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

Obese Zucker rats were either pair-fed to their lean litter-mates or fed ad lib, to determine the effect of hyperphagia on serum hormone levels and tissue metabolism as indicated by enzyme activities and in vitro metabolite flux. Hyperphagia was shown to be non-essential for the elevation in serum insulin and suppression in serum growth hormone and prolactin in the genetically obese rat. It was also shown that the increased liver cell lipogenic rate was not dependent on hyperphagia in the obese rat and that adipose cell lipogenesis was not significantly altered in the pair-fed obese rat. The utilization of alanine for glucose synthesis in vitro was similar for both lean and obese rats, but its utilization for fatty acid synthesis was higher in the obese rat. Data is presented which suggest that the inhibitory effect of glucagon on liver lipogenesis is blunted in the obese rat.
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PMID:Serum hormone levels and tissue metabolism in pair-fed lean and obese Zucker rats. 19 81

Based on the consideration that insulin does not act directly on metabolic processes but affects membrane carriers and key-enzymes that regulate metabolic pathways, determination of insulin responsiveness of the various key-enzymes is suggested as a very appropriate method for studying insulin resistance. Insulin resistance, as it occurs in obese or obese-diabetic humans and animals, is most often associated with hyperinsulinemia, and is characterized not only by increased activity of key-enzymes of pathways known to be stimulated by insulin (glycolysis, lipogenesis), with the possible exception of glycogen synthesis, but also by a trend towards increased activity of key-enzymes of 'catabolic pathways', normally depressed by insulin. In the adipose tissue there is a normal-to-enhanced basal lipolysis, which in man would result from the prevalence of the active over the inactive form of triacylglycerol lipase. In muscle, the increased amino-acid release that can be inferred from the elevated blood level of both alanine and branched-chain amino acids suggests an enhanced proteolysis. In liver, there is an elevation in the activity of the key gluconeogenic enzymes, which forms the basis of the augmented gluconeogenesis. In both muscle and liver, phosphorylase is also elevated with no change in glycogen synthase. Therefore, insulin resistance seems to consist of the failure of insulin to depress the key-enzymes of catabolic pathways. Possible resistance of glycogen synthetase, which might account for decreased glucose utilization in muscle, may be due to the opposing effects of the phosphorylation process on glycogen synthetase and phosphorylase, implying that activation of phosphorylase (which occurs in obesity) entails inhibition of the synthetase. The fact that insulin insensitivity concerns only the 'catabolic' but not most 'anabolic' pathways makes it unlikely that the unresponsiveness is due to a reduction in insulin receptors or increase in insulin degradation. Since resistance to insulin is shown by enzymes regulated by such different mechanisms as induction-repression (gluconeogenic enzymes), covalent modifications (lipase, phosphorylase), and changes in lysosome stability (lysosomal proteases responsible for proteolysis, a single basic mechanism for explaining insulin insensitivity cannot be envisaged at present.
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PMID:Insulin resistance in obesity: a critical analysis at enzyme level. A review. 39 47

Hyperuricaemia was present in 18 out of 73 men with untreated mild hypertension and was related significantly to alcohol intake, serum aspartate transaminase activity, and obesity. In the whole group the mean serum urate concentration correlated highly significantly with alcohol intake and activities of serum aspartate and alanine transferases but not with ponderal index, serum creatinine concentration, age, or blood pressure. Hypertension and hyperuricaemia are related at least in part through their common association with frequent alcohol use. A serum urate concentration exceeding 0.5 mmol/l (8--4 mg/100 ml) in a man with untreated hypertension is highly suggestive of heavy alcohol consumption. There was no evidence that hyperuricaemia had a deleterious effect on renal function.
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PMID:Hyperuricaemia in hypertension: role of alcohol. 43 9

The methods utilized in our laboratory for a biochemical approach of obesity include dietary manipulations, fatty acid analysis of tissue lipids, in vivo lipogenesis from [3H H2O and [1-14C] acetate, in vitro utilization of [3H] H2O, [U-14C] glucose, [U-14C] fructose, [U-14C] alanine and [1-14C] acetate by adipose tissue fragments, hormone sensitivity (to insulin and catecholamines), and the activity of enzymes such as fatty acid synthetase and adenylate cyclase in adipose tissue extracts. With these methods at hand, it is possible to estimate the major biochemical factors responsible for fat accumulation in adipose tissue. As an example, the case of obese (ob/ob) homozygotic animals of the C57BL/6J strain of Bar Harbor, which suffer from an autosomal recessive obese-hyperglycemic (O-H) syndrome, is compared to that of control nonobese (ob+/ob+) mice from the same strain. The hereditary O-H syndrome in ob/ob mice is characterized by obesity, resistance to the action of insulin, and hyperinsulinism. The development of obesity depends on high lipogenesis in fat depots. Contribute also to obesity a large influx of fatty acids of hepatic and dietary origin, and reduced lipolysis. In these mice, a high fat diet is more propitious to fat accretion than a high-carbohydrate diet.
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PMID:Experimental basis of obesity. 62 36

Postabsorptive plasma amino acid and insulin concentrations were determined in subjects with hyperplastic obesity and in nonobese controls before and after a 6-wk period of physical training. After the training period the plasma concentrations of insulin and leucine decreased and the concentration of alanine increased in the obese subjects. No changes were noticed in the controls. The obese subjects had elevated plasma levels of valine, isoleucine, leucine, tyrosine, and phenylalanine before as well as after physical training. The concentrations of these amino acids were correlated to the plasma insulin level and to lean body mass before but only to lean body mass after physical training. It is suggested that the lean body mass, whick is higher in hyperplastic obesity, contributes to the elevated concentrations of amino acids, and it is unlikely that the insulin decreases in the obese subjects after physical training is mediated through an effect of amino acids on insulin secretion.
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PMID:Effects of physical training and lean body mass of plasma amino acids in man. 68 Dec 2

