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)

An increased aspartate transaminase in the liver of dietary (post-cafeteria) obese rats was found. It was consistent with the functionality of the malate-aspartate shuttle, that could be responsible for enhancement of metabolic efficiency. The muscle and intestine of obese rats showed a greater capacity for alanine and glutamine synthesis than the controls. Furthermore, enterocyte adaptations in the obese rats indicated higher capabilities for the intake of nitrogen than in the controls. In conclusion, the pattern of amino-acid enzyme activities reflected adaptations to keep from amino nitrogen depletion in dietary obesity which were compatible with an enhancement of the metabolic efficiency.
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PMID:Dietary obesity shows adaptations of amino-acid metabolism on enzyme activities to save amino nitrogen. 168 27

The published literature on the influence of obesity on intermediary metabolite concentrations does not adequately address the potential confounding effects of the increased prevalence of impaired glucose tolerance in obese subjects. In order to remove this, we studied 109 subjects with proven normal glucose tolerance ranging from underweight to grossly obese (range 15.3-80.9 body mass index). All had blood intermediary metabolites, plasma insulin and C-peptide measured after an overnight fast. Thirty-six (18 from each end of the range of body mass index) received a 3-hour oral glucose tolerance test for metabolites and insulin. Fasting plasma insulin was highly significantly associated with body mass index (r = 0.72; P less than 0.001). Concentrations of lipid intermediaries were better associated with body mass index than with fasting plasma insulin: non-esterified fatty acids (r = 0.36; P less than 0.001), glycerol (r = 0.47; P less than 0.001) and ketone bodies (r = 0.45; P less than 0.001). Fasting concentrations of carbohydrate intermediaries were, however, better correlated with fasting plasma insulin: lactate (r = 0.29; P less than 0.01), pyruvate (r = 0.24; P less than 0.01) and alanine (r = 0.36; P less than 0.001). Glucose concentrations were associated with both to a similar degree (r = 0.33, r = 0.32, respectively; P less than 0.001). After oral glucose, exaggerated rises in plasma insulin and blood glucose were observed in obese subjects but a lesser rise was seen for lactate. Non-esterified fatty acids and ketones, although having higher fasting concentrations in obese subjects, fell to similar concentrations in the two groups after glucose whereas blood glycerol did not fall so far in the obese subjects. The results suggest, even if those subjects with impaired glucose tolerance are excluded, insensitivity to insulin in several aspects of intermediary metabolism in obesity the degree of which may vary in different metabolic pathways or tissues.
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PMID:Effect of obesity on circulating intermediary metabolite concentrations in the absence of impaired glucose tolerance. 175 24

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

The "in vivo" handling of L-alanine in 24 hours starved rats, in which obesity was induced by feeding with cafeteria diet, was compared with that of starved control rats. 14C-alanine was administered in trace amounts in order not to affect the normal handling of this amino acid. The results obtained in blood and liver support a lowered glucose formation from alanine. The specific radioactivities corresponding to lactate, glutamate + glutamine and asparagine as well as total protein and total lipid, were all lowered in the obese group. This strongly suggests that glucose formation from alanine in the liver was impaired. The specific radioactivity of the metabolites studied in the striated muscle are compatible with the above suggestion. It can be concluded that the glucose alanine cycle operation is inhibited in the cafeteria diet starved obese rats.
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PMID:In vivo C14-L-alanine metabolism in rat dietary obesity induced by cafeteria diet. 231 16

