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

The metabolic and hormonal changes during a standard physical exercise were studied in healthy subjects and in insulin-dependent diabetics well matched for body weight, and therefore submitted to a similar work load in a physiologic range, and in obese subjects that, owing to their weight, faced a significant heavier work in the same environmental conditions. Moderate work load did not lead to significant changes in metabolic and hormonal blood parameters (blood glucose, FFA and glycerol; insulin, glucagon, growth hormone and cortisol) in healthy subjects. A similar substrate homeostatis was seen in insulin-dependent diabetics, that however showed marked hormonal alterations. In these subjects, indeed, higher levels of plasma glucagon and GH were reached during work and in the recovery phase. Obese subjects, submitted to a heavier work load, presented a marked increase in blood glucose and glycerol which agrees with high GH and cortisol levels, and a subsequent increment of IRI which corresponds to a normalization of blood glucose and glycerol. Obese subjects, therefore, show a normal sensitivity to work load. Considerations about the work load in everyday life are discussed.
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PMID:Metabolic and hormonal changes during exercise in healthy, diabetic and obese subjects. 45 17

The effect of intravenous injection of 0.1 I.U./kg insulin on blood glucose response and on lipolysis, induced by intravenous infusion of 0.2 microgram/kg - min norepinephrine, were studied in 12 normal subjects and 17 obese patients with normal 50 g oral glucose tolerance test and normal thyroid function. In the obese group the insulin-induced hypoglycemia during norepinephrine-infusion was significantly less than in normal subjects. Moreover, the inhibition of norepinephrine-stimulated FFA and glycerol-release by insulin was significantly less in obesity as compared with the non-obese group. It is concluded that in obesity the action of insulin is decreased both in carbohydrate metabolism and in lipolysis. These results provide arguments for the role of an impaired antilipolytic insulin effect in the pathogenesis of hyperinsulinism in obesity.
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PMID:[Effect of insulin on stimulated lipolysis in obesity with normal carbohydrate tolerance and unimpaired thyroid function]. 59 Feb 7

Effects of insulin (1 mU/ml) on diaphragms removed from older-obese (70--110 days, 350--520 g) male Sprague-Dawley rats were compared to responses on muscle removed from younger-lean (27--36 days, 80--150 g) animals. Insulin antagonism on glucose transport (2DG uptake), glucose uptake, glycogen synthesis, glycolysis (lactate production), and glucose oxidation was demonstrated in tissue from the older-obese rats. Extracellular water spaces (measured with inulin-H3) were significantly decreased in these tissue. To determine if insulin antagonism of glucose transport could be secondary to inhibition of a rate-limiting reaction in the Embden-Meyerhof pathway with a subsequent negative feedback on transport, both tissue levels of glycolytic intermediates and oxidation of intracellular lipids were measured. No free intracellular glucose was found in diaphragms from either group of rats. Levels of G-6-P, F-6-P, F-1, 6-diP, PEP, and pyruvate were all lower in muscle from the older-obese animals. Incorporation of C14-FFA into tissue TG was slightly, but significantly, lower in this same tissue. Oxidation of intracellular TG and PL was similar in the two groups. In conclusion, diaphragms from older-obese rats manifest insulin antagonism of glucose transport that is probably responsible for the diminished hormonal effect on glucose uptake and the intracellular pathways of glycogen synthesis, glycolysis, and glucose oxidation. This inhibition of insulin action cannot be accounted for by changes in glycolytic intermediates causing a negative feedback on transport or enhanced lipid oxidation and therefore should be considered primary. The relative effects of age and obesity will need to be evaluated in future studies.
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PMID:Primary insulin antagonism of glucose transport in muscle from the older-obese rat. 72 47

Colony-bred Wistar-rats develop obesity after long term feeding with a high-fat diet (50% fat, w/w). According to previous investigations a disturbed glucose tolerance after i.v. glucose load could be described for obese rats. Therefore, we measured peripheral IRI-concentrations before and after glucose stimulation in controls and fat-fed rats. In obese animals we observed a basal hyperinsulinemia in the dynamic phase of development of obesity. In controls and fatty rats, no differences in the peripheral insulin response to an i.v. glucose stimulation could be demonstrated, nor did we find indications of an impaired early insulin response in fatty rats. In accordance with the glucose tolerance study, obese rats in the dynamic phase showed lower FFA-levels (fasting state) and a slower decrease of FFA-concentrations after the glucose-induced insulin enhancement. Changing the feeding schedule at 20 weeks of age, e.g. feeding control diets to fatty rats for 4 weeks, reduced basal IRI-concentrations in these animals to control values. Assuming the secondary nature of the basal hyperinsulinemia in obese rats, our present results demonstrate that the observed impairment of glucose tolerance may be related to the peripheral insulin resistance of skeletal muscle and/or hypertrophied adipose tissue.
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PMID:Plasma concentrations of insulin and free fatty acids in dietary-induced obesity of Wistar-rats before and after glucose stimulation. 74 34

