to eat at the next meal. It also discusses the likelihood that a disturbance in this mechanism is involved in producing the "carbohydrate-craving" that is frequently associated with obesity. (This behavior which has been studied by allowing hospitalized subjects to choose freely among isocaloric meals and snacks of varying protein/carbohydrate ratios, typically manifests itself as a propensity to consume 30 per cent or more of the total daily calorie intake in the form of sweet or starchy snacks, usually at a characteristic time of day.) D-Fenfluramine, a drug that selectively enhances serotonin-mediated neurotransmission, also selectively suppresses "carbohydrate-craving" in these subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carbohydrate craving, obesity and brain serotonin. 352 63

Very-low-calorie diets (less than 500 kcal/day; VLCD) are widely used for the treatment of severe obesity. We report the effects of such diets, consisting of proteins only or proteins and carbohydrates (CH), on nitrogen balance and protein nutritional status of morbidly obese patients. Cumulative nitrogen loss, serum albumin, transferrin, prealbumin (PA) and retinol-binding protein (RBP) concentrations, and plasma amino acid profile were determined in two groups of obese patients: 5 subjects (3 women, 2 men: BMI 55.3 +/- 2.2 kg/m2) subjected for 4 weeks to a protein VLCD (40 g protein + 2 g fat) and 7 others (4 women, 3 men: BMI 45.6 +/- 2.8 kg/m2) received for the same length of time a protein + CH VLCD (34 g protein + 26 g CH). Nitrogen balance was determined weekly whilst plasma and serum variables were measured on days 0, 3, 5, 10, 20 and 28 of treatment. Nitrogen balance did not significantly differ between the two groups of patients throughout the treatment. Serum PA and RBP concentrations decreased from day 5 and day 10, respectively, in both groups. Plasma amino acids showed a similar pattern in the protein and protein + CH groups. Alanine gradually decreased below baseline values; after a peak value on day 5, branched-chain amino acids (valine, leucine, isoleucine) returned to baseline values in both groups. In conclusion, in severely obese patients subjected to VLCD, nitrogen balance, labile protein concentrations and plasma amino acid profile are not significantly affected by adding CH to proteins.
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PMID:Protein balance during very-low-calorie diets for the treatment of severe obesity. 359 20

In order to test the hypothesis that serotonergic activity is abnormal in the brains of genetically obese Zucker rats, levels of serotonin (5-HT); its amino acid precursor, tryptophan (Trp), and its major metabolite, 5-hydroxyindoleacetic acid (5-HIAA) were measured in eight brain regions in groups of obese and non-obese male rats. Plasma albumin levels as well as levels of amino acids and related compounds in plasma and in a cortical sample were also determined in the same animals. While Trp was lower in several brain regions of the obese animals, the only region showing a depressed level of 5-HT in the obese group was the mesencephalon. Obese animals also had a lower amount of 5-HIAA in the diencephalon, but no other differences were significant. Both elevations and depressions were observed in cortical amino acid levels in obese animals. The level of plasma albumin was increased in the obese group. Free Trp was decreased in the plasma of obese rats while levels of other amino acids (methionine, leucine, isoleucine, valine and phenylalanine) which compete with Trp for transport across the blood-brain barrier were elevated. Thus the combination of lower plasma free Trp and increased levels of competitive amino acids appears to contribute to decreased levels of Trp in the brain of genetically obese rats.
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PMID:Brain serotonergic activity and plasma amino acid levels in genetically obese Zucker rats. 618 36

The effect of euglycemic hyperinsulinism on branched-chain amino acids (BCAA; valine, isoleucine and leucine) was evaluated in five obese subjects and five controls. A continuous intravenous insulin infusion raised plasma insulin to a steady-state level. An artificial endocrine pancrease that infused glucose was used to sustain euglycemia. Basal and steady-state insulin levels were significantly higher in the obese subjects than in the controls. The amount of glucose infused to maintain euglycemia and its ratio to steady-state insulin levels was significantly lower in the obese subjects, suggesting an impaired insulin action on glucose metabolism. Basal BCAA levels were similar in the two groups of subjects. During insulin infusion the decremental areas of BCAA below basal levels were significantly lower in the obese patients (63 +/- 5 nmol/mL X min v 143 +/- 8 nmol/mL X min, P less than 0.001), as was the ratio of the decremental areas of BCAA to the incremental areas of insulin (1.11 +/- 0.05 nmol/microU v 3.30 +/- 0.24 nmol/microU, P less than 0.001). Our data suggest that insulin resistance in obesity reduces hormonal effects on glucose as well as on BCAA metabolism.
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PMID:Insulin-dependent metabolism of branched-chain amino acids in obesity. 636 75

The ratio of plasma concentrations of tryptophan to the sum of neutral amino acids (valine, isoleucine, leucine, phenylalanine and tyrosine) was found to be significantly lower in formula-fed infants as compared to breast-fed infants and to newborns at birth. This tryptophan to neutral amino acids ratio in the blood is thought to control the synthesis of serotonin in the brain. Serotonin deficiency in the developing brain based on a decreased plasma tryptophan to neutral amino acids ratio may contribute to developmental obesity and/or permanent changes of mental capacity and social adaptability as observed in human subjects who had been formula-fed as compared to those who had been breast-fed in neonatal life.
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PMID:Changes of the plasma tryptophan to neutral amino acids ratio in formula-fed infants: possible effects on brain development. 668 52


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