Alcohol abuse is usually regarded as the most likely cause of elevated serum liver enzyme values in those attending for well population screening, but we have found increased body weight to be an important contributing factor. We have measured serum levels of alanine amino-transferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (GGT) in approximately 21,000 men attending for routine health screening, and related these to behavioural factors such as alcohol consumption, cigarette smoking, exercise level and obesity. The levels of all three enzymes were positively correlated with levels of alcohol consumption. Decreasing levels of physical activity were associated with increases in mean ALT and GGT levels. Cigarette smoking showed only a weak effect on ALT and AST, which became non-significant after multivariate statistical analysis, but increasing consumption of cigarettes was associated with increased mean levels of GGT. In contrast, all three enzymes showed marked increases in mean levels with increasing body mass index (BMI). The effect of obesity was particularly important in the case of ALT: the prevalence of increased ALT values in obese subjects (BMI greater than or equal to 31 kg/m2) was more than eight times that in those with normal weight (BMI less than or equal to 25 kg/m2), even after allowing for the confounding effect of alcohol consumption. This study is concerned solely with male subjects, but we hope to extend the analysis to females in the near future.
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PMID:Effect of body mass and other factors on serum liver enzyme levels in men attending for well population screening. 257 11

To investigate glucagon (IRG) and insulin (IRI) responses to alanine infusion in obesity and to assess the effect of body weight reduction with respect to hormonal balance, we compared six obese subjects with nine normal weight controls. None of the subjects were diabetic by OGTT criteria. Plasma IRI and IRG were measured following IV alanine at a rate of 0.1 g/kg over a period of 2 min. Our obese subjects had an increase in IRG response to alanine, which was due to decreased suppression of alpha-cell function due to insulin resistance. Weight reduction via calorie restriction reduced insulin demand, resulting in reduced plasma IRI by restoring beta-cell function, and the IRG response was paradoxically decreased as compared with that before weight loss. It is conceivable that improvements in insulin sensitivity after body weight reduction may re-establish the normalization of pancreatic beta-cell function and the insulin-induced inhibition of IRG secretion. Our obese subjects were characterized by decreased IRG secretion which was reflected in a change in body weight reduction.
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PMID:Plasma glucagon response to intravenous alanine in obese and non-obese subjects. 269 21

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

Plasma concentrations of glucagon, insulin, glucose, and individual plasma amino acids were measured in normal nonobese and obese subjects before and after 3 days of dexamethasone treatment (2 mg/day) and in patients with Cushing's syndrome. The subjects were studied in the basal postabsorptive state and following the infusion of alanine (0.15 g/kg) or ingestion of a protein meal. In nonobese subjects dexamethasone treatment resulted in a 55% increment in basal glucagon levels and in a 60-100% increase in the maximal glucagon response to alanine infusion or protein ingestion. In obese subjects, basal glucagon rose by 110% following dexamethasone, while the response to alanine increased fourfold. In patients with Cushing's syndrome basal glucagon levels were 100% higher and the glucagon response to alanine infusion was 170% greater than in normal controls.Dexamethasone treatment in normal subjects resulted in a 40% rise in plasma alanine concentration which was directly proportional to the rise in basal glucagon. The remaining 14 amino acids were unchanged. In the patients with Cushing's syndrome alanine levels were 40% higher than in normal controls and were directly proportional to basal glucagon concentrations. No other plasma amino acids were significantly altered in the group with Cushing's syndrome. It is concluded that (a) glucocorticoids increase plasma glucagon concentration in the basal state and in response to protein ingestion or aminogenic stimulation; (b) this effect of glucocorticoids occurs in the face of obesity and persists in chronic hypercorticism; (c) hyperalaninemia is a characteristic of acute and chronic glucocorticoid excess, and may in turn contribute to steroid-induced hyperglucagonemia; and (d) increased alpha cell secretion may be a contributory factor in the gluconeogenic and diabetogenic effects of glucocorticoids.
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PMID:Influence of glucocorticoids on glucagon secretion and plasma amino acid concentrations in man. 474 10