Studies of fat mobilization and transport are reported in six patients with the Prader-Willi syndrome. Two patients had carbohydrate intolerance. One of these had a low and the other an augmented insulin response to glucose challenge. Following challenge with glucose, three of the four nondiabetics had normal insulin responses or increased responses consistent with their obesity; the other nondiabetic had insulinopenia. Measurements of the effects of norepinephrine, insulin, glucose, and 5-methylpyrazole-3-carboxylic acid on plasma levels of FFA, glycerol, and ketones provide no evidence for abnormal regulation of mobilization of fat from adipose tissue. Measurements of plasma lipids and postheparin lipolytic activity are consistent with normal uptake of fat into adipose tissue, and normal fatty acid composition of adipose tissue gives no evidence for abnormal lipogenesis.
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PMID:The Prader-Willi syndrome. Regulation of fat transport. 89 39

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

The lipolysis induced by i.v. injection of caffeine (3 mg/kg body weight) has been investigated in 11 normal subjects and 18 obese patients with normal 50 g oral glucose tolerance test and normal thyroid-function. The pattern of blood-glucose and immunoreactive insulin (IRI) secretion were not influenced by caffeine in both groups. Both in the controls and obese group a significant response of FFA and glycerole were noted. In the obese group the caffeine-induced lipolysis was slightly higher as compared with controls. There are no differences in FFA-response between obese group and controls. The observations suggest that an impaired lipolysis is not a pathogenetic factor for development of obesity.
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PMID:[Lipid mobilization in obesity without carbohydrate intolerance. 2. Caffeine-stimulated lipolysis]. 100 10

Blood glucose, free fatty acid and insulin responses to oral glucose and the fasting serum lipids were measured in 3 groups: 32 non-obese (mean age: 47.5 years) and 9 obese (mean age: 84.5 years), male patients with coronary heart disease and 12 non-obese male controls (mean age: 46.5 years). The oral glucose tolerance tests were repeated after 3 years in 16 of the non-obese patients with coronary heart disease. The results were as follows: 1) Glucose tolerance was impaired in 19 of 32 non-obese patients (59.4%). There was a significant correlation between impaired glucose tolerance and hyperlipidemia (hypercholesterolemia and/or hypertriglyceridemia). 2) In obese patients FFA levels at 30, 60, and 120 min after oral glucose administration were significantly elevated and FFA decrease was delayed with a drop to minimum levels at 180 min. 3) The insulin response after oral glucose administration in the group of non-obese patients with normal glucose tolerance was similar to that of non-obese controls. In the group of non-obese patients with impaired glucose tolerance, serum insulin levels went up to normal levels, but the peak was delayed. The serum insulin levels in obese patients were significantly higher than those of controls of 0, 60, 120, and 180 min. After 3 years the change in insulin response to oral glucose was not related to anginal symptoms or ECG findings, but was related to body weight change in patients with minor changes in glucose tolerance. 4) The metabolic pattern in the non-obese group with impaired glucose tolerance resembled that of "mild diabetes" in delayed response of insulin and FFA, and mild hyperlipidemia. These findings suggest that obesity may contribute to hyperinsulinemia in patients with coronary heart disease and that impaired glucose tolerance observed in patients with coronary heart disease is in part due to "latent diabetes".
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PMID:Glucose tolerance, serum insulin and lipid abnormalities in patients with coronary heart disease. 118 89

1. In obese patients with normal glucose tolerance the norepinephrine-induced lipolysis in vivo was significantly higher as compared with a non-obese group. This was observed both during weight-related and constant norepinephrine infusion. 2. In the obese group a discordant release of free fatty acids and glycerol and a significantly lower quotient of FFA/Glycerol than in the controls was found. It is supposed that in obesity the re-esterification of FFA is increased.
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PMID:[Studies on lipid mobilization in obesity without glucose intolerance. 1st communication. Noradrenaline-stimulated lipolysis]. 121 97

The turnover rate of plasma FFA measured by constant infusion of albumin-complexed labeled palmitate in a group of 16 patients with Cushing's syndrome was significantly lower than in a group of 6 controls. Seven patients reexamined after correction of the hypercortisolism showed a normalization of the plasma FFA turnover rate. By contrast, 7 patients with simple obesity had a normal or increased plasma FFA turnover rate depending on the way this parameter is expressed.
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PMID:Depressed plasma FFA turnover rate in Cushing's syndrome. 124 92


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