The most serious adverse effect of standard intestinal bypass for obesity is the high incidence of hepatic dysfunction and death from hepatic failure. We therefore examined the long-term effects of a modified form of jejunoileal bypass (in which a greater continuous length of ileum is retained), on liver function in 120 patients. Substantial weight loss (119-0+/-SD 23-3 kg to 82-3+/-18-8 kg) occurred during the first nine months after surgery, accompanied by a significant rise in serum concentrations of bilirubin, alanine transferase, and alkaline phosphatase, and a significant reduction in albumin concentrations. Biochemical changes were unrelated to weight loss or halothane anaesthesia. After weight stabilisation liver function reverted to normal, and four years after bypass sulphobromophthalein retention and hepatic histology did not differ from those in obese controls. There were two postoperative deaths. Three other patients died during the period of rapid weight loss with severe hepatic steatosis. While transient mild impairment of liver function is common after modified jejunoileal bypass, clinically significant hepatic dysfunction is a rare and unexplained early complication.
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PMID:Hepatic structure and function after modified jejunoileal bypass surgery for obesity. 91 71

Effects of a 24 hour fast were studied in 21 obese children aged 7 to 14 and in 8 controls. Mean blood glucose (BG) during fast dropped more in controls (0.88 to 0.54 g/l) than in obese (0.90 to 0.63 g/l) Plasma cortisol changes were similar in the 2 groups, FFA increased (p less than 0.01) in the 2 groups, but the 24 hour mean level was higher in controls (4.0 mEq/l) than in obese (2.06 mEq/l). At the end of the fast, a ketonuria was present in all obese children except 2. Serum alanine dropped similarly in obese (28 to 24 muM p. cent ml) and in controls (30 to 22 muM p. cent ml). All obese exhibited at the end of the fast a significant rise (p less than 0.01) of branched chain aminoacids, not observed in controls. Responses to glucagon (0.03 mg/kg I.M.) were studied before and after fast. At time 0, BG response was higher and more prolonged in obese in spite of hyperinsulinism. At time 24 hours, BG raised from 0.50 to 0.74 g/1 and insulin from 8 to 35 muU/ml in controls, while in obese BG raised from 0.63 to 1.06 g/l and insulin from 25 to 88 muU/ml. Concomitant hyperinsulinsim and biological criteria of hypoinsulinism demonstrated in obese children the peripheral resistance to insulin. The contrast between a normal degree of protein gluconeogenesis and a reduced rate of fat mobilization during fast may be a major biological feature of obesity in childhood.
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PMID:Effect of 24 hour fast in obese children. 100 33

Liver biopsy and liver function tests were performed in 17 obese patients before and 14 months after intestinal shunt operation for obesity. In another 20 patients liver biopsy was performed postoperative only, in 12 patients preoperatively only. Steatosis was present in 85 per cent. of the patients before the operation. After the operation steatosis decreased in half the patients and increased in the other half. In patients with biopsy twice postoperatively there was a significant trend of decreasing steatosis up to 56 months after the operation. No patient developed cirrhosis during the time of observation. Within the first postoperative year there was a substantial and significant increase in serum alanine-aminotransferase and a minor increase in alkaline phosphatases and BSP. There was no correlation between the rate of weight loss and the change in steatosis or liver function.
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PMID:Liver morphology and liver function before and after intestinal shunt operation for obesity. 115 33

In this study of spontaneous obesity of pigs, specific metabolic shifts were observed, which explain an increase in fat deposition. Liver tissue utilization of pyruvate and glucose for oxidation and lipogenesis showed no significant difference between lean and obese pigs. Adipose tissue utilization of glucose, acetate and glycerol for triglyceride and fatty acid synthesis was greater in obese pigs than lean pigs (P less than 0.01). No significant difference in leucine incorporation into lipid fractions was found. Of the substrates utilized, glucose supplied 86 and 94% of the glyceride-glycerol synthesized in lean and obese pigs, respectively. Glycerol was not a major contributor to glyceride-glycerol synthesis (3.5 to 5.5%), in spite of the presence of adipose tissue glycerokinase. An increase (P less than 0.05) in alanine incorporation into glucose was observed in liver tissue from obese pigs. In general, the levels of enzymes activities associated with gluconeogenesis, glycolysis, and lipogenesis supported the findings of in vitro utilization of these substrates.
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PMID:A comparison of the enzyme levels and the in vitro utilization of various substrates for lipogenesis in pair-fed lean and obese pigs. 125 Aug 52

The effects of cafeteria diet-induced obesity upon in vitro uptake of L-Alanine, Glycine, L-Lysine, L-Glutamine, L-Glutamic acid, L-Phenylalanine and L-Leucine by isolated rat erythrocytes have been studied. The total Phe and Leu uptakes followed Michaelis-Menten kinetics. The Glu uptake was fitted to diffusion kinetics. The uptakes of Ala, Gly, Lys and Gln were best explained by a two-component transport: one saturable and one diffusion. Obesity increased the Km value for Ala, Gln and Leu, and the Vmax value for Ala, but decreased the Vmax for Lys. Kinetic parameters of Phe uptake were unaffected by obesity. In addition, the pseudo-first order rate constant (Vmax/Km) for Ala, Gly, Gln, Lys and Leu uptake decreased as a result of cafeteria diet-induced obesity. The Kd value for Ala, Gly, Gln and Glu decreased and that of Lys increased as result of obesity. These adaptations could, at least in part, explain alterations in amino acid distribution between blood cells and plasma related to overfeeding or obesity.
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PMID:Effect of diet-induced obesity on kinetic parameters of amino acid uptake by rat erythrocytes. 148 91


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