Hormone and metabolite profiles were investigated over a 12-hr period in six patients with Cushing's syndrome, ten age- and sex-matched normal controls, and six moderately obese subjects matched for weight with the patient group. Mean diurnal plasma cortisol levels were 563 +/- 74 nmole/liter in the patients, 275 +/- 22 nmole/liter in normal controls and 241 +/- 32 nmole/liter in obese subjects, with total loss of diurnal changes in Cushing's syndrome. Fasting blood glucose concentration was similar in all groups although mild hyperglycemia occurred after meals in the Cushing's patients compared with normal and obese subjects (mean 12-hr blood glucose: Cushing's 6.31 +/- 0.39 mmole/liter; normal controls, 5.32 +/- 0.14 mmole/liter, p < 0.01; obese subjects, 5.41 +/- 0.18 mmole/liter, p < 0.05) despite marked hyperinsulinemia (mean 12-hr serum insulin: Cushing's 57.3 +/- 18.2 mU/liter; normal controls, 19.7 +/- 2.5 mU/liter, p < 0.02; obese subjects, 18.1 +/- 4.0 mU/liter, p < 0.05). Concentrations of the gluconeogenic precursors lactate, pyruvate, and alanine were raised in Cushing's syndrome, particularly postprandially. Plasma nonesterified fatty acids (NEFA), blood glycerol, and blood ketone body concentrations were comparable in all three groups although the normal diurnal variation in circulating NEFA and ketone body levels was lost in Cushing's syndrome. Serum triglyceride (TG) concentrations were grossly elevated in the Cushing's patients (mean 12-hr serum TG: Cushing's 3.51 +/- 1.23 mmole/liter; normal controls 0.89 +/- 0.19 mmole/liter, p < 0.02; obese subjects, 0.93 +/- 0.23 mmole/liter, p < 0.05) and correlated positively with serum insulin levels. Plasma glucagon concentrations were raised in Cushing's syndrome (mean 12-hr plasma glucagon: Cushing's 23.2 +/- 3.7 pmole/liter; normal controls 12.3 +/- 1.5 pmole/liter p < 0.01; obese subjects 12.2 +/0 2.0 pmole/liter, p < 0.02) and correlated positively with the serum cortisol but not with blood alanine, suggesting that some stimulatory factor other than alanine was responsible. The metabolic effects of chronic glucocorticoid excess thus may not be explained on the basis of obesity alone. Compensatory hyperinsulinemia limits the disturbance of carbohydrate and lipid metabolism in Cushing's syndrome but may be important in production of the hypertriglyceridemia observed.
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PMID:Hormonal and metabolic rhythms in Cushing's syndrome. 700 Nov 75

The small intestine of obese animals supplies nutrients to a metabolic live mass (body weight 0.75) that is much higher than that of age- and sex-matched lean animals. To determine the mechanisms of adaptation of the small intestine to obesity, we determined the rate of uptake of D-glucose and five amino acids, the site density of intestinal D-glucose transporters, and the permeability of the absorptive mucosa in isolated everted intestinal sleeves of genetically obese male mice (C57BL/6J ob/ob) and their lean male littermates. Intestinal D-glucose, proline, alanine, aspartate, leucine, and lysine uptakes per milligram were each similar in the small intestine of obese and control mice. Mucosal permeability, site density of intestinal D-glucose transporters, and their affinity for phlorizin were also each similar between obese mice and their lean controls. In contrast, intestinal D-glucose, proline, alanine, aspartate, leucine, and lysine uptakes per centimeter of small intestine were each approximately 40% greater in obese mice compared with lean controls (P < 0.001 to P < 0.08, depending on the nutrient and intestinal region). Differences in total absorptive capacity for any nutrient between the small intestine of obese and lean mice reflect mainly differences in intestinal weights. Thus, genetic obesity is associated with increased intestinal growth, which augments absorption of all types of nutrients. The ratio of intestinal absorptive capacity to metabolic mass, and of intestinal mass to metabolic mass, does not change with obesity, indicating that in mice, changes in intestinal mass and in absorptive capacity are directly proportional to changes in metabolic mass.
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PMID:Intestinal nutrient transport in genetically obese mice. 766 Nov 15


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